Washington, January 5 (ANI): A cocktail of three specific genes can reprogram cells in the scars caused by heart attacks into functioning muscle cells, and the addition of a gene that stimulates the growth of blood vessels enhances that effect, researchers say.

"The idea of reprogramming scar tissue in the heart into functioning heart muscle was exciting," Dr. Todd K. Rosengart, corresponding author of the study from Baylor College of Medicine, said.

"The theory is that if you have a big heart attack, your doctor can just inject these three genes into the scar tissue during surgery and change it back into heart muscle. However, in these animal studies, we found that even the effect is enhanced when combined with the VEGF gene," he said.

During a heart attack, blood supply is cut off to the heart, resulting in the death of heart muscle. The damage leaves behind a scar and a much weakened heart. Eventually, most people who have had serious heart attacks will develop heart failure.

Changing the scar into heart muscle would strengthen the heart. To accomplish this, during surgery, Rosengart and his colleagues from Weill Cornell Medical College and Stony Brook University Medical Center transferred three forms of the vascular endothelial growth factor (VEGF) gene that enhances blood vessel growth or an inactive material (both attached to a gene vector) into the hearts of rats.

Three weeks later, the rats received either Gata4, Mef 2c and Tbx5 (the cocktail of transcription factor genes called GMT) or an inactive material. (A transcription factor binds to specific DNA sequences and starts the process that translates the genetic information into a protein.)

The GMT genes alone reduced the amount of scar tissue by half compared to animals that did not receive the genes, and there were more heart muscle cells in the animals that were treated with GMT.

The hearts of animals that received GMT alone also worked better as defined by ejection fraction than those who had not received genes. (Ejection fraction refers to the percentage of blood that is pumped out of a filled ventricle or pumping chamber of the heart.)

The hearts of the animals that had received both the GMT and the VEGF gene transfers had an ejection fraction four times greater than that of the animals that had received only the GMT transfer.

Rosengart emphasizes that more work needs to be completed to show that the effect of the VEGF is real, but it has real promise as part of a new treatment for heart attack that would minimize heart damage.

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Gene therapy helps patients with damaged hearts grow new blood vessels

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January 5, 2013

redOrbit Staff & Wire Reports Your Universe Online

A team of US researchers has reportedly developed a way to reprogram scar tissue from damaged hearts into healthy muscle through gene therapy a discovery which could help strengthen hearts harmed as a result of cardiovascular events.

According to a recent statement, scientists from Weill Cornell Medical College, along with colleagues from the Baylor College of Medicine (BCM) and Stony Brook University Medical Center have discovered that a combination of three specific genes can turn cells in the scar tissue into fully-functioning muscle cells, and that the addition of a fourth can stimulate blood vessel growth and make the process even more effective.

Typically, the hearts blood supply is cut off during a heart attack, causing muscles to die off and become scarred, the researchers explained. The result is a weakened heart which will eventually lead to heart failure for those who have experienced serious cardiovascular events. This, however, could be avoided if medical experts could find a way to transform scar tissue into normal heart tissue, thus strengthening the heart as a whole.

To that end, Dr. Todd K. Rosengart, chair at BCMs Michael E. DeBakey Department of Surgery, and colleagues implanted either three forms of a gene that encourages blood vessel growth known as the vascular endothelial growth factor (VEGF) gene or an inactive material into the hearts of rats.

Three weeks later, the rats received either Gata4, Mef 2c and Tbx5 (the cocktail of transcription factor genes called GMT) or an inactive material. (A transcription factor binds to specific DNA sequences and starts the process that translates the genetic information into a protein), the researchers explained. The GMT genes alone reduced the amount of scar tissue by half compared to animals that did not receive the genes, and there were more heart muscle cells in the animals that were treated with GMT.

The hearts of animals that received GMT alone also worked better as defined by ejection fraction than those who had not received genes. (Ejection fraction refers to the percentage of blood that is pumped out of a filled ventricle or pumping chamber of the heart), they added. The hearts of the animals that had received both the GMT and the VEGF gene transfers had an ejection fraction four times greater than that of the animals that had received only the GMT transfer.

