Archive for the ‘Gene Therapy Research’ Category

FREE QVprep Lite Genetic Engineering App
QVprep Lite Genetic Engineering is FREE and has limited content. The app gives you the option to buy the paid QVprep Genetic Engineering app which has exhaus...

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QVprep Genetic Engineering App - Learn, Review and Test in Genetics
Covers * Introduction History of Genetic Engineering * Genetic Engineering Techniques * Genetic Engineering Experiments * Molecular Cloning * Gene Targetin...

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Sep. 4, 2013 Researchers at Johns Hopkins and the National Institutes of Health have identified a compound that dramatically bolsters learning and memory when given to mice with a Down syndrome-like condition on the day of birth. As they report in the Sept. 4 issue of Science Translational Medicine, the single-dose treatment appears to enable the cerebellum of the rodents' brains to grow to a normal size.

The scientists caution that use of the compound, a small molecule known as a sonic hedgehog pathway agonist, has not been proven safe to try in people with Down syndrome, but say their experiments hold promise for developing drugs like it.

"Most people with Down syndrome have a cerebellum that's about 60 percent of the normal size," says Roger Reeves, Ph.D., a professor in the McKusick-Nathans Institute of Genetic Medicine at the Johns Hopkins University School of Medicine. "We treated the Down syndrome-like mice with a compound we thought might normalize the cerebellum's growth, and it worked beautifully. What we didn't expect were the effects on learning and memory, which are generally controlled by the hippocampus, not the cerebellum."

Reeves has devoted his career to studying Down syndrome, a condition that occurs when people have three, rather than the usual two, copies of chromosome 21. As a result of this "trisomy," people with Down syndrome have extra copies of the more than 300 genes housed on that chromosome, which leads to intellectual disabilities, distinctive facial features and sometimes heart problems and other health effects. Since the condition involves so many genes, developing treatments for it is a formidable challenge, Reeves says.

For the current experiments, Reeves and his colleagues used mice that were genetically engineered to have extra copies of about half of the genes found on human chromosome 21. The mice have many characteristics similar to those of people with Down syndrome, including relatively small cerebellums and difficulty learning and remembering how to navigate through a familiar space. (In the case of the mice, this was tested by tracking how readily the animals located a platform while swimming in a so-called water maze.) Based on previous experiments on how Down syndrome affects brain development, the researchers tried supercharging a biochemical chain of events known as the sonic hedgehog pathway that triggers growth and development. They used a compound -- a sonic hedgehog pathway agonist -- that could do just that.

The compound was injected into the Down syndrome-like mice just once, on the day of birth, while their cerebellums were still developing. "We were able to completely normalize growth of the cerebellum through adulthood with that single injection," Reeves says.

But the research team went beyond measuring the cerebellums, looking for changes in behavior, too. "Making the animals, synthesizing the compound and guessing the right dose were so difficult and time-consuming that we wanted to get as much data out of the experiment as we could," Reeves says. The team tested the treated mice against untreated Down syndrome-like mice and normal mice in a variety of ways, and found that the treated mice did just as well as the normal ones on the water maze test.

Reeves says further research is needed to learn why exactly the treatment works, because their examination of certain cells in the hippocampus known to be involved in learning and affected by Down syndrome appeared unchanged by the sonic hedgehog agonist treatment. One idea is that the treatment improved learning by strengthening communication between the cerebellum and the hippocampus, he says.

As for the compound's potential to become a human drug, the problem, Reeves says, is that altering an important biological chain of events like sonic hedgehog would likely have many unintended effects throughout the body, such as raising the risk of cancer by triggering inappropriate growth. But now that the team has seen the potential of this strategy, they will look for more targeted ways to safely harness the power of sonic hedgehog in the cerebellum. Even if his team succeeds in developing a clinically useful drug, however, Reeves cautions that it wouldn't constitute a "cure" for the learning and memory-related effects of Down syndrome. "Down syndrome is very complex, and nobody thinks there's going to be a silver bullet that normalizes cognition," he says. "Multiple approaches will be needed."

