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

Advanced Cell Technology, Inc. (ACT)(ACTC), a leader in the field of regenerative medicine, today issued a statement on the U.S. Appeals Courts ruling, upholding a lower courts dismissal of the case, Sherley v. Sebelius, 11-5241, U.S. Court of Appeals for the District of Columbia Circuit (Washington), on the permissibility of federal funding of embryonic stem cell research.

This court ruling should be of considerable benefit to ACT and our embryonic stem cell-based clinical programs, commented Gary Rabin, chairman and CEO. It effectively removes major speed bumps for the National Institutes of Health (NIH) in terms of approving the several stem cell lines that we have submitted for their consideration for funding. With Fridays decisive ruling, we expect that a number of our embryonic stem cell lines will be approved for funding in coming months.

Sherley v. Sebelius had sought to block the United States Health and Human Services Department and the NIH from spending federal funds for research with hESCs, contending that doing so would violate the Dickey-Wicker Amendment, a short rider attached to legislation passed in 1996.

This ruling removes a great deal of the ambiguity that has hampered legislative attempts to provide an efficient mechanism for federal funding of hESC research, continued Mr. Rabin. The path for legislators to enact such legislation has now been cleared, and in that case we are optimistic that there could be encouraging new developments in the legislative arena, as well, in coming months. We would certainly hope that our patented, proprietary embryo-safe single-cell blastomere technique would be a part of any such conversation. We feel that if we could educate more Americans about this technique, and how directly and effectively it addresses the various ethical objections to hESC research, that broad support for the technique and the field overall would quickly fall into place.

More commentary on Fridays court ruling will be posted today on Mr. RabinsChairmans blog.

About Advanced Cell Technology, Inc.

Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.

Forward-Looking Statements

Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words will, believes, plans, anticipates, expects, estimates, and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, protection of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the companys periodic reports, including the report on Form 10-K for the year ended December 31, 2011. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the companys management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. There can be no assurance that the Companys clinical trials will be successful.

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ACT Comments on U.S. Appeals’ Court’s Dismissal Ruling in Case Challenging Federal Funding of Embryonic Stem Cell ...

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NORTHRIDGE, CA and CAMBRIDGE, UNITED KINGDOM--(Marketwire -08/27/12)- Avita Medical Ltd. (AVH.AX), (AVMXF), (AVMXY), the regenerative medicine company, announced a brief summary of recent manufacturing improvements, a direct result of the combined efforts of R&D and Operations and implementation of the company's commitment to a Continuous Improvement Model.

Modifications and improvements in manufacturing have generated a reduction of greater than 33% in cost of goods of the company's products over the past 18 months. Recent manufacturing changes and product improvements will be yielding significant additional increases in margins in the near term. These include:

"The significant improvements to Avita's products and manufacturing process have yielded important and quantifiable benefits in product quality, increased margins and reductions in operating costs," said Dr. William Dolphin, CEO of Avita Medical. "Moreover, the new manufacturing ensures ready availability of the ReCell Enzyme, a critical factor as demand for ReCell grows worldwide.

"The company is committed to our Continuous Improvement model with tight control of our Quality and Manufacturing Systems a prerequisite for efficient operations. We look forward to announcing additional improvements as we continue to reach our key milestones."

ABOUT AVITA MEDICAL LTD.Avita Medical (http://www.avitamedical.com/) develops and distributes regenerative and tissue-engineered products for the treatment of a broad range of wounds, scars and skin defects. Avita's patented and proprietary tissue-culture, collection and application technology provides innovative treatment solutions derived from a patient's own skin. The company's lead product, ReCell Spray-On Skin, is used in a wide variety of burns, plastic, reconstructive and cosmetic procedures. ReCell is patented, CE-marked for Europe, TGA-registered in Australia, and SFDA-cleared in China. ReCell is not available for sale in the United States; in the U.S. ReCell is an investigational device limited by federal law to investigational use. A Phase III FDA trial is in process.

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Japanese scientists from the NIMS International Center for Materials Nanoarchitectonics (MANA) have developed a nanostructured sheets film capable of introducing designated genes into animal cells. The scientists also demonstrated the safety and efficacy of the new nanosheet film as a substrate for reverse gene transfection.

The methods of introducing genes into cells can be performed in liquids (solution-based) or on the surface of a solid substrate (solid phase gene transfection). In the solid phase gene transfection, DNA is fixed on the solid surface and then cells adhere on the DNA-bearing surface. The objective of the present research is to explore new solid substrates for the reverse gene transfection. This solid-mediated transfection has attracted attention due to the higher delivery efficiency of DNA than liquid phase transfection method. Different types of DNA are possible to arrange on a solid surface and introduce into cells. This technology is also effective in systematic analysis and profiling of the effects of genes.

Until now, an extracellular matrix called fibronectin, which is an animal-derived protein, or other similar substances, had been used as an accelerant in solid phase gene transfection. However, this approach had been considered problematic in clinical application situations, where the gene transferred cells are returned to the patient's body. Thus, the use of animal-derived substances has a serious concern from the viewpoint of safety, etc.

In the present research, the MANA researchers prepared a nanosheets film through a near-infinite number of nanoscale walls protruding from the surface. The film is composed of only inorganic silica without any animal sources. The MANA team found that genes can be introduced into cells with extremely high efficiency when fixing DNA on the nanostructured silica film and contacting with cells. Since an animal-derived supplements is not necessary, this should be a safe and simple solid phase transfection system.

This research result is applicable to gene therapy and offers a revolutionary gene introduction method. It is expected to make a valued contribution to gene therapy for hereditary diseases such as diseases of inborn error of metabolism, hemophilia, etc., and for intractable diseases such as diabetes and the like.

More information: pubs.rsc.org/en/Content/ArticleLanding/2012/CC/c2cc34289h

Provided by National Institute for Materials Science

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ScienceDaily (Aug. 27, 2012) Some of the body's own genetic material, known as small interfering RNA (siRNA), can be packaged then unleashed as a precise and persistent technology to guide cell behavior, researchers at Case Western Reserve University report in the current issue of the journal, Acta Biomaterialia.

The research group, led by Eben Alsberg, associate professor in the departments of Biomedical Engineering and Orthopedic Surgery, have been pursuing experiments that seek to catalyze stem cells to grow into, for example, bone and cartilage cells, instead of fat, smooth muscle and other cell types.

Beyond tissue engineering, the scientists believe that their technology could be used to starve a tumor by blocking growth of blood vessels that carry nutrition to a malignancy. Or the siRNA could bring on cancer cell death by interfering with other cellular processes.

siRNA is a short section of double-stranded RNA that inhibits gene expression. The molecule can jam up the machinery that produces specific proteins important to cell processes.

A current challenge to using siRNA to block growth of cancerous tumors or guide cell behavior in tissue engineering, is that the tiny material rapidly disperses when injected in the bloodstream or directly into target tissues.

Alsberg, Khanh Nguyen, a postdoctoral researcher, and Phuong N Dang a doctoral student here, packaged siRNA in a mix of polymeric materials. Under ultraviolet light, the mix is induced to form hydrogels connected by a network of polymer threads.