The idea of reprogramming scar tissue in the heart into functioning heart muscle was exciting, Dr. Rosengart, the corresponding author of the study, said. The theory is that if you have a big heart attack, your doctor can just inject these three genes into the scar tissue during surgery and change it back into heart muscle. However, in these animal studies, we found that even the effect is enhanced when combined with the VEGF gene.

This experiment is a proof of principle. Now we need to go further to understand the activity of these genes and determine if they are effective in even larger hearts, added Dr. Ronald G. Crystal, chairman and professor of genetic medicine at Weill Cornell Medical College. We have shown both that GMT can effect change that enhances the activity of the heart and that the VEGF gene is effective in improving heart function even more.

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Damaged Heart Strengthened Using New Gene Therapy Method

Recommendation and review posted by Bethany Smith

Written by Kait Shea, Assistant Editor Friday, 04 January 2013 11:00

There may not be a cure for cancer just yet, but the Alliance for Cancer Gene Therapy (ACGT), a nonprofit established by a Greenwich couple thats dedicated to gene therapy, is making big strides in treatment.

The Stamford-based organization is the only nonprofit in the United States dedicated exclusively to cell and gene cancer therapy research. One hundred percent of all contributions to ACGT go directly to research and fund grants with leading scientists in the country, representing 28 prestigious medical institutions. Many feel that because of this ACGT has played a major role in what many doctors believe may be the key to healing those plagued by the disease.

In an interview with the Post, Ms. Netter said she and her late husband realized this really is a key to perhaps finding the answers to cancer and immediately sought to put their energies and resources into it on hope and faith. After a year of fund raising, the couple officially embarked on their mission to provide grants to the nations leading scientific investigators for cancer gene therapy research.

With the help of ACGTs Scientific Advisory Council, a group composed of leading scientists and doctors who conduct rigorous reviews of grants to ensure that the most promising cancer gene therapy projects are given funding, the Netters awarded more than $22 million in grants within the first 10 years of launching their organization.

The latest strides in gene therapy projects funded by ACGT, however, are the most exciting the organization has seen, Ms. Netter said. The alliance played a significant part in the recent leukemia study pioneered by scientists at the Perelman School of Medicine at the University of Pennsylvania. ACGT provided the initial funds for the study, which has found success using immune-mediated gene therapy for leukemia and lymphoma.

According to Ms. Netter, the therapy used involves removing immune cells from the body of the patient, bioengineering and strengthening them, then reinfusing them into the patient using a gutted out HIV vector, which reprograms the patients immune system genetically to kill cancer. The T cells directly target and kill cancer cells and circulate through the body for at least a few years, and Ms. Netter called it an enormous breakthrough.

Initial ACGT grants for the immune mediated gene therapy project were awarded in 2004 to Carl June of the Abramson Family Cancer Research Institute at the University of Pennsylvania and to Michel Sadelain, of Memorial Sloan-Kettering Cancer Center, Gene Therapy and Gene Expression Laboratory, in New York City. Preliminary results were issued by Dr. June in August 2011, with additional results released in December 2012, delivering some of the most promising results seen to date in the search for a cure.

The clinical trial participants, all of whom had advanced cancers, included 10 adult patients with chronic lymphocytic leukemia who were treated at the Hospital of the University of Pennsylvania and two children with acute lymphoblastic leukemia who were treated at the Childrens Hospital of Philadelphia. Two of the first three adult patients treated with the protocol remained healthy and in full remission more than two years after their treatment, with the engineered cells still circulating in their bodies. Currently, nine out of the 12 participants show their disease in remission.

Perhaps the most amazing story of recovery, Ms. Netter said, was that of now 7-year-old Emma Whitehead, who was on the brink of death, suffering from acute lymphoblastic leukemia. After trying traditional cancer treatments like chemotherapy without any improvement, Emmas parents decided to try the experimental T-cell therapy. And although the treatment nearly killed Emma, her health rapidly improved and she emerged cancer-free, Ms. Netter said. The young girl is now out of the hospital and leading the life of a regular second grader, with eight months of remission from the disease under her belt.