Other authors on the paper were Jung H. Shin of the National Institute on Alcohol Abuse and Alcoholism, and Ishita Das, Joo-Min Park, Soo Kyeong Jeon, Hernan Lorenzi, David J. Linden and Paul F. Worley, all of the Johns Hopkins University School of Medicine. The study was funded by the Down Syndrome Research and Treatment Foundation, Research Down Syndrome, the National Institute of Child Health and Human Development (grant number R01 HD38384), the intramural programs of the National Institute on Alcohol Abuse and Alcoholism, the National Institute of Mental Health (grant number MH51106) and the National Institute of Neurological Disorders and Stroke (grant number R01 NS39156).

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Experimental compound reverses down syndrome-like learning deficits in mice

Newswise Case Western Reserve researchers have identified a genetic factor that blocks the blood vessel inflammation that can lead to heart attacks, strokes and other potentially life-threatening events.

The breakthrough involving Kruppel-like factor (KLF) 15 is the latest in a string of discoveries from the laboratory of professor of medicine Mukesh K. Jain, MD, FAHA, that involves a remarkable genetic family. Kruppel-like factors appear to play prominent roles in everything from cardiac health and obesity to metabolism and childhood muscular dystrophy.

School of Medicine instructor Yuan Lu, MD, a member of Jains team, led the study involving KLF-15 and its role in inflammation, which appears online this week in the Journal of Clinical Investigation. Lu and colleagues observed that KLF-15 blocks the function of a molecule called NF-kB, a dominant factor responsible for triggering inflammation.

This finding reveals a new understanding of the origins of inflammation in vascular diseases, and may eventually lead to new, targeted treatment options.

It had been suspected that smooth muscle cells were related to inflammation, but it hadnt been pinpointed and specifically linked to disease, said Jain, Ellery Sedgwick Jr. Chair and director, Case Cardiovascular Research Institute at Case Western Reserve School of Medicine. Jain also is chief research officer for the Harrington Heart & Vascular Institute at University Hospitals Case Medical Center. This work provides cogent evidence that smooth muscle cells can initiate inflammation and thereby promote the development of vascular disease.

Smooth muscle cells are only one of two major cell types within blood vessels walls. The other cell type, endothelium, has traditionally taken the blame for inflammation, but Jains study suggests that both cells are critically important in the development of vascular disease.

The researchers learned that expression of this factor appeared mainly in smooth muscle cells and that levels were markedly reduced in atherosclerotic human blood vessels. To establish causality, the team generated genetically-modified mice where they deleted KLF-15 gene in smooth muscle cells.

We expected to see more proliferation of the smooth muscle cells as this is a common response of this cell type in disease, Lu said, first author on the paper. Instead, we were surprised to see rampant vascular inflammation and hyper activated NF-kB, the master regulator of inflammation.

The results offer hope for the development of specific anti-inflammatory therapies for vascular disease. Cholesterol-lowering drugs such as statins have some anti-inflammatory effects, but despite their widespread use, the burden of vascular disease remains high.

Jains previous research of the KLF family of genetic factors revealed regulator functions in blood vessels. KLF4 was shown to potently inhibit inflammation in the endothelium, the other major cell type in vessels. The current work is first to establish a role for these factors in smooth muscle inflammation.

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Researchers Discover a New Pathway in Blood Vessel Inflammation and Disease

Sep. 4, 2013 Case Western Reserve researchers have identified a genetic factor that blocks the blood vessel inflammation that can lead to heart attacks, strokes and other potentially life-threatening events.

The breakthrough involving Kruppel-like factor (KLF) 15 is the latest in a string of discoveries from the laboratory of professor of medicine Mukesh K. Jain, MD, FAHA, that involves a remarkable genetic family. Kruppel-like factors appear to play prominent roles in everything from cardiac health and obesity to metabolism and childhood muscular dystrophy.

School of Medicine instructor Yuan Lu, MD, a member of Jains team, led the study involving KLF-15 and its role in inflammation, which appears online this week in the Journal of Clinical Investigation. Lu and colleagues observed that KLF-15 blocks the function of a molecule called NF-kB, a dominant factor responsible for triggering inflammation.