As the threads of the hydrogels break down, the siRNA molecules are cut loose to redirect the fate of the targeted cells. Ultimately, this system can be injected into a target tissue and application of light from outside the body will induce hydrogel formation.

"Local delivery helps target the siRNA to specific cell populations of interest, such as cancer cells in a tumor or stem cells in a bone fracture," Alsberg said. "The ability to alter cell behavior with siRNA can depend on the length of exposure time to the genetic material.

"We can tune the material properties so we can control the dose and rate at which cells are exposed to siRNA. This capacity may prove to be therapeutically valuable."

Tests showed the siRNA effectively interfered with a signal pathway of cells surrounding and inside the hydrogels over an extended period of time.

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ScienceDaily (Aug. 26, 2012) A team of scientists, including faculty at the University of Massachusetts Medical School (UMMS), have discovered a gene that influences survival time in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease). The study, published August 26 in Nature Medicine, describes how the loss of activity of a receptor called EphA4 substantially extends the lifespan of people with the disease. When coupled with a UMMS study published last month in Nature identifying a new ALS gene (profilin-1) that also works in conjunction with EphA4, these findings point to a new molecular pathway in neurons that is directly related to ALS susceptibility and severity.

"Taken together, these findings are particularly exciting because they suggest that suppression of EphA4 may be a new way to treat ALS," said Robert Brown, MD, DPhil, a co-author on the study and chair of neurology at UMass Medical School.

ALS is a progressive, neurodegenerative disorder affecting the motor neurons in the central nervous system. As motor neurons die, the brain's ability to send signals to the body's muscles is compromised. This leads to loss of voluntary muscle movement, paralysis and eventually respiratory failure. The cause of most cases of ALS is not known. Approximately 10 percent of cases are inherited. Though investigators at UMMS and elsewhere have identified several genes shown to cause inherited or familial ALS, almost 50 percent of these cases have an unknown genetic cause. There are no significant treatments for the disease.

Wim Robberecht, MD, PhD, lead investigator of the Nature Medicine study and a researcher at the University of Leuven in Belgium and the Vesalius Research Center, screened for genes in zebrafish that blunt the adverse effect of the ALS mutant gene SOD1. Through this process, his team identified EphA4 as an ALS modifier. Dr. Robberecht's team went on to show that when this gene is inactivated in mice with ALS, the mice live longer.

Dr. Robberecht then turned to UMass Medical School to confirm that turning off EphA4 in human ALS cells would slow the progression of the disease. Dr. Brown and his team identified two human ALS cases with mutations in the EphA4 gene which, like the zebrafish and the mice, had unusually long survival times. This suggests that blocking EphA4 in patients with ALS may be a potential therapeutic target in the future.

In an exciting, related development, a new ALS gene (profilin-1) identified last month by UMMS scientists works in conjunction with EphA4 in neurons to control outgrowth of motor nerve terminals. In effect, gene variants at both the top and the bottom of the same signaling pathway are shown to effect ALS progression. Together these discoveries highlight a new molecular pathway in neurons that is directly related to ALS susceptibility and severity and suggests that other components of the pathway may be implicated in ALS.

"It is exciting that these two studies identify the same pathway in ALS," said John Landers, PhD, associate professor of neurology and lead author of the PFN1 study. "Hopefully this discovery will accelerate efforts to finding a treatment for ALS."

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Public release date: 26-Aug-2012 [ | E-mail | Share ]

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, MA A team of scientists, including faculty at the University of Massachusetts Medical School (UMMS), have discovered a gene that influences survival time in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease). The study, published today in Nature Medicine, describes how the loss of activity of a receptor called EphA4 substantially extends the lifespan of people with the disease. When coupled with a UMMS study published last month in Nature identifying a new ALS gene (profilin-1) that also works in conjunction with EphA4, these findings point to a new molecular pathway in neurons that is directly related to ALS susceptibility and severity.

"Taken together, these findings are particularly exciting because they suggest that suppression of EphA4 may be a new way to treat ALS," said Robert Brown, MD, DPhil, a co-author on the study and chair of neurology at UMass Medical School.

ALS is a progressive, neurodegenerative disorder affecting the motor neurons in the central nervous system. As motor neurons die, the brain's ability to send signals to the body's muscles is compromised. This leads to loss of voluntary muscle movement, paralysis and eventually respiratory failure. The cause of most cases of ALS is not known. Approximately 10 percent of cases are inherited. Though investigators at UMMS and elsewhere have identified several genes shown to cause inherited or familial ALS, almost 50 percent of these cases have an unknown genetic cause. There are no significant treatments for the disease.

Wim Robberecht, MD, PhD, lead investigator of the Nature Medicine study and a researcher at the University of Leuven in Belgium and the Vesalius Research Center, screened for genes in zebrafish that blunt the adverse effect of the ALS mutant gene SOD1. Through this process, his team identified EphA4 as an ALS modifier. Dr. Robberecht's team went on to show that when this gene is inactivated in mice with ALS, the mice live longer.

Dr. Robberecht then turned to UMass Medical School to confirm that turning off EphA4 in human ALS cells would slow the progression of the disease. Dr. Brown and his team identified two human ALS cases with mutations in the EphA4 gene which, like the zebrafish and the mice, had unusually long survival times. This suggests that blocking EphA4 in patients with ALS may be a potential therapeutic target in the future.

In an exciting, related development, a new ALS gene (profilin-1) identified last month by UMMS scientists works in conjunction with EphA4 in neurons to control outgrowth of motor nerve terminals. In effect, gene variants at both the top and the bottom of the same signaling pathway are shown to effect ALS progression. Together these discoveries highlight a new molecular pathway in neurons that is directly related to ALS susceptibility and severity and suggests that other components of the pathway may be implicated in ALS.

"It is exciting that these two studies identify the same pathway in ALS," said John Landers, PhD, associate professor of neurology and lead author of the PFN1 study. "Hopefully this discovery will accelerate efforts to finding a treatment for ALS."

###

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Scientists identify new gene that influences survival in ALS

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ScienceDaily (Aug. 26, 2012) Two opposing teams battle it out to regulate gene expression on the DNA playing field. One, the activators, keeps DNA open to enzymes that transcribe DNA into RNA. Their repressor opponents antagonize that effort by twisting DNA into an inaccessible coil around histone proteins, an amalgam called chromatin, effectively blocking access to DNA by enzymes that elongate an RNA strand.

Both teams maneuver by chemically modifying histones -- the activators by decorating histones with acetyl groups -- let's call them green flags -- causing them to loosen their grip on DNA. The repressors retaliate by marking histones with red flags, often methyl groups, which call in de-acetylase enzymes to clip off the green flags, restore the chromatin barrier and end that round of gene expression. Disturbing this biochemical balance lies at the heart of many diseases, particularly cancer.