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Gene therapy: Local group seeks ‘answers to cancer’

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Cost of Stem Cell Therapy | Malaysia Stem Cell Therapy Cost
stemcellmalaysia.com Stem cell therapy is not a cheap medical treatment. In fact, it is very expensive treatment to the majority of people. The high price of stem cell therapy becomes not only a deterrent to the majority but also creates room for non-medical sector to fill the void of demands for disease treatment. This video addresses the issues surrounding the cost of stem cell therapy, particularly in Malaysia. For more information on stem cell therapy, please visit Stem Cell Malaysia at stemcellmalaysia.com

By: stemcells2012

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Cost of Stem Cell Therapy | Malaysia Stem Cell Therapy Cost - Video

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IRVINE A variant of a gene associated with active personality traits in humans seems also to be involved with living a longer life, UC Irvine and other researchers have found.

This derivative of a dopamine-receptor gene called the DRD4 7R allele appears in significantly higher rates in people more than 90 years old and is linked to lifespan increases in mouse studies.

Robert Moyzis, professor of biological chemistry at UC Irvine, and Dr. Nora Volkow, a psychiatrist who conducts research at the Brookhaven National Laboratory and also directs the National Institute on Drug Abuse, led a research effort that included data from the UC Irvine-led 90+ Study in Laguna Woods, Calif. Results appear online in the Journal of Neuroscience.

The variant gene is part of the dopamine system, which facilitates the transmission of signals among neurons and plays a major role in the brain network responsible for attention and reward-driven learning. The DRD4 7R allele blunts dopamine signaling, which enhances individuals' reactivity to their environment.

People who carry this variant gene, Moyzis said, seem to be more motivated to pursue social, intellectual and physical activities. The variant is also linked to attention-deficit/hyperactivity disorder and addictive and risky behaviors.

"While the genetic variant may not directly influence longevity," Moyzis said, "it is associated with personality traits that have been shown to be important for living a longer, healthier life. It's been well documented that the more you're involved with social and physical activities, the more likely you'll live longer. It could be as simple as that."

Numerous studies including a number from the 90+ Study have confirmed that being active is important for successful aging, and it may deter the advancement of neurodegenerative diseases, such as Alzheimer's.

Prior molecular evolutionary research led by Moyzis and Chuansheng Chen, UC Irvine professor of psychology & social behavior, indicated that this "longevity allele" was selected for during the nomadic out-of-Africa human exodus more than 30,000 years ago.

In the new study, the UC Irvine team analyzed genetic samples from 310 participants in the 90+ Study. This "oldest-old" population had a 66 percent increase in individuals carrying the variant relative to a control group of 2,902 people between the ages of 7 and 45. The presence of the variant also was strongly correlated with higher levels of physical activity.

Next, Volkow, neuroscientist Panayotis Thanos and their colleagues at the Brookhaven National Laboratory found that mice without the variant had a 7 percent to 9.7 percent decrease in lifespan compared with those possessing the gene, even when raised in an enriched environment.

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'Fountain of youth' gene?

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Jan. 3, 2013 In a novel use of gene knockout technology, researchers at the University of California, San Diego School of Medicine tested the same gene inserted into 90 different locations in a yeast chromosome -- and discovered that while the inserted gene never altered its surrounding chromatin landscape, differences in that immediate landscape measurably affected gene activity.

The findings, published online in the Jan. 3 issue of Cell Reports, demonstrate that regulation of chromatin -- the combination of DNA and proteins that comprise a cell's nucleus -- is not governed by a uniform "histone code" but by specific interactions between chromatin and genetic factors.

"One of the main challenges of epigenetics has been to get a handle on how the position of a gene in chromatin affects its expression," said senior author Trey Ideker, PhD, chief of the Division of Genetics in the School of Medicine and professor of bioengineering in UC San Diego's Jacobs School of Engineering. "And one of the major elements of that research has been to look for a histone code, a general set of rules by which histones (proteins that fold and structure DNA inside the nucleus) bind to and affect genes."

The Cell Report findings indicate that there is no singular universal code, according to Ideker. Rather, the effect of epigenetics on gene expression or activity depends not only on the particular mix of histones and other epigenetic material, but also on the identity of the gene being expressed.

To show this, the researchers exploited an overlooked feature of an existing resource. The widely-used gene knockout library for yeast, originally created to see what happens when a particular gene is missing, was built by systematically inserting the same reporter gene into different locations. Ideker and colleagues focused on this reporter gene and observed what happens to gene expression at different locations along yeast chromosome 1.