This finding reveals a new understanding of the origins of inflammation in vascular diseases, and may eventually lead to new, targeted treatment options.

It had been suspected that smooth muscle cells were related to inflammation, but it hadnt been pinpointed and specifically linked to disease, said Jain, Ellery Sedgwick Jr. Chair and director, Case Cardiovascular Research Institute at Case Western Reserve School of Medicine. Jain also is chief research officer for the Harrington Heart & Vascular Institute at University Hospitals Case Medical Center. This work provides cogent evidence that smooth muscle cells can initiate inflammation and thereby promote the development of vascular disease.

Smooth muscle cells are only one of two major cell types within blood vessels walls. The other cell type, endothelium, has traditionally taken the blame for inflammation, but Jains study suggests that both cells are critically important in the development of vascular disease.

The researchers learned that expression of this factor appeared mainly in smooth muscle cells and that levels were markedly reduced in atherosclerotic human blood vessels. To establish causality, the team generated genetically-modified mice where they deleted KLF-15 gene in smooth muscle cells.

We expected to see more proliferation of the smooth muscle cells as this is a common response of this cell type in disease, Lu said, first author on the paper. Instead, we were surprised to see rampant vascular inflammation and hyper activated NF-kB, the master regulator of inflammation.

The results offer hope for the development of specific anti-inflammatory therapies for vascular disease. Cholesterol-lowering drugs such as statins have some anti-inflammatory effects, but despite their widespread use, the burden of vascular disease remains high.

Jains previous research of the KLF family of genetic factors revealed regulator functions in blood vessels. KLF4 was shown to potently inhibit inflammation in the endothelium, the other major cell type in vessels. The current work is first to establish a role for these factors in smooth muscle inflammation.

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New pathway discovered in blood vessel inflammation and disease

Ulisses Jr talks genetics

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Ulisses Jr talks genetics - Video

Wheat Genetics Resource Center at K State
The director of the Wheat Genetics Resource Center at K-State, Bikram Gill, talks about the selection of K-State as the home for the National Science Foundat...

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Let #39;s Play Spore In 2013! - Part 5: That #39;s Genetics
Subscribe: http://www.youtube.com/subscription_center?add_user=nunny0206 Twitter: https://twitter.com/Nunny0206 Let #39;s Play Spore Hey everyone! Spore is back,...

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Genetics problems 3 (incomplete dominance)
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Genet...

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Genetics problems 3 (incomplete dominance) - Video

Elk Broken Pedicle and Genetics
Many believe that a broken pedicle on a bull elk is caused from an injury. Here are some examples of why some believe that it is actually genetics that cause...

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Elk Broken Pedicle and Genetics - Video

SALT LAKE CITY, Sept. 4, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) announced today that it has entered into an expanded, nonexclusive global collaboration agreement with AstraZeneca to provide companion diagnostics for the olaparib Phase 3 clinical development program. Olaparib is an investigational orally active poly-ADP ribose polymerase (PARP) inhibitor being developed by AstraZeneca for the treatment of various tumor types including BRCA-mutated breast and ovarian cancers.

Under the expanded agreement, Myriad will build out a new laboratory within its Salt Lake City facility in accordance with U.S. Food and Drug Administration (FDA) regulations for companion diagnostic devices. In August, the FDA approved the Investigational Device Exemption (IDE) for BRACAnalysis(R) filed by Myriad, enabling clinical studies with olaparib to include BRACAnalysis testing as a companion diagnostic.

"We are excited to be expanding our companion diagnostic collaboration with AstraZeneca," said Peter D. Meldrum, president and CEO of Myriad. "We are working together to transform the future of personalized medicine and to deliver significant value for patients and the healthcare system, and we are committed to being a leader in companion diagnostics."

The collaboration builds on an existing agreement through which Myriad provided supply of BRACAnalysis to support the Phase 2 development program for olaparib in breast and ovarian cancers. Specific terms were not disclosed.