Recently, the lab of Jerry Workman, Ph.D., investigator at the Stowers Institute for Medical Research, reported in the journal Nature that a reserve of "pre-acetylated" histones sits on the chromatin sidelines ready to sub for histones whose green flags get clipped by repressors, a tactic aiding the activators called "histone exchange." In a companion study published in the Aug. 26, 2012 Advance Online Publication of Nature Structural & Molecular Biology the Workman lab now shows that a repressor called Set2 in yeast recruits a protein assistant to block the histone exchange. That study reveals a heretofore unknown mechanism to keep gene activation under control and ensure that erroneous transcription does not occur.

"Accurate gene expression is critical for normal cell function, and when this control is lost cells grow abnormally," says Workman. "These two studies identify mechanisms used by cells to regulate gene expression, which is important for our understanding of what goes wrong in diseases marked by unregulated cell growth, like cancer."

The study began when the group, in collaboration with Stowers proteomics experts Michael Washburn, Ph.D., and Laurence Florens, Ph.D., applied mass spectrometry analysis to identify any protein expressed in yeast Saccharomyces cerevisiae that bound to chromatin in regions patrolled by Set2. Those regions were readily apparent by the presence of Set2's red flag methyl group planted in a specific histone protein interacting with DNA.

"We knew that Set2 added this mark in the middle and downstream parts of genes to recruit de-acetylases," says the study's lead author Michaela Smolle, Ph.D., a postdoctoral researcher in the Workman lab. "But the proteomic search allowed us to cast a wide net for other proteins associated with that mark -- a bit like fishing."

Among the fish caught was a component of a yeast chromatin "remodeler" known as Isw1, providing circumstantial evidence that the Set2 red flag attracts Isw1 as well as de-acetylases. Additional genomic experiments evaluating the entire genome of a yeast mutant lacking Set2 supported that idea: not only were the red methyl flags missing but the chromatin landscape was devoid of Isw1 as well.

To assess Isw1's biological function the group exploited yet another yeast mutant, this one lacking the ISW1 gene itself. Microarray analysis of global transcription in ISW1 CHD1 mutants showed widely perturbed gene expression marked by aberrant expression of RNA snippets rather than complete transcripts. Biologists view the presence of such "cryptic transcripts" as indicators of cellular stress.

Analysis of acetylation and methylation patterns in chromatin of ISW1 mutants revealed the probable cause: mutants showed ramped up histone exchange activity marked by excessive levels green-flagged pre-acetylated histones along the length of many genes, a condition likely favoring initiation of truncated RNAs.

"Our work shows that the Set2 methylation mark plays two important roles to ensure that RNA transcription starts only at the beginning of the gene and not in the middle," says Workman. "On one hand, it recruits Isw1 to block incoming histones, and on the other it also recruits a deacetylase to remove any acetylation marks that might happen to have sneaked in."

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Controlling gene expression: How chromatin remodelers block a histone pass

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Newswise People who carry a G instead of an A at a specific spot in the sequence of their genetic code have roughly a six-fold higher risk of developing certain types of brain tumors, according to a study by researchers at the University of California, San Francisco and Mayo Clinic.

The study was jointly led by geneticists Margaret Wrensch, PhD, and John Wiencke, PhD, professors in the Department of Neurological Surgery at UCSF, and Robert Jenkins, MD, PhD, professor of Laboratory Medicine in the Department of Laboratory Medicine and Pathology and the Division of Laboratory Genetics at the Mayo Clinic. The findings, published on August 26, 2012 in the journal Nature Genetics, could help researchers identify people at risk of developing certain subtypes of gliomas, which account for about 4,600 of the 23,000 brain cancers newly diagnosed annually in the US.This information could lead to better surveillance, diagnosis and treatment.

Based on their findings, the scientists already are starting to think about clinical tests that could tell patients with abnormal brain scans what kind of tumor they have, by simply testing their blood.

Researchers still need to understand how the specific DNA change actually causes the tumors, said Wrensch, since this is among the first examples that a change in a non-coding portion of DNA can be so strongly associated with cancer risk.

The study began a few years ago when researchers started hunting for regions of the genome that might be associated with glioma development. They observed that a portion of chromosome 8 contained single nucleotide polymorphisms, or SNPs, that were associated with brain tumors. Then, Wrensch, Wiencke, Jenkins and their colleagues used a combination of sophisticated genomic techniques to search for the SNP that was causing brain tumors to form.

They honed in on seven candidates, including the SNP called rs55705857, which confers a relative risk for glioma approaching that seen with changes in BRCA1 for breast cancer.

Interestingly, this region was only found through the most laborious method used by the researchers next generation sequencing suggesting that experimental and mathematical shortcuts may miss such rare, highly potent gene variants, the authors say.

Wrensch and Jenkins found that having the G, or guanine, version of this SNP rather than the more common A adenine version was strongly associated with slower growing gliomas.

Understanding how this variant causes people to get these less aggressive, but still lethal, tumors will be extremely important, Wrensch said. It may eventually lead to methods to reverse the course of these tumors or possibly to prevent their formation.

As part of their work, the researchers compared the sequence of the gene variant throughout mammalian evolution and found that it has been conserved as far back as the platypus. Computer modeling indicated that the region may be a microRNA, a special kind of nucleic acid that controls the activity of genetic messages within cells. The modeling places the SNP within the functional part of the microRNA, suggesting that a change in genetic code from an A to a G could have significant consequences. The research team is investigating whether the microRNA actually exists, and what its functional implications might be.

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UCSF, Mayo Team Discovers Genomic Variant That Increases Risk of Some Brain Tumors

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Geneticists soon will be able to identify an unborn childs risk of developing chronic diseases later in life and possibly shed light on other traits, such as athletic ability and intelligence, medical experts say.

The source of such information probably will be the expectant mothers blood sample. For the first time, researchers recently extracted fetal DNA from a pregnant womans blood and examined the unborn babys genome.

The procedure prenatal whole genome sequencing is not yet available in the clinical setting. But some health professionals expect that pediatricians and family doctors soon will be sifting through sequencing results of infants and older children.

Key goals of the procedure are improving detection of serious genetic disorders before a child is born and helping create preventive care plans for conditions that young patients are at risk of developing as they age.

My instinct is this will be available certainly in the next decade, and probably sooner, said Benjamin E. Berkman, MPH, deputy director of the Bioethics Core at the National Human Genome Research Institute in Bethesda, Md.

But the medical community is not prepared to address the clinical challenges and ethical issues that probably will accompany the procedure, say some bioethicists and geneticists.

Such concerns could include physician uncertainty about which results to give to families and a potential rise in abortions due to parents worries about the comprehensive genetic findings, said an article in the July-August issue of The Hastings Center Report, a bioethics journal. Berkman is a senior author of the article.

The report calls for professional medical organizations to begin educating physician members about prenatal whole genome sequencing and how to discuss the procedure with expectant couples. Although the sequencing probably will be ordered by obstetrician-gynecologists, some patients might ask their primary care physicians about the procedure, health professionals say.

The report encourages the medical community to offer guidance on the types of genetic findings physicians should offer expectant parents. It also urges scientists to conduct more research into the kinds of information parents find relevant to reproductive decision-making and how health care systems should accommodate adoption of prenatal whole genome sequencing.