"If epigenetics didn't matter -- the state of histones and DNA surrounding the gene -- the expression of a gene would be the same regardless of where on the chromosome that gene is positioned," said Ideker. But in every case, gene expression was measurably influenced by interaction with nearby epigenetic players.

Ideker said the work provides a new tool for more deeply exploring how and why genes function, particularly in relation to their location.

Co-authors are first author Menzies Chen, UCSD Department of Bioengineering; Katherine Licon, UCSD Department of Medicine and UCSD Institute for Genomic Medicine; Rei Otsuka and Lorraine Pillus, UCSD Department of Molecular Biology and UCSD Moores Cancer Center.

Funding for this research came, in part, from NIH grants R21HG005232, R01GM084279, P50GM085764 and P30CA023100.

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In epigenomics, location is everything: Researchers exploit gene position to test 'histone code'

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If you lead an active, extroverted life and are something of a thrill seeker, you might be genetically primed to live into your 90s or longer, according to a new study by a team that included UC Irvine researchers.

A variation of a much-studied gene involved in transmission of dopamine, a key component of the brain's reward and learning system, was found to be far more frequent among the very old.

Martha Ettl celebrates her 100th birthday in San Clemente in February. UC Irvine scientists say they've found a variant of a single gene that promotes longer life in humans as well as laboratory mice.

FIL EPHOTO: ORANGE COUNTY REGISTER

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And the same gene variant was also linked to longer life in mice.

The variant itself might not extend lifespan directly, said Robert Moyzis, a UCI biological chemistry professor and an author of the study.

Instead, it appears to predispose those who bear it to a more vigorous lifestyle.

"This particular variation has already been associated with personality traits that are much more outgoing, much more socially engaged," Moyzis said. "We think it's a simple as that. Obviously, if you are much more likely to be engaged in physical and intellectual activities as you age, there have been many studies that have shown that is a good predictor of adding a few more years to your life."

The human subjects in the study came from Laguna Woods, part of a group involved in the Leisure World Cohort Study that began in 1981. It included people who were 90 years old or older in 2003; most of them have since passed away, Moyzis said.

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Longer-life gene variant found in study

Recommendation and review posted by Bethany Smith

CLARENCE, N.Y.--(BUSINESS WIRE)--

22nd Century Group, Inc. (OTCBB: XXII), a company that has developed groundbreaking technology for tobacco harm reduction and smoking cessation products, today announced that the United States Patent and Trademark Office (USPTO) has issued a Notice of Allowance for the N-methylputrescine oxidase (MPO) gene technology. MPO is essential for production of nicotine in the tobacco plant.

The allowed claims of Patent Application No. 12/305,483, entitled, NUCLEIC ACID ENCODING N-METHYLPUTRESCINE OXIDASE AND USES THEREOF, cover nucleic acids encoding MPO, methods for producing tobacco plants with either reduced or increased nicotine levels, and tobacco cells and tobacco plants produced by the foregoing. The Notice of Allowance was issued on December 24, 2012 to the National Research Council Canada (NRC). 22nd Century is NRCs exclusive worldwide licensee of MPO and other technologies. A patent will be issued by the USPTO within the next few months. Including the patent term adjustment, this U.S. patent will expire in December 2027 and will be the first MPO gene patent issued anywhere in the world.

The MPO gene encodes a protein involved in a key step of nicotine biosynthesis. Scientists have attempted to clone the MPO gene for decades. MPO expression can be either down-regulated or up-regulated to produce tobacco plant varieties and tobacco products with a wide range of nicotine levels (from very low to high), or altered ratios of nicotine and other nicotinic alkaloids such as anatabine and nornicotine. Dr. Jonathon Page and Enwu Liu of the NRC Plant Biotechnology Institute are the inventors of the MPO technology. 22nd Century funded subject patent and research and development expenses at NRC from 2006 to 2008. Patent Application PCT/IB2007/003550 is the related international application to U.S. Patent Application No. 12/305,483.