"Our hope is that the Phase 3 development program for olaparib will result in a new treatment option for patients suffering from BRCA-mutated ovarian and breast cancers, accompanied by a diagnostic to help physicians identify the patients for whom the therapy might be most appropriate," said Ruth March, vice president and head of Personalised Healthcare and Biomarkers at AstraZeneca. "Myriad is well positioned to provide high quality BRCA mutation testing services and the infrastructure to offer testing to support therapy choices."

Olaparib is a novel investigational PARP inhibitor that induces synthetic lethality in homozygous BRCA-deficient cells. Phase II clinical data presented at ASCO 2013 demonstrated that patients with BRCA mutated ovarian cancers received the most clinical benefit from maintenance treatment with olaparib. BRACAnalysis is the gold standard diagnostic test to confirm the presence of a BRCA gene mutation.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

Myriad, the Myriad logo and BRACAnalysis are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and other countries. MYGN-F, MYGN-G

About AstraZeneca

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Myriad Genetics Expands Collaboration with AstraZeneca on Olaparib Phase 3 Clinical Trials

September 4, 2013

April Flowers for redOrbit.com Your Universe Online

There is no simple recipe for raising children, as any parent will tell you. Parents receive hefty doses of advice often unsolicited from others, however the advice generally fails to consider one critical factor: the child. A new literature review of dozens of studies, performed by Hebrew University of Jerusalem, used more than 14,600 pairs of twins to reveal that childrens genetics significantly affect how they are parented.

There is a lot of pressure on parents these days to produce children that excel in everything, socially and academically, says Reut Avinun of the Hebrew University of Jerusalem. Since children are not born tabula rasa [blank slate], I felt it was important to explore their side of the story, to show how they can affect their environment, and specifically parental behavior. The research team found that most studies had focused on how parents affect their childrens experiences instead of the reverse.

Avinun and his colleague Ariel Knafo looked to twins to explore the other side of the equation. Identical twins share 100 percent of their genes, while fraternal twins share an average of 50 percent of their genes. The researchers reasoned that if parents treat identical twins more similarly than fraternal twins, it suggests that the childs genes shape parenting behaviors.

The research team found that childrens genetically-influenced characteristics do affect parental behavior across 32 studies involving twins. They estimated that a childs genetics influenced 23 percent of genetic differences in parenting. Children evoke different responses from their environment through genotype-related differences. An antisocial child, for example, is more likely to elicit harsh discipline than a more social child.

Boys with less self-control are more likely to experience lower levels of maternal behavior, according to one recent study the team examined. A particular genotype a polymorphic region in the gene that codes for the serotonin transporter predicted mothers levels of positive parenting and the boys level of self-control. This was not true for girls. In other words, boys genetically influenced level of self-control affected the behavior of their mothers toward them, Avinun says.

The research team found that childrens shared environment including socioeconomic factors, cultural exposure and others accounted for 43 percent of parenting differences. The non-shared environment different schools, friends, etc. accounted for 34 percent of the differences. The researchers suggest that parenting does not necessarily affect children in the same family similarly.

The extent to which parenting is influenced by genetics is influenced by several factors. For example, the researchers found that age was important. This supports the theory that the childs genetic influence on parenting increases with age. As children become increasingly autonomous, their genetic tendencies are more likely to be able to affect their behavior, which in turn influences parental behavior, Avinun says.

Overall, Avinun says that their research means that parenting should not be viewed solely as a characteristic of the parent, but as something that results from both parental and child attributes. This means that any interventions or treatments considered to help parenting should take into account both the parents and children. These interventions could vary even within a family.

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Parenting 101: Genetics Of The Child Can Influence Parenting Style

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (SGEN) announced today that Clay B. Siegall, Ph.D., President and Chief Executive Officer, will present at the Morgan Stanley Global Healthcare Conference on Tuesday, September 10, 2013, at 2:05 p.m. Eastern Time. The presentation will be webcast live and available for replay from Seattle Genetics website at http://www.seattlegenetics.com in the Investors and News section.

