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Healthier orange juice could be the result of British scientists seeing red.

Researchers hope to turn ordinary fruit into blood oranges by manipulating their genes.

The distinctive red pigment is believed to have health benefits which include combating obesity and heart disease.

One recent study found that drinking blood orange juice with a full English breakfast reduced the harmful effects of a fat-laden fry-up.

Scientists writing in The Plant Cell journal described how they identified the "ruby" gene that makes the blood orange red. They also discovered how the gene is activated, raising the possibility of switching it on in ordinary "blond" orange varieties.

Blood oranges need a period of cold as they ripen and currently the only place where they can be reliably grown on a commercial scale is in the foothills of Mount Etna in Sicily in the Mediterranean. As a result, blood orange juice is hard to come by and a carton costs about 1 more than ordinary orange juice.

Professor Cathie Martin, who led the research team from the John Innes Centre in Norwich, said: "Blood oranges contain naturally occurring pigments associated with improved cardiovascular health, controlling diabetes and reducing obesity.

"Our improved understanding of this trait could offer relatively straightforward solutions to growing blood oranges reliably in warmer climates through genetic engineering."

A test batch of genetically created blood oranges is currently being grown in Valencia, Spain.

Speaking at a press conference in London, Prof Martin said: "Hopefully in the near future, seven years down the line, we will have blood orange varieties which can be grown in the major orange growing areas like Brazil and Florida. So blood orange juice will become more available worldwide and the healthy properties enjoyed by more and more people."

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Gene for blood orange identified

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Published: March. 12, 2012 at 7:15 PM

ADELAIDE, Australia, March 12 (UPI) -- Australian researchers say they've bred salt tolerance into a variety of wheat, resulting in a 25 percent increase in grain yield in salty soils.

Using 'non-GM,' crop breeding techniques, scientists have introduced a salt-tolerant gene into commercial durum wheat, with field tests confirming the benefits to yield figures, the University of Adelaide reported Sunday.

"This work is significant as salinity already affects over 20 percent of the world's agricultural soils, and salinity poses an increasing threat to food production due to climate change," Commonwealth Scientific and Industrial Research Organization scientist Rana Munns said.

While domestication and breeding have narrowed the gene pool of modern wheat, leaving it susceptible to environmental stress, wild relatives of modern-day wheat remain a significant source of genes for a range of traits including salinity tolerance, the researchers said.

A salt-tolerant gene in an ancestral cousin of modern-day wheat, Triticum monococcum, has been introduced into modern commercial durham wheat, they said.

"Salinity is a particular issue in the prime wheat-growing areas of Australia, the world's second-largest wheat exporter after the United States," Adelaide researcher Matthew Gilliham said.

"With global population estimated to reach 9 billion by 2050, and the demand for food expected to rise by 100 percent in this time, salt-tolerant crops will be an important tool to ensure future food security."

While durham what is used mainly for foods like pasta and couscous, the researchers said they've now crossed the salt-tolerance gene into bread wheat and are beginning field trials.

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Wild gene makes wheat crops salt-tolerant

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A drug found to slow some of the physical problems and reduce the number of flareups of multiple sclerosis (MS) could also show promise for treating spinal cord injuries, according to a new Japanese study.

Researchers from the Jichi Medical University School of Medicine and the Universisty of Tokyo's Graduate School of Medicine found that FTY720, also known as Gilenya, helped mice with spinal cord injuries (SCIs) recover some motor function when they were given the drug immediately after the injuries.

FTY720 acts in a number of ways, the study authors wrote. The drug, provided by its manufacturer, Novartis, for this study, suppresses the immune system, which reduces inflammation that occurs after injuries. Inflammatory effects, they explained, can worsen the damage done by SCIs. The drug also helped the mice's damaged tissue regenerate, among other effects.

"The main biological activity responsible for these actions is believed to be immunological, but our data suggest that nonimmunological role(s) of FTY720 are also important in the treatment of SCI," they wrote.

The drug still needs to be evaluated in larger animals before determining whether it is effective in treating SCIs, but still has promise, the authors added.

Experts not involved with the study, however, are a bit more skeptical. Many interventions work in mice, so determining the utility of Gilenya for SCIs in humans is a long way off, if it happens at all.

"Another issue is that in this study, the drug was given immediately after the SCI, and rarely do we have the opportunity to give a drug immediately after this type of injury in humans," said W. Dalton Dietrich, professor and scientific director of the Miami Project to Cure Paralysis at the University of Miami's Miller School of Medicine. "One big question is if the drug delivery is delayed, will it work?"

Studies have found that in some people, the steroid drug methylprednisolone has been effective at restoring a little bit of function if given within eight hours of injury.

But other drugs -- mostly experimental -- that clinicians have tried with post-SCI patients have not been particularly effective.

"Acutely, we really don't have any drugs to try to protect the nervous system," said Dr. Bruce Dobkin, director of the Neurologic Rehabilitation and Research Program at UCLA's Geffen School of Medicine. "The most important thing is rehabilitation."

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Could MS Drug Treat Spinal Cord Injuries?

Recommendation and review posted by sam

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

Contact: David Sampson ajpmedia@elsevier.com 215-239-3171 Elsevier Health Sciences

Philadelphia, PA, March 13, 2012 A new study suggests that administering FTY720, an oral drug that has shown promise in trials for human multiple sclerosis, significantly improves locomotor recovery in mice with spinal cord injury (SCI). The research suggests a possible new avenue to counteract the degeneration of the spinal cord in human SCI. The study will be published in the April 2012 issue of The American Journal of Pathology.

Beyond the initial tissue damage, much of the degradation of the spinal cord in SCI is due to a cascade of secondary injuries, including neuronal and glial apoptosis, inflammation, glial scar formation, local edema and ischemia, and oxidative stress. The aim of current SCI treatment is to counteract the mechanisms of secondary injury and prevent their pathological consequences, because central nervous system (CNS) neurons have very limited capacity to self-repair and regenerate.