22nd Centurys vice president of research and development, Dr. Michael Moynihan stated, We are very pleased that the USPTO has allowed the MPO patent. The MPO gene technology is one of several 22nd Century patent families representing our second-generation gene technology for modifying the content of nicotine and other nicotinic alkaloids in the tobacco plant. Our second-generation technology has significant advantages over our first generation technology.

Upon this MPO patent issuing, 22nd Century will have a portfolio of 15 issued U.S. patents and 8 pending U.S. patent applications. Globally, 22nd Century owns or is the exclusive licensee of 107 issued patents in 78 countries plus an additional 38 pending patent applications mainly related to all of the key nicotine biosynthesis genes and potential modified risk tobacco products produced therefrom.

For additional information, please visit: http://www.xxiicentury.com.

Cautionary Note Regarding Forward-Looking Statements: This press release contains forward-looking information, including all statements that are not statements of historical fact regarding the intent, belief or current expectations of 22nd Century Group, Inc., its directors or its officers with respect to the contents of this press release. The words may, would, will, expect, estimate, anticipate, believe, intend and similar expressions and variations thereof are intended to identify forward-looking statements. We cannot guarantee future results, levels of activity or performance. You should not place undue reliance on these forward-looking statements, which speak only as of the date that they were made. These cautionary statements should be considered with any written or oral forward-looking statements that we may issue in the future. Except as required by applicable law, including the securities laws of the United States, we do not intend to update any of the forward-looking statements to conform these statements to reflect actual results, later events or circumstances or to reflect the occurrence of unanticipated events. You should carefully review and consider the various disclosures made by us in our annual report on Form 10-K for the fiscal year ended December 31, 2011, filed on April 16, 2012, including the section entitled Risk Factors, and our other reports filed with the U.S. Securities and Exchange Commission which attempt to advise interested parties of the risks and factors that may affect our business, financial condition, results of operation and cash flows. If one or more of these risks or uncertainties materialize, or if the underlying assumptions prove incorrect, our actual results may vary materially from those expected or projected.

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22nd Century Group Announces Allowance of U.S. Patent for MPO Nicotine Biosynthesis Gene

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Public release date: 3-Jan-2013 [ | E-mail | Share ]

Contact: Tom Vasich tmvasich@uci.edu 949-824-6455 University of California - Irvine

Irvine, Calif., Jan. 3, 2013 A variant of a gene associated with active personality traits in humans seems to also be involved with living a longer life, UC Irvine and other researchers have found.

This derivative of a dopamine-receptor gene called the DRD4 7R allele appears in significantly higher rates in people more than 90 years old and is linked to lifespan increases in mouse studies.

Robert Moyzis, professor of biological chemistry at UC Irvine, and Dr. Nora Volkow, a psychiatrist who conducts research at the Brookhaven National Laboratory and also directs the National Institute on Drug Abuse, led a research effort that included data from the UC Irvine-led 90+ Study in Laguna Woods, Calif. Results appear online in The Journal of Neuroscience.

The variant gene is part of the dopamine system, which facilitates the transmission of signals among neurons and plays a major role in the brain network responsible for attention and reward-driven learning. The DRD4 7R allele blunts dopamine signaling, which enhances individuals' reactivity to their environment.

People who carry this variant gene, Moyzis said, seem to be more motivated to pursue social, intellectual and physical activities. The variant is also linked to attention-deficit/hyperactivity disorder and addictive and risky behaviors.

"While the genetic variant may not directly influence longevity," Moyzis said, "it is associated with personality traits that have been shown to be important for living a longer, healthier life. It's been well documented that the more you're involved with social and physical activities, the more likely you'll live longer. It could be as simple as that."

Numerous studies including a number from the 90+ Study have confirmed that being active is important for successful aging, and it may deter the advancement of neurodegenerative diseases, such as Alzheimer's.

Prior molecular evolutionary research led by Moyzis and Chuansheng Chen, UC Irvine professor of psychology & social behavior, indicated that this "longevity allele" was selected for during the nomadic out-of-Africa human exodus more than 30,000 years ago.

Original post:
Dopamine-receptor gene variant linked to human longevity

Recommendation and review posted by Bethany Smith

Jan. 3, 2013 A variant of a gene associated with active personality traits in humans seems to also be involved with living a longer life, UC Irvine and other researchers have found.