About Seattle Genetics

Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The companys lead program, ADCETRIS (brentuximab vedotin), received accelerated approval from the U.S. Food and Drug Administration in August 2011 and approval with conditions from Health Canada in February 2013 for two indications. In addition, under a collaboration with Millennium: The Takeda Oncology Company, ADCETRIS received conditional approval from the European Commission in October 2012. Seattle Genetics is also advancing a robust pipeline of clinical-stage ADC programs: SGN-75, ASG-22ME, SGN-CD19A, SGN-CD33A, ASG-15ME and SGN-LIV1A. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including AbbVie, Agensys (an affiliate of Astellas), Bayer, Celldex, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys and Genmab. More information can be found at http://www.seattlegenetics.com.

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Seattle Genetics to Present at Morgan Stanley Global Healthcare Conference

Researchers at the National Institutes of Health have found that suppressing the expression of a single gene in mice extends their average lifespan by about 20 percent the equivalent of humans living an average of 95 years. While modification of the so-called mTOR gene may not lead to the fountain of youth, further study could open up a path to keeping us healthier and more alert in our old age.

The findings of the NIH study indicate that the median lifespan of the wild-type mice was 25.4 months, compared to 30.3 months for the mTOR-suppressed mice, an increase of over 19 percent. The maximum lifespan of the mTOR-suppressed mice was increased by about 12 percent, to about 1.5 times the median lifespan of the wild-type mice. In human terms, this would correspond to nearly 120 years of age, which is getting close to the 122 years survived by Jeanne Calment, the oldest human on (reliable) record.

There were a mixed bag of other effects on the mTOR-suppressed mice. They tended to suffer more infections and more severe age-related bone density loss than did wild-type mice. On the other hand, the genetically engineered mice had fewer tumors (one of the primary causes of death of laboratory mice), and experienced a slower transition into senility (mental and physical) than did the wild-type mice.

The mTOR gene is associated with metabolism and energy balance, suggesting that its suppression may have effects similar to those of caloric restriction. Previous research has shown that eating a very-low calorie diet increases the lifespan of mice and rhesus macaques, inspiring some people to follow such a diet. However, a recent study of 41 strains of mice found that one-third of the strains showed no change in lifespan in response to caloric restriction, and of the remainder, more strains had shorter rather than longer lifespans. An analysis of the studies on rhesus monkeys showed that if you include all forms of death, they do not on average live longer on calorie restricted diets.

The structure of the rapamycin-FKBP12-mTOR complex - pink is rapamycin, blue is FKBP12, and red is mTOR (Photo: Fvasconcellos via Wikipedia)

The immunosuppressant drug rapamycin shows effects similar to those claimed for caloric restriction. The mode of operation is thought to be suppression of the mTOR gene, which regulates numerous metabolic and inflammation pathways. However, rapamycin does not appear to be a musine fountain of youth. A recent study shows that populations of mice treated with rapamycin do appear to live longer, but the rate at which they age is not slowed. The effect now appears not to be a general slowing of aging (although senility appears to have a slower onset), but rather that fewer premature deaths occur from formation of tumors.

The NIH team decided to study suppression of the mTOR gene in a more focused way. They used a new technique to genetically engineer a strain of mice which produced only about one-quarter of the mTOR protein found in normal mice. They found mTOR suppression does correlate with 20 percent longer lifespan, but there is no consistent slowing of the aging process.

These findings suggest that mTOR suppression could provide benefits to an aging population by keeping people healthier as they get older. This is clearly a worthwhile target for further research, and if such research also reveals how to extend the human lifespan, well, two birds with one stone.

The NIH study was recently published in the journal Cell Reports [PDF].

Source: National Institutes of Health

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Partial gene knockout produces long-lived mice

Sep. 3, 2013 Ground-breaking new research from a team of evolutionary biologists at Indiana University shows for the first time how asexual lineages of a species are doomed not necessarily from a long, slow accumulation of new mutations, but rather from fast-paced gene conversion processes that simply unmask pre-existing deleterious recessive mutations.

Geneticists have long bet on the success of sexual reproduction over asexual reproduction based in a large part on the process known as Muller's ratchet, the mechanism by which a genome accrues deleterious and irreversible mutations after the host organism has lost its ability to carry out the important gene-shuffling job of recombination.