Researchers from the Jichi Medical University School of Medicine and the Graduate School of Medicine at the University of Tokyo had previously shown that the concentration of the lysophospholipid mediator, sphingosine 1-phosphate (S1P), was significantly increased in the location of a contusion injury, triggering the migration of neural progenitor/stem cells to the site of the injury. They hypothesized that targeting S1P receptors may become a candidate therapy for various refractory central nervous system disorders, including SCI.

FTY720 acts as a broad S1P receptor modulator. Its efficacy in central nervous system disorders is believed to derive from immunomodulation. Researchers found that orally administering FTY720 to mice shortly after contusion SCI significantly improved motor function recovery. Importantly, they found that the therapeutic effects of FTY720 were not solely dependent on immune modulation. The administration of FTY720 induced lymphopenia, clearing lymphocytes from the blood, and reduced T-cell infiltration in the spinal cord. But it did not affect the early infiltration of neutrophils and activation of microglia, and it did not reduce plasma levels and mRNA expression of inflammatory cytokines in the spinal cord. Tests in mice with severe combined immunodeficiency (SCID mice) with SCI found that FTY720 significantly improved recovery of hind limb motor function.

"These data clearly indicate the importance of immune-independent functions of FTY720 in the amelioration of functional deficits after SCI in mice," explains lead investigator Yoichi Sakata, MD, PhD, Research Division of Cell and Molecular Medicine, Center for Molecular Medicine, Jichi Medical University School of Medicine.

Dr. Sakata notes that S1P receptors exist in many types of cells and play a role in many cellular processes. "We observed that FTY720 decreased vascular permeability and astrocyte accumulation in injured spinal cord. These changes were also noted in SCID mice, suggesting they are not dependent on lymphocyte function. Increased vascular permeability can lead to destruction of the blood-brain barrier in spinal cord, and astrocyte accumulation is the main cellular component of glial scar after CNS injury. FTY720 might counteract these secondary injuries and thereby prevent their pathological consequences."

"Our data suggest that targeting S1P receptors with FTY720 is an attractive therapeutic approach for SCI," Dr. Sakata concludes. "However, further evaluation utilizing larger animals such as non-human primates will be necessary to confirm its efficacy in treating SCI. Further, strategies targeted at modulating the SIP concentration in injured CNS may lead to new therapeutic approaches towards repairing various CNS disorders."

###

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LOS ANGELES Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears today in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad stem cell research center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

The study in Cell outlined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression or output of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited and energy production was compromised, leading to stalled cell growth.

The findings from the current study provide a form of gene therapy for mitochondria by compensating for mutations that cause a wide range of diseases, said study co-senior author Koehler.

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Repairing mutations in human mitochondria

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

Contact: Sarah Jackson press_releases@the-jci.org 919-684-0620 Journal of Clinical Investigation

EDITOR'S PICK Restoring what's lost: uncovering how liver tissue regenerates

The liver is unique among mammalian organs in its ability to regenerate after significant tissue damage or even partial surgical removal. Laurie DeLeve and her colleagues at the University of Southern California in Los Angeles wanted to better understand which cells are specifically responsible for driving liver regeneration. A specialized cell type, known as liver sinusoidal endothelial cells, has generally been thought to promote regeneration of liver tissue. However, the DeLeve team suspected that stem cells and progenitor cells, which have the capacity to differentiate into mature cell types, might be responsible for stimulating liver regeneration by generating hepatocyte growth factor. Using a rat model system, they first identified the presence of stem and progenitor cells that give rise to liver sinusoidal endothelial cells in both the liver and the bone marrow. They next sought to determine which population of stem and progenitor cells are required for regeneration. DeLeve and colleagues found that the bone marrow-derived cells were not required for liver cell proliferation in the absence of damage. In contrast, following surgical removal of a portion of the rat liver, an infusion of bone marrow-derived progenitor cells was required for liver regeneration. These results improve our understanding of how liver tissue can regenerate following damage and may shed light on liver complications in patients with suppressed bone marrow tissue.

TITLE: Liver sinusoidal endothelial cell progenitor cells promote liver regeneration in rats

AUTHOR CONTACT: Laurie D. DeLeve University of Southern California Keck School of Medicine, Los Angeles, CA, USA Phone: 323-442-3248; Fax: 323-442-3238; E-mail: deleve@usc.edu

View this article at: http://www.jci.org/articles/view/58789?key=21e2857b21106f232595

ONCOLOGY New Determinant of Human Breast Cancer Metastasis Discovered

Researchers at the University of Kentucky's Markey Cancer Center in Lexington, KY have provided new insight as to why the most severe subtype of breast cancer in humans frequently metastasizes. Tumor cells can exploit a cellular program that promotes cell migration and reduces adhesion between cells to spread to distant sites in the body (metastasis). This cellular program, known as the epithelial-mesenchymal transition, is normally restricted to wound healing, tissue remodeling and embryonic development. Increasing cell motility requires a decrease in E-cadherin, which functions to promote cell-cell adhesion. Led by Binhua Zhou, the research team identified G9a as a major repressor of E-cadherin expression. They found that G9a interacts with Snail, which can repress gene expression, to modify the E-cadherin promoter and block expression of the E-cadherin gene. Their findings establish that G9a is an important determinant of metastasis in the most severe sub-type of breast cancer, and suggest the development of new therapeutics targeting this pathway could potentially disrupt the metastatic disease.

TITLE: G9a interacts with Snail and is critical for Snail-mediated E-cadherin repression in human breast cancer

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JCI early table of contents for March 12, 2012

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

Contact: Sarah Jackson sarah.jackson@the-jci.org 919-684-0620 Journal of Clinical Investigation

The liver is unique among mammalian organs in its ability to regenerate after significant tissue damage or even partial surgical removal. Laurie DeLeve and her colleagues at the University of Southern California in Los Angeles wanted to better understand which cells are specifically responsible for driving liver regeneration. A specialized cell type, known as liver sinusoidal endothelial cells, has generally been thought to promote regeneration of liver tissue. However, the DeLeve team suspected that stem cells and progenitor cells, which have the capacity to differentiate into mature cell types, might be responsible for stimulating liver regeneration by generating hepatocyte growth factor. Using a rat model system, they first identified the presence of stem and progenitor cells that give rise to liver sinusoidal endothelial cells in both the liver and the bone marrow. They next sought to determine which population of stem and progenitor cells are required for regeneration. DeLeve and colleagues found that the bone marrow-derived cells were not required for liver cell proliferation in the absence of damage. In contrast, following surgical removal of a portion of the rat liver, an infusion of bone marrow-derived progenitor cells was required for liver regeneration. These results improve our understanding of how liver tissue can regenerate following damage and may shed light on liver complications in patients with suppressed bone marrow tissue.