This derivative of a dopamine-receptor gene -- called the DRD4 7R allele -- appears in significantly higher rates in people more than 90 years old and is linked to lifespan increases in mouse studies.

Robert Moyzis, professor of biological chemistry at UC Irvine, and Dr. Nora Volkow, a psychiatrist who conducts research at the Brookhaven National Laboratory and also directs the National Institute on Drug Abuse, led a research effort that included data from the UC Irvine-led 90+ Study in Laguna Woods, Calif. Results appear online in The Journal of Neuroscience.

The variant gene is part of the dopamine system, which facilitates the transmission of signals among neurons and plays a major role in the brain network responsible for attention and reward-driven learning. The DRD4 7R allele blunts dopamine signaling, which enhances individuals' reactivity to their environment.

People who carry this variant gene, Moyzis said, seem to be more motivated to pursue social, intellectual and physical activities. The variant is also linked to attention-deficit/hyperactivity disorder and addictive and risky behaviors.

"While the genetic variant may not directly influence longevity," Moyzis said, "it is associated with personality traits that have been shown to be important for living a longer, healthier life. It's been well documented that the more you're involved with social and physical activities, the more likely you'll live longer. It could be as simple as that."

Numerous studies -- including a number from the 90+ Study -- have confirmed that being active is important for successful aging, and it may deter the advancement of neurodegenerative diseases, such as Alzheimer's.

Prior molecular evolutionary research led by Moyzis and Chuansheng Chen, UC Irvine professor of psychology & social behavior, indicated that this "longevity allele" was selected for during the nomadic out-of-Africa human exodus more than 30,000 years ago.

In the new study, the UC Irvine team analyzed genetic samples from 310 participants in the 90+ Study. This "oldest-old" population had a 66 percent increase in individuals carrying the variant relative to a control group of 2,902 people between the ages of 7 and 45. The presence of the variant also was strongly correlated with higher levels of physical activity.

Next, Volkow, neuroscientist Panayotis Thanos and their colleagues at the Brookhaven National Laboratory found that mice without the variant had a 7 percent to 9.7 percent decrease in lifespan compared with those possessing the gene, even when raised in an enriched environment.

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Gene variant linked to active personality traits also linked to human longevity

Recommendation and review posted by Bethany Smith

YAKIMA, Wash. (AP) Companies would be required to label food products made from genetically engineered crops under a Washington state initiative to be submitted Thursday by the proposal's sponsors.

Initiative 522 would require food and seeds produced entirely or partly through genetic engineering and sold in Washington to be labeled as such, effective July 1, 2015. Under the measure, raw foods that are not packaged separately would have to be labeled on the retail shelf.

The proposal comes two months after California voters rejected a similar ballot measure in a nearly $55 million advertising war that pitted food safety advocates against agricultural and biotechnology giants. Supporters argued consumers should have a choice of whether or not to eat genetically engineered products, even though the government and major science groups say such foods are safe to eat. Opponents argued the proposal would raise food prices and hurt farmers.

About 50 countries require genetically modified foods to be labeled, but the U.S. isn't one of them. Only Alaska has enacted legislation at the state level, requiring the labeling of genetically engineered fish and shellfish products.

A bill in the Washington Legislature to require food labeling failed to pass out of committee, despite support from a coalition of local wheat farmers who said they feared their export markets will be hurt if genetically modified wheat gains federal approval.

Biotechnology giant Monsanto Co. has announced plans to begin testing genetically modified wheat, though the product is likely a decade or more from being offered commercially.

An initiative to the Legislature requires at least 241,153 valid signatures of registered state voters to be certified, though the secretary of state's office suggests at least 320,000 as a buffer for any duplicate or invalid signatures.

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Proposal would require genetically modified label

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Brad Shannon | The Olympian Published January 03, 2013 Modified January 03, 2013

Backers of an initiative to require disclosures of genetic alterations of commercially sold food say theyll bring in signatures to state elections official today Initiative 522. (click here for full text) is an initiative to the Legislature, which means it would first go to the Legislature for possible adoption.

Tim Eyman, the professional initiative promoter, also is bringing in signatures this morning for I-517, which he says will protect the initiative process. A background story on it is here and the full text is here.

Friday is the deadline for filing signatures for measures to the Legislature. The petition-filing period begins Saturday for new initiatives to the people.