The new work from the laboratory of IU Distinguished Professor of Biology Michael Lynch instead indicates that most deleterious DNA sequences contributing to the extinction process are actually present in the sexual ancestors, albeit in recessive form, and simply become exposed via fast-paced gene conversion and deletion processes that eliminate the fit genes from one of the parental chromosomes.

After sequencing the entire genomes of 11 sexual and 11 asexual genotypes of Daphnia pulex, a model organism for the study of reproduction that is more commonly known as the water flea, the team discovered that every asexual genotype shared common combinations of alleles for two different chromosomes transmitted by asexual males without recombination.

Asexual males then spread the genetic elements for suppressing meiosis, the type of cell division necessary for sexual reproduction, into sexual populations. The unique feature of this system is that although females become asexual, their sons need not be, and instead have the ability to spread the asexuality gene to sexual populations -- in effect, by a process of contagious asexuality.

"One might think of this process as a transmissible asexual disease," Lynch said. Exposure of pre-existing, deleterious alleles is, incidentally, a major cause of cancer, he added.

In another remarkable finding from the genome-wide survey for asexual markers, the team was also able to determine the age of the entire asexual radiation for D. pulex. Just a few years ago biologists were guessing that asexual daphnia lineages could be millions of years old, and most recent estimates put it between 1,000 years and 172,000 years. But new calculations for the molecular evolutionary rates of the two chromosomes implicated in asexuality date the establishment and spread of the asexual lineage to just 1,250 years ago. Some current asexual lineages, in fact, were only decades old, younger than Lynch himself.

"A pond of asexual daphnia may go extinct quite rapidly owing to these deleterious-gene-exposing processes, but the small chromosomal regions responsible for asexuality survive by jumping to new sexual populations where they again transform the local individuals to asexuality by repeated backcrossing," Lynch said. "Soon after such a transformation, the processes of gene conversion and deletion restarts, thereby again exposing resident pre-existing mutations leading to another local extinction event. As far as the sexual populations are concerned, asexuality is infectious, spreading across vast geographic distances while undergoing no recombination."

Lynch said it remains unclear what the ultimate fate of the entire sexual species will be and whether all sexual populations will be eventually displaced by the westward march of asexual lineages.

The team from the IU College of Arts and Sciences' Department of Biology used sexual and asexual daphnia sourced from ponds and lakes in six states and two Canadian provinces. The new work supported past research showing that a westward expansion of asexual lineages began in northeastern North America.

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Death by asexuality: Biologists uncover new path for mutations to arise

Published: September 03, 2013 6:00 AM

To the Editor,

At a Nanaimo City Council meeting Monday night, I heard speakers opposing genetically engineered foods, and one supporting them.

Former soil biologist Thierry Vrain, who worked for 30 years for Agriculture Canada as a genetic engineer, is well aware that genetic engineering is a very imprecise technology. He explained that when genetic engineering technology began, it was based on the theory that each gene codes for a single protein. But in 2002, the Human Genome Project was completed, making the old scientific paradigm obsolete. The new knowledge means that "every scientist now learns that any gene can give more than one protein, and that inserting a gene anywhere in a plant eventually creates rogue proteins. Some of these proteins are obviously allergenic or toxic."

Professor Robert Wager, who teaches at VIU and is a staunch supporter of GMO technology, told us there are no unintended consequences of GMO foods after 25 years. He has obviously not read a study completed in June of 2012 called GMO Myths and Truths, available for free online at Earth Open Source. He said there are no lawsuits being brought forth, but seems to be unaware of the fact that many US farmers are suing Monsanto whose GMO seeds are contaminating their non GMO crop fields. Mr. Wager continues to claim that "all of the alleged dangers of GM crops and food have been analyzed by global experts and dismissed." He also rejects research that demonstrates harm from GM crops and food as "pseudo-science," and boldly puts Dr. Vrain's research in that dismissive category.