###

TITLE: Liver sinusoidal endothelial cell progenitor cells promote liver regeneration in rats

AUTHOR CONTACT: Laurie D. DeLeve University of Southern California Keck School of Medicine, Los Angeles, CA, USA Phone: 323-442-3248; Fax: 323-442-3238; E-mail: deleve@usc.edu View this article at: http://www.jci.org/articles/view/58789?key=21e2857b21106f232595

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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CARLSBAD, Calif.--(BUSINESS WIRE)--

International Stem Cell Corporation (OTCBB:ISCO.OB - News) http://www.internationalstemcell.com, a California-based biotechnology company focused on therapeutic, cosmetic and research products, announced today that it had obtained new capital financing and made important changes in the composition of its Board of Directors to ensure that Independent Directors hold the majority of Board seats.

The financing consists of $5 million in newly issued Series G Convertible Preferred Stock (without warrants), convertible into Common Stock at a conversion price of $0.40/share, the market price of the Companys Common Stock on the date the offer to purchase was made. This financing was made by AR Partners LLC, a healthcare investment firm owned by Dr. Andrey Semechkin, ISCOs CEO and Co-Chairman of the Board of Directors.

Concurrently with the closing of this financing, the Company elected to its Board of Directors Dr. James Berglund, co-founder of Enterprise Partners Venture Capital - one of the premier venture capital firms in the field of healthcare technology founded in 1985. Dr. Berglund, with his extensive professional experience, continues as an active participant in the biotech and healthcare industries. Dr. Berglund will replace Kenneth C. Aldrich, co-founder and former CEO of the Company during the period 2008-2009, who is stepping down as ISCO Board of Directors Co-Chairman. Although Mr. Aldrich is retiring from our Board, he will remain as one of ISCOs largest shareholders and an active consultant to the Board and executive management and will continue to represent the Company as Chairman Emeritus in a variety of public and private venues.

According to Mr. Aldrich, In my view, Dr. Semechkins willingness to commit such a significant amount of capital to ISCO at the market price of the Companys stock on the date of his offer represents a major vote of confidence in ISCOs future by its most senior executive. We are thankful to Dr. Semechkin for his support that will further advance ISCOs parthenogenetic stem cell-based therapeutic programs and income generating businesses.

Having a majority of independent directors on our companys Board represents an important step in ISCOs development and in transforming ISCO into a leading public company in the field of regenerative medicine.

I want to thank Mr. Aldrich for his long-standing dedication and continued involvement in guiding the Company, said Dr. Semechkin. This long-term investment, along with the new executive management team recruited over the previous twelve months, will provide ISCO with the necessary economic stability and resources to pursue its goals of consolidating our leadership position and accelerating our therapeutic programs, continued Dr. Semechkin.

About International Stem Cell Corporation

International Stem Cell Corporation is focused on the therapeutic applications of human parthenogenetic stem cells and the development and commercialization of cell-based research and cosmetic products. ISCO's core technology, parthenogenesis, results in the creation of pluripotent human stem cells from unfertilized oocytes (eggs). HpSCs avoid ethical issues associated with the use or destruction of viable human embryos. ISCO scientists have created the first parthenogenic, homozygous stem cell line that can be a source of therapeutic cells with minimal immune rejection after transplantation into hundreds of millions of individuals of differing genders, ages and racial backgrounds. This offers the potential to create the first true stem cell bank, UniStemCell. ISCO also produces and markets specialized cells and growth media for therapeutic research worldwide through its subsidiary Lifeline Cell Technology, and cell-based skin care products through its subsidiary Lifeline Skin Care. More information is available at http://www.internationalstemcell.com.

To subscribe to receive ongoing corporate communications, please click on the following link: http://www.b2i.us/irpass.asp?BzID=1468&to=ea&s=0.

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International Stem Cell Corporation Completes $5 Million Financing and Elects Jim Berglund to the Board of Directors

Recommendation and review posted by Bethany Smith

Published: March 12, 2012

(NEW YORK, NY, March 11, 2012) A study by Columbia researchers suggests that cells in the patients intestine could be coaxed into making insulin, circumventing the need for a stem cell transplant. Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

The researchconducted in micewas published 11 March 2012 in the journal Nature Genetics.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose. Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

Gut insulin cells express glucokinase, a key enzyme for glucose processing. Immunostaining detected insulin in red and glucokinase in green. Yellow marked merged colors.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed. Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels. If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, professor of medicine at Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells. Dr. Talchai, who works in Dr. Accilis lab, is a New York Stem Cell Foundation-Druckenmiller Fellow.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

Inactivation of Foxo1, a gene important for metabolism generated insulin producing cells in small intestines of newborn mice, as detected by immunofluorescence in red.Drs. Talchai and Accili found that when they turned off a gene known to play a role in cell fate decisionsFoxo1the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.

Our results show that it could be possible to regrow insulin-producing cells in the GI tracts of our pediatric and adult patients, Dr. Accili says.

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Columbia Researchers Find Potential Role for Gut Cells in Treating Type I Diabetes

Recommendation and review posted by Bethany Smith

London, Mar 12 (ANI): A new study conducted by scientists suggests a new approach that could give patients the ability to make their own insulin-producing cells without a stem cell transplant.

Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose.

Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed.

Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels.

If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai and Domenico Accili from Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

They found that when they turned off a gene known to play a role in cell fate decisions-Foxo1-the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.