I-522 backer Chris McManus the Office of the Secretary of State he plans to submit 340,000 signatures at 1 p.m., which based on the historical invalidity rates of ballot measures should be more than enough to qualify. By law, the measure needs at least 241,153 valid voter signatures to be considered.

Assuming I-522 and I-517 qualify, and that lawmakers choose not to enact either one, each would go to the November ballot for consideration by voters statewide. Lawmakers could also refer a companion or alternative initiative. The Associated Press reports that California voters rejected a food disclosure measure last year.

Dave Ammons of the elections agency said in a blog post that I-522 would require most raw agricultural commodities, processed foods, and seeds and seed stocks, if produced using genetic engineering as defined, to be labeled as genetically engineered when offered for retail sale.

Text of the measure asserts that 49 nations have laws requiring disclosure of genetically modified foods and that the lack of disclosure on U.S. crops is interfering with this countrys ability to export crops to some countries. The measures preamble also says the public wants to know if their food was produced using genetic engineering and that Without disclosure, consumers of genetically engineered food unknowingly may violate their own dietary and religious restrictions.

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I-522 backers turning in signatures to send genetically-modified food measure to Legislature

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Public release date: 3-Jan-2013 [ | E-mail | Share ]

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

New Rochelle, NY, January 3, 2013Penetrating soft tissue injuries that may be caused by bullet wounds or motor vehicle accidents, or exposure to explosive devices in military settings, can cause muscle loss resulting in functional disability and cosmetic deformity. Efforts underway to develop tissue engineering solutions to repair and replace damaged and lost muscle will benefit greatly from the availability of robust animal models to test these innovative therapeutic strategies. A new rat model that simulates traumatic or surgical muscle tissue loss in humans is described in an article in BioResearch Open Access, a bimonthly peer-reviewed open access journal from Mary Ann Liebert, Inc., publishers. The article is available free on the BioResearch Open Access website.

Xiaowu Wu, MD, Benjamin T. Corona, PhD, Xiaoyu Chen, PhD, and Thomas J. Walters, PhD, United States Army Institute of Surgical Research (Fort Sam Houston, TX), Wake Forest Institute for Regenerative Medicine (Winston-Salem, NC), and University of Texas Health Science Center at San Antonio, provide a detailed description of the methods used to create an animal model with approximately 20% volumetric muscle loss (VML) from the middle third of the tibialis anterior muscle. The authors demonstrate successful repair of the injury using a biological scaffold and present their findings in "A Standardized Rat Model of Volumetric Muscle Loss Injury for the Development of Tissue Engineering Therapies."

###

About the Journal

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

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including ASSAY and Drug Development Technologies, Tissue Engineering, Stem Cells and Development, Human Gene Therapy, and AIDS Research and Human Retroviruses. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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

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New rat model for muscle regeneration after trauma-related soft tissue injury

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Jan. 3, 2013 Research out of the George Washington University (GW), published in the journal Proceedings of the National Academy of Sciences (PNAS), reveals another piece of the puzzle in a genetic developmental disorder that causes behavioral diseases such as autism. Anthony-Samuel LaMantia, Ph.D., professor of pharmacology and physiology at the GW School of Medicine and Health Sciences (SMHS) and director of the GW Institute for Neuroscience, along with post-doctoral fellow Daniel Meechan, Ph.D. and Thomas Maynard, Ph.D., associate research professor of pharmacology and physiology at GW SMHS, authored the study titled "Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome."

For the past nine years, LaMantia and his colleagues have been investigating how behavioral disorders such as autism, attention deficit hyperactivity disorder (ADHD), and schizophrenia arise during early brain development. His work published in PNAS focuses specifically on the effects diminished 22q11.2 gene dosage has on cortical circuit development.

This research shows for the first time that genetic lesions known to be associated with autism and other behavioral diseases disrupt cellular and molecular mechanisms that ensure normal development of a key type of cortical neuron: the interneuron. LaMantia and his colleagues had found previously that one type of cortical neuron, the projection neuron, is not generated in appropriate numbers during development in a mouse model of 22q11 Deletion Syndrome. In the current study published in PNAS, LaMantia found that interneurons, while made in the right numbers at their birthplace outside of the cortex, are not able to move properly into the cortex where they are needed to control cortical circuit activity. The research shows that the main reason they don't move properly is due to diminished expression of activity of a key regulatory pathway for migration, the Cxcr4 cytokine receptor.