It is not uncommon to find experts and authorities on both sides of a controversial issue. For such significant issues as the safety of our food supply and planetary environment, is it not appropriate to look at the integrity of the research, who is funding it, and who publishes it? In May of this year, a former Monsanto researcher joined the editorial staff of the journal Food and Chemical Toxicology. Such potential for conflict of interest, where one person can control or prevent the publication of research that would be inconvenient to the biotech industry, means that the public cannot trust peer-reviewed journals to reflect the true state of scientific knowledge. Add to this the well-known fact that scientists often choose to say yes to their research being funded by industry, a fact Dr. Vrain knows very well from being a member of the scientific community for 30 years.

On May 25 of this year, two million people from 52 countries marched against Monsanto, producer of 90 per cent of the world's genetically modified seed. They marched against a trans-national company having monopoly control of the world's food supply. Monsanto forces farmers who buy their seed to sign a contract stating they will not save seed. At a time when the world is focusing on food, it is time we realized that we have food today because farmers have saved seed every year for the next crop. In no way is forcing farmers to buy seed every year a sustainable practice.

If you care about the future of our food supply, I suggest to devote 90 minutes to watch the hard-hitting 2008 documentary, The World According to Monsanto, in which investigative journalist uncovers Monsanto's long track record of environmental crimes and health scandals. It is very important to understand that Monsanto is the same company that brought the world the toxins known as PCBs, dioxins and Agent Orange. Why in the name of everything we hold sacred should we trust the future of our food supply to this company?

Tsiporah Grignon Gabriola Island

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GMO leaves sour taste

Think tank calls for GE-free farming

Media release 3 September 2013 FOR IMMEDIATE RELEASE

A Wellington think tanks call for New Zealand to be a GE-free food and fibre producer has been welcomed by the Soil & Health Association. The latest McGuinness Institute report, An Overview of Genetic Modification in New Zealand, 19732013 was released on 29 August.

This comprehensive and thoroughly researched report sums up a lot of what weve been saying for years, says Marion Thomson, co-chair of Soil & Health Organic NZ. Soil & Health agrees with its recommendations, including a moratorium on growing genetically engineered crops, and a thorough review of the systems and policy gaps around GE.

The McGuinness report also calls for the implementation of all the recommendations made by the Royal Commission on Genetic Modification in 2001. Soil & Health has continued to ask for this. Many of the recommendations have never been carried out, such as adequate liability laws, or have been discontinued, like the Bioethics Council.

The risks of GE are too high, and our laws dont protect the public from financial liability when things go wrong. This is why local governments are moving to protect their communities, says Thomson.

This report should be required reading for all New Zealanders involved in decision-making about genetic engineering. This includes all levels of government, from central government agencies such as the Environmental Protection Agency and CRIs like AgResearch and Scion, to local governments.

The McGuinness Institute report points out the lack of investment value for New Zealanders in genetic engineering. Of the 57 field trials held here since 1988, Not one of these has resulted in any commercial benefit or tangible return on the publics investment, while all experiments have presented a constant risk.1

Soil & Health, established in 1941, is one of the worlds oldest organic organisations and publishes Organic NZ. We advocate for peoples right to have fresh, healthy, organic food and water free of GE, pesticides and additives. Oranga nuku, oranga kai, oranga tangata. http://organicnz.org.nz http://www.facebook.com/OrganicNZ

Reference 1. McGuinness, Wendy, and Mokena-Lodge, Renata, An Overview of Genetic Modification in New Zealand, 19732013: The first forty years, McGuinness Institute, Wellington, 29 August 2013 http://mcguinnessinstitute.org/includes/download.aspx?ID=130247

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Think tank calls for GE-free farming

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

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

New Rochelle, NY, September 3, 2013A new recombinant antibody can detect and isolate mesenchymal stem cells (MSCs), a nonembryonic source of stem cells with promising applications in tissue engineering, blood stem cell transplantation, and treatments for immune-mediated disorders. The antibody recognizes an i blood group antigen present on MSCs in umbilical cord blood, as described in a study published in BioResearch Open Access, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the BioResearch Open Access website.

Tia Hirvonen and coauthors from the Finnish Red Cross Blood Service, Glykos Finland Ltd., and Biova Ltd. (Helsinki), and VTT Technical Research Center of Finland (Espoo), identified a blood donor with high levels of antibody to the i blood group antigen. No antibodies recognizing this antigen are commercially available at present.