Original post:
Gut cells transformed into insulin factories 'could help to treat type I diabetes'

Recommendation and review posted by Bethany Smith

I rarely post anything on space because I really dont know much more than the average reader of this weblog; no value-add from me. But yesterday I ran across an article which reported the financial overruns in the Mars Science Laboratory project. Today NASA said that the project will launch on schedule. It seems that to make this work theyll have to ax some other missions, though theyre putting a happy-face on their claims today (as if the money will magically appear in these strained financial times!).

Im very happy that the is all-go. Space exploration and science is something I really care about. I remember how angry I was when I saw a speech in Congress by representative Joe Kennedy II where he argued for the cutting of the NASA budget by suggesting that people were going hungry so that we could launch vehicles into earth orbit. I thought that was a low blow; after all, why doesnt Joe Kennedy and his clan divest themselves of their wealth and funnel it to organizations which aid the needy? Why dont obese & consumerist Americans start diverting their economic wealth to those in need, especially to places where malnutrition and hunger are endemic? Ive lived in very progressive & conscious locales where theres plenty of affluence and useless bling. Its more complicated than a simple trade-off between basic blue sky science and human necessities. Why do we continue to fund space science is something that cant be resolved through material utilitarian calculus; rather, it is an issue of values, dare I say, a matter of transcendence?* Those who support unmanned space exploration often gripe about the costs of the manned projects and their lack of basic science yield. But of course, that too is an issue of values. At the end of the day reasonable people can disagree. I accept that many humans do not share my fascination with space science, and appreciation of its fruits. In fact, it may be that my relative security in terms of basic necessities allow my head to be in the clouds. But, I would offer that all humans are in the clouds in some way. Even the poor in many developing nations give some of their meager income to religions and bow to social custom which demand that they take on debt so as to finance outrageous displays such as weddings for their children. I could ask why Joe Kennedy allowed children to starve so that he could afford ski trips to Aspen? And yet I am sure he could make a case for the joy and the intrinsic value of racing down a ski slope at incredible velocities. I dont begrudge him that. * I am not persuaded that the engineering byproducts of space exploration warrant the enormous cost. Zero gravity might be the ideal laboratory for some experiments, but the cost to attain zero gravity could probably be better allocated so as to the make the research in regular gravity more productivity.

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Mars Science Laboratory on schedule! | Gene Expression

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Enlarge Michelle Campbell/Birmingham News /Landov

Sunflowers in Birmingham, Ala.

Sunflowers in Birmingham, Ala.

I'm rounding out The Salt's impromptu Pest Resistance Week (which started with stories about weeds and corn rootworms) with a little-known tale that may scramble your mental categories.

You've heard about herbicide-resistant weeds (which farmers hate) and herbicide-resistant crops like Roundup Ready soybeans or corn (which farmers like). But here's a case the only one I know of in which a weed helped create a herbicide-resistant crop.

The story begins in 1996, in a soybean field in Kansas. The soybeans in this field were able to tolerate a class of weedkillers known as "ALS inhibitors." This line of soybeans had been created through "mutation breeding."

This technique involves exposing thousands of seeds to chemicals that cause genetic mutations. One of those mutations allowed the resulting soybean plant to withstand the herbicides. (Similar kinds of herbicide-tolerant wheat, rice, and other crops have been created using the same method.)

Among the soybeans in this Kansas field, however, a few weeds also survived after the farmers sprayed their herbicide. The weeds were native sunflowers, wild relatives of the sunflowers that farmers grow as a crop. (As I reported a few months ago, sunflowers are one of a very small handful of crops that originated in our part of the world.)

The farmer contacted Kassim Al-Khatib, who was then a weed expert at Kansas State University. Al-Khatib collected some of the surviving weeds from this field, did some tests on them, and confirmed that these sunflowers were indeed resistant to ALS inhibitor herbicides.

A few months later, through a chance encounter at a scientific meeting, word of this discovery reached Jerry Miller, a sunflower breeder at the U.S. Department of Agriculture's Sunflower Research Unit in Fargo, N.D. "I couldn't believe it. I called Kassim right away," recalls Miller. He saw the possibility of a herbicide-tolerant commercial sunflower created through traditional breeding, avoiding controversies over genetic engineering.

Originally posted here:
How A Sunflower Gene Crossed The Line From Weed To Crop

Recommendation and review posted by Bethany Smith

When men get stressed, their bodies get more revved up than women's. Now, two Australian researchers have a theory as to why and it all boils down to a single gene.

The classic "fight-or-fight" response to stress is controlled by the sympathetic nervous system the part of our nervous system that deals with automatic functions such as breathing. Under stress, this system goes wild, increasing heart rate and blood pressure, hastening breathing, and otherwise readying you to face down your enemy or to run.

But most of the research that established this fight-or-flight paradigm was done on men. About 12 years ago, researchers started to pull together evidence from that women don't respond to stress in the same way. In fact, they found, women do show a fight-or-flight response to immediate stress, but it's dampened by a tendency to "tend and befriend," or to seek out social support in stressful times.

Neuroscientist Joohyung Lee of Prince Henry's Institute of Medical Research in Melbourne, Australia, and his colleague Vincent Harley of Monash University in Melbourne now suspect that a Y-chromosome gene called SRY may be at the root of why men's response to stress is more aggressive than women's. [6 Gender Myths Busted]

The gene is known for its role in prenatal testes development; without it, the testes don't form. But new research has shown that SRY plays a role in the heart, lungs and brain. It's involved in the release of the neurotransmitter dopamine, which is crucial to movement. It also shows up in the adrenal glands, which secrete norepinephrine and epinephrine. All three chemicals are important in regulating how our bodies respond to stress.

This male-only SRY gene may "prime" the male body for a more aggressive stress response, Lee and Harley reported March 7 in the journal BioEssays. Their idea is still speculative. To find out if it's true, researchers will need to determine how SRY acts in the brain and in other tissues. They'll need to find out what happens when the SRY gene is blocked from being expressed. And they'll have to study other sex-linked genes to understand how they work in tandem with gonadal (sex) hormones, to create sex differences in the brain.