"This gives us two pieces of the puzzle for this genetic developmental disorder," said LaMantia. "These two pieces tell us that in very early development, those with 22q11.2 deletion syndrome do not make enough cells in one case, and do not put the other cells in the right place. This occurs not because of some degenerative change, but because the mechanisms that make these cells and put them in the right place during the first step of development have gone awry due to mutation."

The next step in LaMantia's research is to probe further into the molecular mechanisms that disrupt the proliferation of projection neurons and migration of interneurons. "If we understand that better and understand its consequences, we can go about fixing it," said LaMantia. "We want to understand why cortical circuits don't get built properly due to the genetic deletion of chromosome 22."

LaMantia recently received the latest installment of a 10-year RO1 grant from the National Institutes of Health and the Eunice Kennedy Shriver National Institute of Child Health & Human Development for his project, titled "Regulation of 22q11 Genes in Embryonic and Adult Forebrain." This will allow him to further his research.

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The above story is reprinted from materials provided by George Washington University, via Newswise.

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New information on autism and genetics

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Public release date: 3-Jan-2013 [ | E-mail | Share ]

Contact: Lisa Anderson lisama2@gwu.edu 202-994-3121 George Washington University

WASHINGTON (Jan. 3, 2012) Research out of the George Washington University (GW), published in the journal Proceedings of the National Academy of Sciences (PNAS), reveals another piece of the puzzle in a genetic developmental disorder that causes behavioral diseases such as autism. Anthony-Samuel LaMantia, Ph.D., professor of pharmacology and physiology at the GW School of Medicine and Health Sciences (SMHS) and director of the GW Institute for Neuroscience, along with post-doctoral fellow Daniel Meechan, Ph.D. and Thomas Maynard, Ph.D., associate research professor of pharmacology and physiology at GW SMHS, authored the study titled "Cxcr4 regulation of interneuron migration is disrupted in 22q11.2 deletion syndrome."

For the past nine years, LaMantia and his colleagues have been investigating how behavioral disorders such as autism, attention deficit hyperactivity disorder (ADHD), and schizophrenia arise during early brain development. His work published in PNAS focuses specifically on the effects diminished 22q11.2 gene dosage has on cortical circuit development.

This research shows for the first time that genetic lesions known to be associated with autism and other behavioral diseases disrupt cellular and molecular mechanisms that ensure normal development of a key type of cortical neuron: the interneuron. LaMantia and his colleagues had found previously that one type of cortical neuron, the projection neuron, is not generated in appropriate numbers during development in a mouse model of 22q11 Deletion Syndrome. In the current study published in PNAS, LaMantia found that interneurons, while made in the right numbers at their birthplace outside of the cortex, are not able to move properly into the cortex where they are needed to control cortical circuit activity. The research shows that the main reason they don't move properly is due to diminished expression of activity of a key regulatory pathway for migration, the Cxcr4 cytokine receptor.

"This gives us two pieces of the puzzle for this genetic developmental disorder," said LaMantia. "These two pieces tell us that in very early development, those with 22q11.2 deletion syndrome do not make enough cells in one case, and do not put the other cells in the right place. This occurs not because of some degenerative change, but because the mechanisms that make these cells and put them in the right place during the first step of development have gone awry due to mutation."

The next step in LaMantia's research is to probe further into the molecular mechanisms that disrupt the proliferation of projection neurons and migration of interneurons. "If we understand that better and understand its consequences, we can go about fixing it," said LaMantia. "We want to understand why cortical circuits don't get built properly due to the genetic deletion of chromosome 22."

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LaMantia recently received the latest installment of a 10-year RO1 grant from the National Institutes of Health and the Eunice Kennedy Shriver National Institute of Child Health & Human Development for his project, titled "Regulation of 22q11 Genes in Embryonic and Adult Forebrain." This will allow him to further his research.

To interview Dr. LaMantia, please contact Lisa Anderson.

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GW professor discovers new information in the understanding of autism and genetics

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