The tests are here, said New York geneticist Robert W. Marion, MD. Technology is going to advance, and the public is going to learn about this. The medical community cant sit back and wait for this to happen. We have to be very aggressive in getting the word out and training doctors in the significance of this procedure. Dr. Marion is chief of the divisions of genetics and developmental medicine in the Dept. of Pediatrics at the Childrens Hospital at Montefiore and the Albert Einstein College of Medicine in New York.

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Dr. Robert C. Green, an associate professor of medicine at Harvard, sees practical as well as ethical issues in trying to warn anonymous study subjects of disease risks. (Gretchen Ertl, The New York Times)

Dr. Arul Chinnaiyan stared at a printout of gene sequences from a man with cancer, a subject in one of his studies. There, along with the man's cancer genes, was something unexpected genes of the virus that causes AIDS.

It could have been a sign that the man was infected with HIV; the only way to tell was further testing. But Chinnaiyan, who leads the Center for Translational Pathology at the University of Michigan, was not able to suggest that to the patient, who had donated his cells on the condition that he remain anonymous.

Around the world, genetic researchers using tools that are ever more sophisticated to peer into the DNA of cells are finding things they were not looking for, including information that could make a big difference to an anonymous donor.

The question of how, when and whether to return genetic results to study subjects or their families "is one of the thorniest current challenges in clinical research," said Dr. Francis Collins, the director of the National Institutes of Health.

The federal government has made the issue a priority, spending millions of dollars on research on questions unique to this new genomics era.

Researchers are divided on what counts as an important finding. Some say it has to suggest prevention or treatment. Others say it can suggest a clinical trial or an experimental drug. Then there is the question of what to do if the genetic findings only sometimes lead to bad outcomes and there is nothing to do to prevent them.

"If you are a Ph.D. in a lab in Oklahoma and think you made a discovery using a sample from 15 years ago from a subject in California, what exactly are you supposed to do with that?" asked Dr. Robert C. Green, an associate professor of medicine at Harvard.

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Public release date: 26-Aug-2012 [ | E-mail | Share ]

Contact: Julie Robert julie.robert@muhc.mcgill.ca 514-934-1934 x71381 McGill University Health Centre

This release is available in French.

Vitamin B12 is essential to human health. However, some people have inherited conditions that leave them unable to process vitamin B12. As a result they are prone to serious health problems, including developmental delay, psychosis, stroke and dementia. An international research team recently discovered a new genetic disease related to vitamin B12 deficiency by identifying a gene that is vital to the transport of vitamin into the cells of the body. This discovery will help doctors better diagnose this rare genetic disorder and open the door to new treatments. The findings are published in the journal Nature Genetics.

"We found that a second transport protein was involved in the uptake of the vitamin into the cells, thus providing evidence of another cause of hereditary vitamin B12 deficiency", said Dr. David Rosenblatt, one of the study's co-authors, scientist in medical genetics and genomics at the Research Institute of the McGill University Health Centre (RI MUHC) and Dodd Q. Chu and Family Chair in Medical Genetics and the Chair of the Department of Human Genetics at McGill University. "It is also the first description of a new genetic disease associated with how vitamin B12 is handled by the body".

These results build on previous research by the same team from the RI MUHC and McGill University, with their colleagues in Switzerland, Germany and the United States. In previous work, the researchers discovered that vitamin B12 enters our cells with help from of a specific transport protein. In this study, they were working independently with two patients showing symptoms of the cblF gene defect of vitamin B12 metabolism but without an actual defect in this gene. Their work led to the discovery of a new gene, ABCD4, associated with the transport of B12 and responsible for a new disease called cblJ combined homocystinuria and methylmalonic aciduria (cblJ-Hcy-MMA).

Using next generation sequencing of the patients' genetic information, the scientists identified two mutations in the same ABCD4 gene, in both patients. "We were also able to compensate for the genetic mutation by adding an intact ABCD4 protein to the patients' cells, thus allowing the vitamin to be properly integrated into the cells," explained Dr. Matthias Baumgartner, senior author of the study and a Professor of metabolic diseases at Zurich's University Children's Hospital.

Vitamin B12, or cobalamin, is essential for healthy functioning of the human nervous system and red blood cell synthesis. Unable to produce the vitamin itself, the human body has to obtain it from animal-based foods such as milk products, eggs, red meat, chicken, fish, and shellfish or vitamin supplements. Vitamin B12 is not found in vegetables.

"This discovery will lead to the early diagnosis of this serious genetic disorder and has given us new paths to explore treatment options. It also helps explain how vitamin B12 functions in the body, even for those without the disorder," said Dr. Rosenblatt who is the director of one of only two referral laboratories in the world for patients suspected of having this genetic inability to absorb vitamin B12. Dr. Rosenblatt points out that the study of patients with rare diseases is essential to the advancement of our knowledge of human biology.

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26 August 2012 Last updated at 19:58 ET

A centre for research into genetics at Edinburgh University is to benefit from almost 60m of funding.

The money, from the Medical Research Council, will help scientists gain fresh insights into conditions such as cancer, arthritis, and schizophrenia.

The grants could also help doctors develop and deliver new tests and therapies for patients.

Edinburgh University said its Institute of Genetics and Molecular Medicine is already one of the largest in Europe.

The funding - paid over the next five years - aims to consolidate the IGMM's position as a world leader in genetics research.

Institute director, Prof Nick Hastie said: "The challenge we face is to work out how human genes work together to build a human.

"We also want to find out how subtle DNA differences help shape human diversity and influence susceptibility to a wide range of common diseases. This funding will help us to turn the potential of the genetic revolution into reality."

The money has been awarded to teams carrying out research on schizophrenia, cystic fibrosis, cancer, osteoarthritis and genetic eye disorders, amongst other conditions.

The IGMM is a partnership between the Medical Research Council, the University of Edinburgh's Centre for Molecular Medicine and Cancer Research UK.

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Funding boost for genetics centre

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Phosphorus Starvation Tolerance (PSTOL1) gene helps rice plants produce around 20 percent more grain. Credit: IRRI

In a discovery that could help boost food output across the globe, scientists have discovered a new gene that enables rice plants to produce more grain.

An international team of scientists has found the gene, Phosphorus Starvation Tolerance (PSTOL1), which helps rice plants produce around 20 percent more grain by increasing the uptake of phosphorus, a key plant nutrient. The gene helps rice grow a longer and better root system enabling it to gain access to more phosphorus.

"For many years we have searched for genes that improve phosphorus uptake," saidDr Sigrid Heuer, senior scientist at theInternational Rice Research Institute(IRRI).

Usually, farmers apply phosphorus fertilisers to increase productivity but on problem soils phosphorus often gets locked in the soil making it unavailable to plants. Now scientists have found the gene that helps grow rice plants even in low phosphorus soil. A study conducted on rice plants in Indonesia and the Philippines found that the PSTOL1 gene helps produce more grain evenin soil that has low phosphorus.

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During the experiment, scientists bred the rice with the PSTOL gene. The plants are not genetically modified but just bred using smart modern breeding techniques. Then they planted the rice in soil that is very low in phosphorus.

The study found that the rice bred with PSTOL gene produced about 20 percent more grain than rice without the gene.