If their hypothesis is right, the researchers wrote, SRY could have medical implications. Disorders such as Parkinson's disease, autism, attention deficit/hyperactive disorder and schizophrenia are all more common in men than in women, and they all involve alterations in the body chemicals, such as dopamine, that the SRY gene influences.

"Better understanding the degree and nature of interactions between the sex-specific genes, gonadal hormones and epigenetic pathways will undoubtedly shed light on what predisposes men or women to certain behavioral phenotypes and neuro-psychiatric disorders," the researchers wrote.

You can follow LiveSciencesenior writer Stephanie Pappas on Twitter @sipappas. Follow LiveScience for the latest in science news and discoveries on Twitter @livescienceand on Facebook.

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Single Gene May Drive Men's Aggressive Stress Response

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A year after introducing the first pair of rare African black-footed kittens conceived through in vitro fertilization, the scientists at the Audubon Center for Research of Endangered Species in Algiers have announced the arrival of another kitten that, genetically, is their sister, and the first kitten of her type to be carried in the womb of a domestic cat. The same parents contributed to the frozen embryos that produced the two males born last year and this year's female.

A black-footed cat served as the surrogate mother for last year's litter. Researchers next sought to show that vastly more plentiful domestic cats can serve as surrogate mothers in efforts to save the small wild cat from extinction.

"Being able to use domestic cats adds another extra dimension to that, being able to produce more," said Earle Pope, acting director of the center. Only 53 of the cats, which are native to South Africa, live in zoo collections in the United States.

Domestic and African black-footed are different species of cat but members of the same group of felines. Their similar sizes and gestation lengths, Pope said, appear to be what made the pregnancy and birth physically possible even though the genetic makeup of the kitten differed from the mother.

"They're considered to be of the same lineage," he said. "Somewhere back a couple of million years ago, they're descended from the same ancestor."

The kitten, named Crystal, was born on Feb. 6 to domestic cat Amelie without any human assistance in the birth itself. It exhibits all the characteristics of a black-footed cat despite being nurtured by a domestic cat mother, Pope said.

"It's not changed genetically in any way," from other black-footed cats, he said. "It is totally a black-footed cat in behavior."

Researchers handle the kitten almost every day as they study it, but she remains decidedly unadapted to human contact.

"It just wants you to leave it alone and stay away from it," Pope said. "It gets along beautifully with the domestic cat mother. They don't know, or do not care, that it's a different species."

Scientists started gathering the genetic material that eventually created the kitten in 2003, when they collected and froze a sperm sample from a black-footed cat named Ramses that lived at a research center in Nebraska. In 2005, they thawed the sperm and combined them with eggs from Zora, a cat living at Audubon. That produced 11 embryos, which went into deep freeze.

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Audubon center in Algiers logs another breakthrough in genetic engineering of endangered cats

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The Los Angeles Times this week reports on a new UnitedHealth Group study that "estimates spending on genetic tests at $5 billion in the US in 2010," adding that it "could reach $25 billion within a decade." The LA Times says that the increasing availability of genetic tests and molecular diagnostics "offers the promise of earlier detection of disease and more personalized treatments that could wring substantial savings from the nation's $2.6 trillion-a-year healthcare tab." However, the LA Times adds, some "worry that those benefits may be outweighed by indiscriminate use of genetic testing."

The research arm of UnitedHealth surveyed physicians and patients on their attitudes toward genetic testing, and estimates that its members in private plans, Medicare, and Medicaid "spent $483 million on genetic tests in 2010, with 40 percent related to infectious diseases, 16 percent for cancer, and the rest for inherited disorders and other conditions." UnitedHealth also found that "more than half the 1,506 consumers surveyed were concerned about their physician's ability to know when a genetic test is needed and interpret it, the confidentiality of test results and about possible discrimination," the LA Times adds.

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Physicians, Patients Talk Genetic/MDx Tests

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On Feb. 28, European and American scientists, including Stanford School of Medicine genetics professor Carlos Bustamante, PhD, and senior research associate Peter Underhill, PhD, announced the sequencing of Otzis entire genome. It is the oldest human sample to undergo such an analysis. Postdoctoral scholars Andres Moreno-Estrada, PhD; Brenna Henn, PhD; and Martin Sikora, PhD, also worked on the study, which appeared in Nature Communications. High-throughput DNA sequencing was performed at Massachusetts-based Life Technologies Corp.

The sequence revealed some things impossible to learn by studying the body: the color of his eyes, for example, (brown) and the fact that he was likely lactose-intolerant. But more importantly, it also gave clues to where his ancestors lived and how humans may have migrated across Europe during the Copper Age, which started about 7,000 years ago. The answer surprised some people:

The Icemans ancestry most closely mirrors that of modern-day Sardinians, said Underhill, who, with Bustamante, came to the conclusion by analyzing the mummys Y chromosome. His lineage is very rare in mainland Europe only 1 percent or less share the same sequence but is rather frequent in northern Sardinia and southern Corsica.

Sardinia is the second-largest island in the Mediterranean Sea. It lies 120 miles west of Italys mainland and 7.5 miles south of the French island of Corsica.

Enlarge

The mummy of the Iceman is kept in a refrigerated cell in the South Tyrol Museum of Archaeology. Credit: South Tyrol Museum of Archaeology

Obtaining and sequencing DNA from such an ancient source was challenging. Ancient DNA, which has been exposed to the elements for thousands of years, is plagued by contamination both from the environment and anyone who has handled Otzi since his discovery, said Timothy Harkins, PhD, of Life Technologies who led the sequencing effort. To limit contamination, researchers used a long needle to tap the inner part of the femur.

As it was, the researchers obtained only about 20 nanograms of genomic DNA for sequencing, which is hundreds of times less than the amount usually used for whole-genome sequencing of modern-day samples. From this, the scientists were able to identify about 2 million unique sequence variants for population studies. One small variation on the Y chromosome pointed researchers to Otzis island heritage.