ThePSTOL1gene is also being tested in rice varieties for more productive irrigated rice-growing areas and initial results show that the plants grow a better root system and yield higher production too. This means it could help farmers in these areas reduce their fertiliser use and expenditure without compromising productivity, according to a Eurekalert report.

Globally, more than 43.3 million tons of rice is produced. Despite this, an estimated five million children die due to starvation across the globe. The present discovery is expected to increase rice output significantly and fight hunger.

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Gene That Can Boost Rice Output Discovered by Scientists

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Race is everywhere in medicine. Mosthealth statistics are broken down by race. We routinely characterize diseases by which populations they affect more and less and medications by which ethnicities respond better or worse.

Its so ubiquitous that its easy to take for granted as justified. But the use of race in medicine is a subject that is vigorously debated. Whenever a new study comes out stratifying results by race, there are inevitably supporters and critics.

The question under debate: is there a place for race in medicine?

Theres a growing number who say we should toss this way of thinking entirely. Many scholars now contend that race is closer to a social construct than a biological category, and theres the legitimate fear that pointing out differences between races sends the message that the difference is biological. Even if there are certain genetic differences among populations, we know that self-reported race is at best a crude proxy for indicating them. Moreover, studies often do not adjust for all other variables besides genetics, such as socioeconomic status, culture, and discrimination meaning if differences are shown, the knee-jerk tendency to think biology might overshadow important environmental disparities that deserve our attention. There are social concerns too, in that historically ethnicity in research has been abused by pseudoscientists with racist agendas of demonstrating the superiority of certain people over others. In light of that history, profound sensitivity toward using race as a variable in medicine is understandable and warranted.

Part of the problem may be that some simply do not give it enough thought. There are some who stratify any data they collect on any health-related subject by race because thats what others did before them, along with others before that. But when you do any data analysis, you need to justify its being done. Theres no such thing as just laying out the facts because there is no such thing as a predetermined set of facts that we either expose or hide. We make choices with everything. Collecting, breaking down, and representing data all involve choices. When comparing groups, we can draw the lines wherever we want. Telling of this point is that many studies that talk about race still only compare blacks to whites, ignoring all other groups along with cases of mixed ancestry.

When the choice lies with the researcher, she has an obligation to use it responsibly. As such, its not enough to enough to justify a project with some ambiguous version of: this will contribute to the literature by showing something we do not know. We dont know infinite numbers of things. Research has to have value. At the forefront of every decision should be the questions: Whats the point? Are the differences Im trying to show relevant to anything? Are there implications for disease prevention, diagnosis, management, or treatment?

Sometimes, indeed the answer is yes. There have been cases where thinking about race, even as a rough guide, have led to benefits for patients. Knowing that sickle cell anemia is more prevalent among populations of sub-Saharan African ancestry can tip physicians off for earlier and thereby more effective diagnosis and management. Since Tay-Sachs is a genetic disease with increased prevalence among Ashkenazi Jews, Jewish communities early on welcomed genetic testing for prospective parents and by doing so dramatically reduced the incidence of the disease. Individuals of Asian descent are more likely to carry certain genetic polymorphisms resulting in slower drug metabolism meaning patients need lower doses to achieve the desired effects and avoid toxicity. There are many more examples. While it is such an important point that Ill say it again that race is only a very imperfect proxy for genetics there has been demonstrated medical value in being aware of these trends.

The reason is that medicine is a field that uses heuristics simple rules of thumb that help home in on best guesses when comprehensive searches are not feasible. These shortcuts are so frequently employed because medicine is the perfect storm of information overload combined with limited time. Best guesses in medicine are probabilistic; doctors collect clues from various sources to select more likely and less likely options. Every test, every new piece of information contributes to that ranking. Thus, some argue that just as doctors clue into best guesses based on a patients constellation of symptoms and test results, so too can race be used as an approximate guide. With the recognition that heuristics can lead to biases, the solution is not to discard them but rather to make doctors more cognizant of biases so they can work to eliminate them and use heuristics more effectively.

The use of race in medicine is a deeply sensitive issue and should be treated as such. One thing to note is that in contrast to shameful periods in history that focused on race with unethical agendas, the vast majority of current research is completely well-intentioned, toward the goal of optimally tailoring medical care to a diverse patient population. Those on both extremes of the debate are looking out for patients. So where does that leave us? While there is a place for race in medicine, the literature also remains rife with studies with seem to point out differences with no valid reason for pointing out differences, and my sense is that theres a greater tendency to overuse race when its not appropriate than to neglect it when it is. The burden should be on every medical researcher who wants to talk about race to be explicit as to what contribution this data would make to the world. And, if those measures fail, it would behoove readers and patients to apply just as critical an eye.

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When should medicine talk about race?

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Otago University Genetics Lecture 'Outdated' and Likely to Mislead

The University of Otago is being challenged to put caveats on claims made in its Genetics lectures, that international consumer concern over Genetically Modified food can be ignored.

The lectures based onresearch over ten years, claim our overseas customers won't care about GE in our food exports, and that there is no risk to Brand New Zealand from Genetically Engineered foods.One study also shows nuclear power stations, and intensive feed-lots are fine for our Brand and international reputation.

However, the claims are based on research that with hindsight is clearly flawed.

Work bya team led by Otago University Marketing lecturer Associate Professor John Knight, included running food stalls in different countries to test consumer acceptance of GE food, and interviewing first-time tourists on arrival in Auckland.

Much of the research was based on the assumption that a key consumer benefit would be that GE food will have fewer toxic chemical sprays than conventional crops. But data on chemical exposure are showing this to be the least likely outcome from GE foods over the past decade.

Another assumption was that consumer concerns for food safety were unfounded, and the result of media hype and scaremongering. The fact that Food Authorities had approved these foods as safe was taken as doctrine. Today scientists are warning of serious risks evidenced in peer-reviewed studies.

"These basic assumptions are now highly doubtful, which means the data is unreliable and could likely mislead decision-makers,"says Jon Carapiet, spokesman for GE-Free NZ in food and environment.

"The rosy picture painted that consumers don't mind GE is based on incomplete knowledge on the part of the consumer to make a reasonable judgement."

The research is also totally blind to Brand marketing:promoting New Zealand products as GE-free and meeting the highest organic standards for purity in the world, both of which fit our values and clean green image.

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Otago Uni Genetics Lecture Outdated and Likely to Mislead

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TORONTO, ON Stem cells hold great promise for treating and curing numerous diseases; however, a major challenge facing scientists is how to produce stem cells in the massive quantities required for clinical use. The McEwen Centre for Regenerative Medicine (McEwen Centre) and the University of Toronto-based Centre for Commercialization of Regenerative Medicine (CCRM) are partnering to establish a fund that will drive research in this area. Several University of Toronto regenerative medicine scientists are affiliated with CCRM and the Scientific Director is Dr. Peter Zandstra of the Institute of Biomaterials and Biomedical Engineering.