The finding suggests two scenarios: either the mummys ancestors were once more prevalent in mainland Europe than they are now (and some unknown selection process caused them to die off everywhere but the island strongholds), or they actively immigrated to the mainland from the island. Because there is little archeological evidence of the large, rapid population change required in the first possibility, the Stanford researchers favor the second.

Its thought that Sardinia was first peopled about 11,000 years ago by sedentary hunter-gatherers, said Underhill. Some samples of volcanic glass, or obsidian, found in mainland Italy and southern France have been shown to come from Mount Arci in Sardinia. This implies that there were episodes of trading between the island and mainland. If so, the mummys ancestors could have arrived in Europe as traders.

Link:
Genetic analysis of ancient 'Iceman' mummy traces ancestry from Alps to Mediterranean isle

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By a GenomeWeb staff reporter

NEW YORK (GenomeWeb News) Baylor College of Medicine's Medical Genetics Laboratory and Brazil's Dasa medical diagnostic laboratory announced on Friday an agreement to provide advanced genetic testing technology in that country.

Under the terms of the deal, Baylor's lab in Houston will conduct genetic testing and prepare a clinical report for Dasa, which will convey the results to the ordering physician in Brazil. The agreement also provides Dasa access to Baylor's database of clinical microarray results and access to Baylor's genetic research and diagnostic laboratory expertise, BCM said.

Luis Franco, assistant professor of molecular and human genetics at BCM, said in a statement that the collaboration is expected to create opportunities for technology transfer and the joint development of tests tailored to the Brazilian market.

Financial and other terms were not disclosed.

Dasa is Latin America's largest medical reference lab and the world's fourth-largest provider of diagnostic services, according to BCM.

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Baylor, Dasa Partner to Bring Genetic Testing to Brazil

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By Alex Nussbaum - Mon Mar 12 04:00:00 GMT 2012

Genetic tests may become a $25 billion annual market in the U.S. within a decade, highlighting the need to identify which exams work the best, insurer UnitedHealth Group Inc. (UNH) said.

A majority of the 1,800 DNA tests developed to identify or manage medical conditions still havent been studied enough to prove their effectiveness, UnitedHealth, the biggest U.S. insurer by sales, said in a report today. The technology generated $5 billion in 2010, the insurer said, and three to five new tests are being introduced each month.

The projections bode well for diagnostics companies including Genomic Health Inc. (GHDX), Myriad Genetics Inc. (MYGN) and Life Technologies Corp. (LIFE), said Daniel Leonard, a Leerink Swann & Co. analyst in New York. They also raise questions about the effect on consumers, doctors and governments struggling with rising medical bills, UnitedHealth said.

While genetic exams hold great promise for better health and medical care, the Minnetonka, Minnesota-based insurer said in the report. They also pose significant challenges to a system that is increasingly unaffordable.

The paper, released to coincide with a Washington D.C. conference on gene testing, calls for cheaper, quicker methods to evaluate the quality of the technology, as well as better education for consumers about privacy protections.

The report echoed concerns from a study last week in the New England Journal of Medicine that found cancer screening may be less useful than hoped because of the wide variety of mutations found in tumors. That may explain why some oncology drugs become less effective even when targeted at specific genes, scientists from the U.K. said.

Genetic tests can be used to identify cancers, judge a persons predisposition to Alzheimers disease or gauge how well a particular medicine will work in a specific patient.

UnitedHealth, which covers 36 million people in its medical plans, spent about $500 million for genetic exams and molecular diagnostics in 2010, mostly to detect cancers and infectious diseases like HIV, todays report said.

The national figure may swell to $15 billion to $25 billion in 2021, with annual growth rates of more than 10 percent, the company said. It based the projections on internal claims and government Medicare and Medicaid data. The ultimate number depends on how popular the tests grow, how expensive they get and insurers willingness to pay, among other factors.

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Genetic Tests to Generate $25 Billion a Year, UnitedHealth Says

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WASHINGTON--(BUSINESS WIRE)--

A new report by UnitedHealth Groups (NYSE: UNH - News) Center for Health Reform & Modernization finds that a majority of physicians are utilizing genetic testing. The report, titled Personalized Medicine: Trends and prospects for the new science of genetic testing and molecular diagnostics, presents new findings on how genetic tests can help diagnose disease, target prevention, and ensure that patients receive the medicines that will best treat their conditions.

Genetic testing is currently available for about 2,500 conditions, including cancers and communicable diseases, and it is estimated to be growing by double digits annually. Full genome sequencing, which maps an individuals entire genetic code, is also expected to become widely available, possibly beginning as soon as later this year.

Genetic science offers unprecedented potential to prevent disease and improve diagnosis and treatment, ushering in an era of truly personalized care, said Simon Stevens, executive vice president, UnitedHealth Group, and chairman of the UnitedHealth Center for Health Reform & Modernization. But for patients to realize these practical benefits, we will also need new models of research and care delivery combined with informed choice and appropriate consumer safeguards.

The report sheds new light on three important questions:

What do U.S. doctors and patients think about genetic testing and molecular diagnostics?

How are these tests currently being used, and how might their use grow?

What practical action can be taken to ensure proper safeguards while accelerating progress for patients?

Report Includes New Survey Results on Patient and Physician Views on Genetic Testing

Most American consumers are optimistic about the potential benefits from advances in genetic testing, according to a national survey of U.S. adults conducted by UnitedHealth Group/Harris Interactive, included in the report. About three-quarters of survey respondents agree that genetic tests help doctors diagnose preventable conditions and offer more personalized treatment options. Most consumers expect that five years from now the use of testing will have increased. However, the coding system used across the country to monitor medical tests offers few codes to describe genetic tests for specific diseases.

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New Report Finds Greater Use of Genetic Testing, but Half of Physicians Concerned About Their Lack of Familiarity With ...

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Newswise CHICAGO, IL March 10, 2012 -- The Genetics Society of America (GSA) and the Drosophila community of geneticists are pleased to announce the six student winners of the Victoria Finnerty Undergraduate Travel Awards, which were used by these students to attend the ongoing 53rd Annual Drosophila Research Conference in Chicago. These students, all juniors or seniors in college are:

Selma Avdagic, Saint Louis University School of Medicine, Missouri Samantha Galindo, University of WisconsinMadison Kenneth B. Hoehn, Duke University, Durham, North Carolina Emily Hsieh, University of Washington and Fred Hutchinson Cancer Research Center, Seattle Jacqueline McDermott, Hofstra University, Hempstead, New York Mohammad Siddiq, Indiana University, Bloomington

It is inspiring to see these undergraduates conducting cutting-edge research so early in their scientific careers, said Adam Fagen, Ph.D., GSA executive director. We at GSA have no doubt that the future of genetics is strong with such talented young people leading the field.

This is the first time these students have attended a professional scientific research conference where they are describing their research to doctoral students, postdoctoral fellows, and principal investigators from research laboratories all over the world. The experience, described by one student as both exciting and intimidating, is an opportunity for them to explore the field of genetics research as a possible career.

Victoria Finnerty was an outstanding scientist and a dedicated teacher and mentor who conveyed her passion for Drosophila genetics in her creative approaches toward undergraduate education and research. We view this award as an important way to encourage our young scientists to pursue research careers and become our future scientific leaders, said Elizabeth Gavis, Ph.D., president of the Drosophila Board of Directors and professor at Princeton University.

The Victoria Finnerty Undergraduate Travel Awards were established last year in memory of its namesake, who was a long-time GSA member, a dedicated undergraduate educator at Emory University for 35 years, and an active member of the Drosophila research community and the genetics community at large. The six undergraduates are the first to receive this funding to attend the annual Drosophila Research Conference.

A list of the students research projects, a brief description of each and the name of their mentor (principal investigator) of the project, is attached.

ABOUT THE GSA DROSOPHILA RESEARCH CONFERENCE: At least 1,500 researchers attend the annual GSA Drosophila Research Conference to share the latest research using the fruit fly Drosophila melanogaster and other insect species. Many of findings from these model organisms have broad application for the study of human genetic traits and diseases. For more information about the conference, see http://www.drosophila-conf.org/2012/.

ABOUT GSA: Founded in 1931, the Genetics Society of America (GSA) is the professional membership organization for scientific researchers, educators, bioengineers, bioinformaticians and others interested in the field of genetics. Its nearly 5,000 members work to advance knowledge in the basic mechanisms of inheritance, from the molecular to the population level. The GSA is dedicated to promoting research in genetics and to facilitating communication among geneticists worldwide through its conferences, including the biennial conference on Model Organisms to Human Biology, an interdisciplinary meeting on current and cutting edge topics in genetics research, as well as annual and biennial meetings that focus on the genetics of particular organisms, including C. elegans, Drosophila, fungi, mice, yeast, and zebrafish. GSA publishes GENETICS, a leading journal in the field and a new online, open-access publication, G3: Genes|Genomes|Genetics. For more information about GSA, please visit http://www.genetics-gsa.org. Also follow GSA on Facebook at facebook.com/GeneticsGSA and on Twitter @GeneticsGSA.

2012 Victoria Finnerty Awardees

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Undergraduate Grant Awardees Present Research at Fly Conference

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

Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-351-0896 Genetics Society of America

Chicago, IL March 10, 2012 -- More than two-thirds of human genes have counterparts in the well-studied fruit fly, Drosophila melanogaster, so although it may seem that humans don't have much in common with flies, the correspondence of our genetic instructions is astonishing. In fact, there are hundreds of inherited diseases in humans that have Drosophila counterparts.

At the ongoing Genetics Society of America's 53rd Annual Drosophila Research Conference in Chicago, several scientific investigators shared their knowledge of some of these diseases, including ataxia-telangiectasia (A-T), a neurodegenerative disorder; Rett Syndrome, a neurodevelopmental disorder; and kidney stones, a common health ailment. All are the subject on ongoing research using the Drosophila model system.

Andrew Petersen, a graduate student in Dr. David Wassarman's laboratory at the University of Wisconsin-Madison, discussed his experiments with a fly model of the rare childhood disease ataxia-telangiectasia. A-T causes cell death within the brain, poor coordination, characteristic spidery blood vessels that show through the skin, and susceptibility to leukemias and lymphomas. A-T generally results in a life expectancy of only 25 years.

A-T is normally lethal in flies, but Mr. Petersen induced a mutant that develops symptoms only when the environmental temperature rises above a certain level, allowing Mr. Petersen to control the lethality by varying the fly's environment. The mutant flies lose their ability to climb up the sides of their vial habitats - a sign of neurodegeneration -- and die prematurely. Their glial cells are primarily affected, rather than the neurons that the glia support. In addition, an innate immune response is activated in the compromised glia, a scenario reminiscent of Alzheimer's and Parkinson's diseases. "We are one step closer to knowing how these diseases occur and possibly how we can treat them," Mr. Petersen concluded.

Sarah Certel, Ph.D., assistant professor of biological sciences at the University of Montana-Missoula, works with flies that have been altered to include the human gene MeCP2. This gene controls how neurons use many other genes, and the amount of the protein that it encodes must be within a specific range for the brain to develop normally. Too little of the protein and Rett syndrome results, a disorder on the X chromosome, which exclusively affects females in childhood. (Males with this mutation are generally miscarried or are stillborn.) It causes a constellation of symptoms including characteristic hand-wringing, autism, seizures, cognitive impairment, and loss of mobility. Yet too much of the protein causes similar problems.

In flies, altered levels of the MeCP2 protein affect sleep and aggression. For flies and most model organisms, sleep is inferred as the absence of activity during the day and night. To study sleep, Dr. Certel conducted "actograms" for individual flies. "The actogram records the activities of individually housed flies when they cross an infrared beam," she explained. The flies' sleep became fragmented, delayed, and shortened. "We're studying the link between the cellular changes and behaviors," she added.