The McEwen Centre-CCRM Commercialization Impact Prize launches today, and will solicit innovative ideas from regenerative medicine scientists working in labs throughout the McEwen Centre. The winning team(s) will be awarded up to $600,000 to pursue research that will determine how to manufacture stem cells for clinical use and drug screening.

This private-public funding partnership is an important step forward to accelerating the advance of a discovery from a lab bench to the patient and onto the global market. Scientists at the McEwen Centre are making significant progress towards finding a cure for diseases such as Type 1 diabetes and heart disease. Collaborative partnerships are the key to discovering the cures sooner! says Rob McEwen, co-founder of the McEwen Centre, and Chief Owner, McEwen Mining.

Deadline for submissions is October 15, 2012. The Prize will fund up to two, 2-year projects that address the following challenges:

Making the transition from pre-clinical to clinical mass production; and, Scaling up stem cell manufacturing for high throughput drug screening.

Overcoming the scale-up and manufacturing challenge of stem cells would be a huge advancement for the regenerative medicine [RM] industry and this initiative fits in perfectly with our mandate to bridge the RM commercialization gap, explains Dr. Michael May, CEO of the Centre for Commercialization of Regenerative Medicine. Were very pleased to be working with the McEwen Centre, already a partner of ours, to make this happen.

The Commercialization Impact Prize budget template and application form can be found here: http://ccrm.ca/Commercialization-Impact-Prize or http://mcewencentre.com/ccrm

About McEwen Centre for Regenerative Medicine The McEwen Centre for Regenerative Medicine was founded by Rob and Cheryl McEwen in 2003 and opened its doors in 2006. The McEwen Centre for Regenerative Medicine, part of Toronto-based University Health Network, is a world leading centre for stem cell research, facilitating collaboration between renowned scientists from 5 major hospitals in Toronto, the University of Toronto and around the world. Supported by philanthropic contributions and research grants, McEwen Centre scientists strive to introduce novel regenerative therapies for debilitating and life threatening illnesses including heart disease, spinal cord injury, diabetes, diseases of the blood, liver and arthritis.

About Centre for Commercialization of Regenerative Medicine (CCRM) CCRM, a Canadian not-for-profit organization funded by the Government of Canadas Networks of Centres of Excellence program and six institutional partners, supports the development of technologies that accelerate the commercialization of stem cell- and biomaterials-based technologies and therapies. A network of academics, industry and entrepreneurs, CCRM translates scientific discoveries into marketable products for patients. CCRM launched in Torontos Discovery District on June 14, 2011.

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New partnership to drive mass production of life-saving stem cells - Commercialization Impact Prize is first of its ...

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NEW YORK (GenomeWeb News) The National Institute of Environmental Health Sciences plans to provide up to $3 million next year to fund research into how exposure to toxic chemicals in the environment affects gene expression.

In a new funding announcement, NIEHS said that it plans to fund grants with up to $400,000 next year that seek to define how environmental exposures affect proteins and other elements that govern gene expression patterns and chromatin states.

Exposure to toxicants that cause changes in gene expression and DNA methylation profiles can lead to diseases such as autoimmune and neurodevelopmental disorders and cancer. NIEHS has over the past decade been supporting projects that focus on exposures to toxicants such as arsenic, tobacco smoke, airborne particulates, and others.

The institute said it has already made "a significant investment" in research to identify epigenetic signatures of exposure, and now it wants to support studies that home in on how these exposures perturb proteins and processes that occur upstream of DNA methylation and other epigenetic marks.

The goal for this program is to begin to move beyond descriptive and correlative studies to understand the mechanisms involved in environmental exposure and gene expression.

Projects funded under this program may include, but are not limited to, research into chromatin accessibility and nucleosome positioning; the role of exposures in influencing the distribution, turnover, and positioning of nucleosomes; chromatin remodeling; the effects of exposures on non-coding RNA DNA/nucleosome binding; and studies that examine mechanisms involved in exposure related to the disruption of normal cis-regulatory functions.

Also under this funding program, the National Institute on Drug Abuse plans to fund one award of $400,000 for research that investigates the impact of drugs of abuse on chromatin. These projects will use high-throughput assays that can reveal changes in chromatin looping, 3D-chromatin structure, or interactions between non-coding RNAs with chromatin to study impacts of drugs such as nicotine, stimulants, opioids, abused prescription medicines, psychedelics, and others.

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NIEHS to Fund Studies of Toxic Exposure Impacts on Gene Expression, Chromatin

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A humble soil bacteria has become a genetically engineered factory capable of making fuel for cars. But the project still has to get out of the lab and scale up to industrial-size production.

The MIT project aims to make transportation fuels 10 times more efficiently than existing biofuels derived from living organisms. Researchers swapped out the genes of the R. eutropha bacterium so that it can create isobutanol an alcohol that can replace or blend with gasoline used by vehicles.

"We've shown that, in continuous culture, we can get substantial amounts of isobutanol," said Christopher Brigham, a biologist at MIT.

Many similar projects use microbes that make the biofuels within their bodies, so that researchers must kill the microbes to get the fuel out. But the MIT effort has succeeded in making the bacteria spit gasoline out into the surrounding liquid medium for easy harvesting.

The natural bacteria usually stores carbon by creating carbon polymers similar to petroleum-based plastics. Brigham and his colleagues Jingnan Lu, Claudia Gai and Anthony Sinskey managed to remove several genes while adding another organism's gene so that the bacteria made isobutanol rather than the carbon polymer.

For their next trick, the MIT researchers hope the genetically engineered bacteria could eventually transform carbon dioxide into fuel a way of using up the greenhouse gas that contributes heavily to global warming. The bacteria already naturally use hydrogen and carbon dioxide for growing.

Additional modifications could allow the bacteria to use carbon from sources such as agricultural field waste or city waste. The research received about $1.8 million from ARPA-E, the U.S. Department of Energy's research arm for high-risk, high-reward projects, from July 2010 until July 2013.

The MIT research is detailed in the August issue of the journal Applied Microbiology and Biotechnology.

Follow InnovationNewsDaily on Twitter @News_Innovation, or on Facebook.

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Genetic Engineering Has Turned Bacteria Into Fuel For Cars

Recommendation and review posted by Bethany Smith

NEW YORK, NY--(Marketwire -08/24/12)- A new shift in thinking about genetics could transform cancer treatment over the next five years, according to Kalorama Information. The healthcare market research publisher says therapies such as monoclonal antibodies may have competition from an unexpected source: changes in the genetic material that occur for reasons other than DNA base pair alteration. The finding was made in its recent report, "Epigenomics, Present and Future Applications for Pharmaceuticals and Diagnostics."

Epigenomics constitutes a challenge to the long-held paradigm of DNA base pair sequences as the prime determinant of the phenotype. Examples of such changes include DNA methylation and histone acetylation, both of which have been known for many years to cause changes in gene expression. The report says that drugs that target the epigenome offer a number of important advantages over other forms of cancer treatment; most notably they can be taken orally, saving the patient discomfort, cost and inconvenience. They are also more focused specifically against their target.

"Rather than blasting away machine gun style at the malignancy, they aim at a very specific reaction site within the cell," said K. John Morrow, Jr., PhD, Kalorama analyst and author of the report. "So far their side effects have proven to be relatively minor."