Switching from the brain to the urinary system, it was noted that "Drosophila get kidney stones too" began Julian Dow, Ph.D., professor of molecular and integrative physiology at the University of Glasgow, United Kingdom. The fly version of a kidney is much simpler in design, a quartet of Malpighian tubules that are conveniently transparent.

Dr. Dow discussed a fly mutant called "rosy," discovered a century ago, that corresponds to the rare human inborn error of metabolism called xanthinuria type 1, as well as a diet-induced blockage that corresponds to the more common human condition of calcium oxalate kidney stones. In time-lapse video, Dr. Dow showed stones appearing and growing in the Malpighian tubule.

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Scientists study human diseases in flies

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SILVER SPRING, Md.--(BUSINESS WIRE)--

Nuvilex, Inc. (OTCQB:NVLX), an emerging biotechnology provider of cell and gene therapy solutions, today discussed the use of the proprietary Cell-in-a-Box technology, being acquired from SG Austria, as an adjunct to chemotherapy across a spectrum of cancer treatments.

The Cell-in-a-Box technology involves the encapsulation of cytochrome P450 expressing cells which are placed beside the target tumor. When the patient is injected with the nontoxic drug ifosfamide, the encapsulated cells transform this prodrug into its active, chemotherapeutic drug. The greatest benefit of this treatment protocol is that the treatment is localized to the tumor, enhancing the chemotherapys effectiveness.

Most chemotherapy drugs affect both normal and cancerous tissue, which is why they also are toxic to naturally fast-growing cells in the body such as hair follicles and intestinal cells. Ifosfamide was one of many drugs originally used for pancreatic cancer that showed an effect against the tumor, but produced severe side effects. By using encapsulated cytochrome P450 expressing cells to convert the ifosfamide at the tumor site, the encapsulated cell treatment was able to localize the drug's effects within the tumor cells. The amount of drug needed was decreased to only one third of the original dose and the side effects were dramatically decreased.

Dr. Robert Ryan, Chief Executive Officer of Nuvilex, commented, Our cell encapsulation technology can help practitioners target the tumors while preserving the health of surrounding tissues and avoiding the often fatal side effects that accompany aggressive chemotherapy. We anticipate that by localizing treatment within the target tumors, we will finally have an effective treatment protocol for cancers that also preserves the quality of life.

About Nuvilex

Nuvilex, Inc. (OTCQB:NVLX) is an emerging international biotechnology provider of live clinically useful, therapeutically valuable, encapsulated cells as well as services for encapsulating live cells for the research and medical communities. Through substantial effort, the aspects of our corporate activities alone and in concert with SG Austria continue to move toward agreement completion and ultimately a strong future. Our companys ultimate clinical offerings will include cancer, diabetes and other treatments using the companys industry-leading cell and gene therapy expertise and cutting edge, live-cell encapsulation technology.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 involving risks and uncertainties. Results, events and performances could vary from those contemplated. These statements involve risks and uncertainties which may cause actual results, expressed or implied, to differ from predicted outcomes. Risks and uncertainties include product demand, market competition, and Nuvilexs ability to meet current or future plans. 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, to reflect events or circumstances afterward, or to disclose unanticipated occurrences, except as required under applicable laws.

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Studies Highlight Nuvilex Cell-In-A-Box® Technology Enhances Chemotherapy Effectiveness

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

Contact: Sarah Jackson press_releases@the-jci.org 919-684-0620 Journal of Clinical Investigation

EDITOR'S PICK Restoring what's lost: uncovering how liver tissue regenerates

The liver is unique among mammalian organs in its ability to regenerate after significant tissue damage or even partial surgical removal. Laurie DeLeve and her colleagues at the University of Southern California in Los Angeles wanted to better understand which cells are specifically responsible for driving liver regeneration. A specialized cell type, known as liver sinusoidal endothelial cells, has generally been thought to promote regeneration of liver tissue. However, the DeLeve team suspected that stem cells and progenitor cells, which have the capacity to differentiate into mature cell types, might be responsible for stimulating liver regeneration by generating hepatocyte growth factor. Using a rat model system, they first identified the presence of stem and progenitor cells that give rise to liver sinusoidal endothelial cells in both the liver and the bone marrow. They next sought to determine which population of stem and progenitor cells are required for regeneration. DeLeve and colleagues found that the bone marrow-derived cells were not required for liver cell proliferation in the absence of damage. In contrast, following surgical removal of a portion of the rat liver, an infusion of bone marrow-derived progenitor cells was required for liver regeneration. These results improve our understanding of how liver tissue can regenerate following damage and may shed light on liver complications in patients with suppressed bone marrow tissue.

TITLE: Liver sinusoidal endothelial cell progenitor cells promote liver regeneration in rats

AUTHOR CONTACT: Laurie D. DeLeve University of Southern California Keck School of Medicine, Los Angeles, CA, USA Phone: 323-442-3248; Fax: 323-442-3238; E-mail: deleve@usc.edu

View this article at: http://www.jci.org/articles/view/58789?key=21e2857b21106f232595

ONCOLOGY New Determinant of Human Breast Cancer Metastasis Discovered

Researchers at the University of Kentucky's Markey Cancer Center in Lexington, KY have provided new insight as to why the most severe subtype of breast cancer in humans frequently metastasizes. Tumor cells can exploit a cellular program that promotes cell migration and reduces adhesion between cells to spread to distant sites in the body (metastasis). This cellular program, known as the epithelial-mesenchymal transition, is normally restricted to wound healing, tissue remodeling and embryonic development. Increasing cell motility requires a decrease in E-cadherin, which functions to promote cell-cell adhesion. Led by Binhua Zhou, the research team identified G9a as a major repressor of E-cadherin expression. They found that G9a interacts with Snail, which can repress gene expression, to modify the E-cadherin promoter and block expression of the E-cadherin gene. Their findings establish that G9a is an important determinant of metastasis in the most severe sub-type of breast cancer, and suggest the development of new therapeutics targeting this pathway could potentially disrupt the metastatic disease.

TITLE: G9a interacts with Snail and is critical for Snail-mediated E-cadherin repression in human breast cancer

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JCI early table of contents for March 12, 2012

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