The report says that while epigenomic therapeutics have been around for a while, a raft of new clinical trials are in progress, and with any luck the next few years will see a number of FDA approvals for these agents. There are already FDA-approved epigenetic anti-cancer drugs available, such as azacytidine, and trials are underway that combine a non-epigenetically-based drug with one of the compounds under evaluation.

Perhaps the only concern to companies wishing to pursue the Kalorama recommendation is the competition, the fact that so many of the major pharmaceutical and biotech players are already building vigorous epigenomics programs. These programs include investigations into epigenomic mechanisms that engage cardiovascular disease and neurological dysfunction. Some may see these as non-cancer-related but they are. It is known that flexible epigenomic parameters exist that can change gene expression under external influences, while endowed with the ability to stably propagate these modifications from one generation to the next.

"At present the major pharmaceutical companies are faced with a downward spiral of profitability," Morrow said. "Epigenomic technologies represent an escape from this corrosive cycle of greater and greater R&D expenditures and poorer and poorer yields of FDA-approved pharmaceuticals."

Kalorama Information's report, "Epigenomics, Present and Future Applications for Pharmaceuticals and Diagnostics," has an extensive survey of information on market forecasts and company activities in the marketplace.

About Kalorama InformationKalorama Information, a division of MarketResearch.com, supplies the latest in independent medical market research in diagnostics, biotech, pharmaceuticals, medical devices and healthcare; as well as a full range of custom research services. We routinely assist the media with healthcare topics. Follow us on Twitter, LinkedIn and our blog.

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Highly-Targeted Epigenomic Treatments May Change Cancer Therapy

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MOBILE, Alabama -- A few years ago, Ronny Laird was perpetually exhausted after work. He was having a hard time losing weight and sometimes felt mentally fuzzy. The 46-year-old embarked on a stringent fitness routine to jump-start his system.

"I was working out and wasn't getting a lot of results," he said, explaining he was struggling to build muscle mass.

A friend told him about Larry Brock, a board-certified regenerative medicine doctor in Mobile who works to balance hormone levels, among other things, as a way to achieve optimum health.

Ready to feel better, Laird made an appointment. After extensive blood tests and other diagnostic exams, Laird found out his testosterone level was below normal. He also had high cholesterol and vitamin deficiencies. Laird started taking hormone shots soon after, and various supplements as directed by Brock.

"There is such a big difference in your energy level and your alertness when you are taking testosterone," said Laird. He continues to give himself an injection of the hormone every five days.

"I just know this works well for me."

Brock, a former surgeon specializing in cancers of the head and neck before an injury to his hand left him unable to operate, said he was intrigued by the tenets of regenerative medicine. After a fellowship and more training, he opened his practice in west Mobile in 2001.

While he doesn't accept private insurance, Brock's cash-only business has grown in recent years so much that he's hired another doctor and is working to bring in several others, he said.

Regenerative medicine, he said, examines the scientific research of what causes illnesses, aging and the decline in physical and mental function as people age.

Brock offers men and women individualized plans to improve health by hormonal balancing using bio-identical hormone therapy and metabolic support of chronic diseases, including cancer, cardiovascular disease and diabetes.

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Patients seeking out regenerative medicine and hormone therapy

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Featured Article Academic Journal Main Category: Bones / Orthopedics Also Included In: Stem Cell Research Article Date: 24 Aug 2012 - 0:00 PDT

Current ratings for: Osteoporosis Clue Found In Stem Cell Signalling Protein

3 (2 votes)

These are the implications of a new study led by Harvard Medical School (HMS) that was published online in The Journal of Clinical Investigation on 13 August.

Senior author Bjorn Olsen, Hersey Professor of Cell Biology at HMS, told the press about what they found:

"It shifts the thinking about what controls the differentiation of stem cells to bone cells instead of fat cells, and how to make sure this mechanism stays active with aging."

Bone is not a dead material: it is living tissue that is changing all the time, as it is continuously formed and reabsorbed.

Osteoporosis is a common bone disease where bone tissue becomes progressively thinner, resulting in higher risk of fracture. It affects about 1 in 5 American women and is thought to be caused by stem cells that normally differentiate into bone-forming cells becoming fat cells instead over time.

For the study, Olsen, who is professor of developmental biology and dean for research at Harvard School of Dental Medicine, and colleagues, decided to investigate the role of vascular endothelial growth factor, or VEGF, a common signalling protein that plays a key role in the development of blood vessels that are important in early bone growth and skeletal maintenance in mammals. The protein works by activating receptors on the surface of cells.

Soon after they were born, the mice's skeletons began to show osteoporosis-like qualities, such as reduced bone tissue and a build up of fat in the bone marrow.

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Osteoporosis Clue Found In Stem Cell Signalling Protein

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SILVER SPRING, Md. and SINGAPORE, Singapore, Aug. 24, 2012 (GLOBE NEWSWIRE) -- Nuvilex, Inc. (OTCQB:NVLX), an international biotechnology provider of cell and gene therapy solutions, announced today that Dr. Robert F. Ryan, President and CEO of Nuvilex, is in Asia and Singapore this week for numerous meetings with the Executives and staff of its wholly-owned subsidiary, Austrianova Singapore (ASPL), as well as other companies and groups in the region.

In addition to specific work with Dr. Walter Gunzburg, ASPL Chairman, and Dr. Brian Salmons, President and CEO of ASPL, and the other ASPL executives and staff regarding Nuvilex's pancreatic cancer treatment, other avenues for the development of Nuvilex and its Cell-in-a-Box(R) live cell encapsulation technology have been discussed.

Since his arrival Tuesday, management has been working closely together discussing possible partnerships with other entities regarding the use of the cell encapsulation technology, a major combined effort for the company. Meetings in Beijing and Singapore have included discussions with previous partners of ASPL regarding potential business opportunities.

In commenting upon his effort in Singapore, Dr. Ryan stated, "These meetings, especially those with the staff of the recently-acquired subsidiary, Austrianova Singapore, have been both timely and crucial as Nuvilex progresses in the biotechnology arena. It's important to establish and solidify the link between our two companies and staff and to ensure a seamless integration of ASPL into Nuvilex for the benefit of all of our staff and future. This is turning out to be a fantastic experience and I believe much will be gained from my visit."

About Nuvilex

Nuvilex, Inc. (OTCQB:NVLX) is an international biotechnology provider of live therapeutically valuable, encapsulated cells and services for research and medicine. A great deal of work is ongoing to move Nuvilex and our Austrianova Singapore subsidiary forward. More information is anticipated to be coming regarding Dr. Ryan's ongoing travel for the Company. Our company's clinical offerings will include cancer, diabetes and other treatments using the company's cell and gene therapy expertise and live-cell encapsulation technology.

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

Safe Harbor Statement

This press release contains forward-looking statements described within the 1995 Private Securities Litigation Reform Act involving risks and uncertainties including product demand, market competition, and meeting current or future plans which may cause actual results, events, and performances, expressed or implied, to vary and/or differ from those contemplated or predicted. Investors should study and understand all risks before making an investment decision. Readers are recommended not to place undue reliance on forward-looking statements or information. Nuvilex is not obliged to publicly release revisions to any forward-looking statement, reflect events or circumstances afterward, or disclose unanticipated occurrences, except as required under applicable laws.

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Nuvilex's President and CEO in Singapore for Meetings With Its Subsidiary Austrianova Singapore

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Public release date: 24-Aug-2012 [ | E-mail | Share ]

Contact: Kim Polacek kim.polacek@moffitt.org 813-745-7408 H. Lee Moffitt Cancer Center & Research Institute

Researchers at Moffitt Cancer Center and colleagues have identified PHF20, a novel transcriptional factor, and clarified its role in maintaining the stability and transcription of p53, a gene that allows for both normal cell growth and tumor suppression. PHF20, the researchers found, plays a previously unknown and unique role in regulating p53.

When p53 is activated, it can mend DNA damage and eliminate cancer cells by binding to DNA. How p53 maintains its basal level and becomes activated remain elusive, but identifying transcription factor PHF20 and understanding its interaction with p53 and its induction of p53 protein stability and transcription has provided a clue.

Results of their research appeared in a recent issue of Nature Structural & Molecular Biology and also in The Journal of Biological Chemistry.

"When a cell undergoes alterations that predispose it to become cancerous, p53 is activated to either mend the DNA damage or eliminate the affected cells, thereby preventing the development of tumors," said Jin Q. Cheng, Ph.D., M.D., a senior member of the Molecular Oncology Department and Molecular Oncology and Drug Discovery Program at Moffitt. "A number of mechanisms normally keep a regulatory strong check on p53 and allow for rapid activation. Still much is unknown about the mechanism of p53 regulation."

After identifying PHF20 as a novel transcriptional factor, the researchers set out in subsequent studies to probe the function of human PHF20 and its effect on p53. They found that PHF20 not only transcriptionally induces p53 but also directly interacts with and stabilizes p53. Akt negatively regulates these processes by interaction and phosphorylation of PHF20.

To determine whether the absence of PHF20 might regulate stress-induced p53 expression, the researchers "knocked down" PHF20. In doing so, they demonstrated that in the absence of PHF20, p53 was reduced. These findings established the role of PHF20 as a key regulator of p53 and additional link between Akt and p53.

According to Cheng, the identification of PHF20 as a regulator of p53 is significant because PHF20 "participates in simultaneous multiple interactions with other proteins and DNA" and serves to stabilize and induce p53.

"Regulation of p53 is critical to allow both normal cell growth and tumor suppression," explained Cheng. "However, further investigation is required to understand PHF20 tumor suppressor function and its possible involvement in human malignancy."

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Moffitt Cancer Center researchers and colleagues identify PHF20, a regulator of gene P53

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August 23, 2012

Brett Smith for redOrbit.com Your Universe Online

In a discovery that could have major implications for the worldwide food supply, scientists at the International Rice Research Institute (IRRI) in the Philippines have identified and leveraged a gene that allows rice to thrive in nutrient deficient soil.

According to their report published this week in the journal Nature, the researchers were able to improve test yields of rice planted in the Philippines, Japan, and Indonesia by 20 percent.

We found a gene that enhances phosphorus uptake in low phosphorus conditions. We have been looking for it for many years, said lead author Sigrid Heuer.

The gene, phosphorus-starvation tolerance 1 (PSTOL1), was first identified in the Kasalath rice variety that is native to India and grows well in soils low in phosphorus. About a decade ago, scientists identified one or more genes in the plant that allowed it to grow successfully in these scarce conditions. Because of the complexity of the genetic mechanism that imparts this unique ability to the Kasalath plants, it took the IRRI team three years to identify the specific gene responsible.

Heuer and his team were able to isolate and breed the gene through cross-pollination, an important distinction for those against using genetic engineering techniques on food products. Advocates of genetic technology say using traditional pollination techniques can translate into years or even decades of testing before a new strain reaches the market.

The PSTOL-1 gene enables developing rice plants by maximizing their roots extraction of phosphorus from the soil. Successful breeding to the gene would reduce the dependence on phosphorus-rich fertilizer in poorer sections of Asia that are known to have nutrient deficient soil.

Because many plant roots are only able to extract a tiny amount of phosphorus from the soil, farmers around the world spread phosphorus-based fertilizer on their fields. In poorer countries, this solution is often too costly, resulting in less than optimal yields when the plants mature. In wealthier countries, more robust rice plants would need less fertilizer, meaning lower costs and less damaging phosphate runoff into the water table.

Fifty percent of worlds arable land is too low in phosphorus. Its not like if you have this gene that the plants dont need phosphorus anymore, Heuer told Tan Ee Lyn of Reuters.

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Rice Gene Allows Crop To Thrive In Nutrient Deficient Soil

Recommendation and review posted by Bethany Smith

By Michelle Fay Cortez - 2012-08-23T04:01:00Z

Scientists using rapid genetic testing to track the path of a deadly bacterium in a Maryland medical center discovered unsuspected ways pathogens can spread and learned a new tool to combat hospital-acquired infections.

The DNA screening allowed staff at the National Institutes of Healths research hospital in Bethesda, Maryland, to link infections with a multidrug resistant strain of Klebsiella pneumoniae weeks after the first case was found, even though there were no obvious ties among the patients. Uncovering the way the bacteria moved silently though the hospital for weeks confirmed an outbreak was under way and prompted aggressive measures to control the pathogen that infected 18 people.

This has changed the practice of medicine in our hospital and we hope it will change the way other hospitals would control a similar outbreak, said Julie Segre, a senior investigator at the National Human Genome Research Institute.

Advances in genetic sequencing allowed researchers to map minute differences in the DNA of the bacterium in less than a week, proving all 18 cases began with a single patient in June 2011.

The first patient, a 43-year-old New York woman, was isolated as soon as she arrived at NIHs 243-bed hospital in Bethesda. Infection-control procedures, such as gloves and gowns for all staff and visitors, were used to contain the dangerous bacteria.

The effort was unsuccessful. Seventeen other patients subsequently fell ill, at an alarming rate of one a week. Eleven people died, six from K. pneumoniae and five from underlying diseases that were exacerbated by the bacteria, which evaded all commonly used antibiotics, including carbapenem, one of the most potent germ-killers.

Its an emerging pathogen, but weve never had a patient with it in our hospital or in this area that we were aware of, Segre said.

Hospital-acquired infections arent new, occurring in more than 1 million patients each year in the U.S. The mystery of the K. pneumoniae case, detailed yesterday in the journal Science Translational Medicine, arose because the second case of infection didnt emerge until three weeks after the first patient was treated and discharged. The bacteria turned up in a trachea of an immune-compromised patient, who had never been in the same hospital ward as the woman from New York.

After the first patient was released, we did routine surveillance to see if anyone in the hospital was exposed and the tests came back negative for weeks, Segre said. On August 5, we got our second patient with a Klebsiella infection. We were stunned.

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Gene Detectives Find New Tool to Contain Deadly Bacteria

Recommendation and review posted by Bethany Smith