In the article "Production of a Recombinant Antibody Specific for i Blood Group Antigen, a Mesenchymal Stem Cell Marker," the authors explain that the i antigen can serve as a marker to detect and isolate MSCs in umbilical cord blood (UCB). They describe the use of antibody phage display technology to produce a recombinant anti-i antibody that recognizes i antigen on the surface of UCB-MSCs as well as on red blood cells.

"The authors have used antibody phage display technology to generate an anti-i antibody," says BioResearch Open Access Editor Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland. "The advantage of this technique is that antibodies against poorly immunogenic molecules can be generated, as an immunization strategy is not required. The availability of an anti-i antibody has the potential to improve the isolation efficiency of MSCs from umbilical cord blood samples."

###

About the Journal

BioResearch Open Access is a bimonthly peer-reviewed open access journal led by Editor-in-Chief Robert Lanza, MD, Chief Scientific Officer, Advanced Cell Technology, Inc. and Editor Jane Taylor, PhD. The Journal 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.

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New recombinant antibody can isolate stem cells from umbilical cord blood

Published: Monday, September 2, 2013 at 11:49 p.m. Last Modified: Monday, September 2, 2013 at 11:49 p.m.

The 29-year-old Auburndale woman, a private nanny, represents one of the millions of U.S. consumers the Florida citrus industry will have to deal with if it takes the path of using genetically engineered trees as a solution to citrus greening, a fatal bacterial disease threatening commercial citrus production in the state.

Citrus growers are desperate for a long-term solution to greening, and most agree developing new trees tolerant or resistant to greening would be the best solution. But many in the Florida citrus community, fearing a consumer backlash from people such as Harp, question that scientists should pursue genetic engineering in breeding a greening-resistant tree.

Meanwhile, the debate continues with GMO supporters, including chemical and food companies and farmers who grow GMO crops, claiming there's no scientific proof the technology is unsafe. On the other side are people such as Harp with the support of some scientists who argue the GMO technology must be proven safe before its products are released into the marketplace.

Harp was one of the local organizers of the May 25 international "March Against Monsanto," the St. Louis-based company that is one of the leading producers of plants containing genetically modified organisms (GMOs). The Winter Haven march drew a few dozen people, she said.

Harp became an anti-GMO activist because of her 14-year struggle with an intestinal disorder that several doctors could not diagnose, she said. Beginning at age 14 and with increasing regularity into her 20s, Harp experienced debilitating intestinal inflammation that caused "excruciating pain" that kept her bed-ridden, sometimes for days.

She did not return to health until she eliminated meat, wheat, gluten, soy, dairy and most processed foods from her diet, Harp said.

Because many of those products have GMO ingredients, notably soy, Harp associates GMOs with her health problems. She also has religious and moral objections.

"I believe your body is a vessel. In order for your spirit and soul to be in the best shape it can be, you've got to take care of your body," Harp said. "I think it (genetic engineering) is wrong. When you genetically modify something by manipulating its genes, you create a mutant. You don't know what would happen to the human body."

Jan Allen, who runs Pat's Apiaries in Auburndale with husband Patrick, takes a more pragmatic stance against GMO foods.

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Nature Vs. GMO: Sides Face Off Over Genetically Modified Food

Glendale, CA (PRWEB) September 03, 2013

Audio-Digest Foundation Announces the Release of Gastroenterology Volume 27, Issue 11: Celiac Disease.

The goal of this program is to improve the diagnosis and management of patients with celiac disease (CD). After hearing and assimilating this program, the clinician will be better able to:

1. Review the pathophysiology of CD 2. Assess the clinical manifestations of CD 3. Analyze the histologic findings associated with CD 4. Implement genetic and serologic testing for CD 5. Formulate a multidisciplinary management plan for patients diagnosed with CD

The original programs were presented by Dora M. Lam-Himlin, MD, Assistant Professor of Pathology and Senior Associate Consultant, Mayo Clinic, Arizona, Phoenix, and Joseph A. Murray, MD, Professor of Medicine, Consultant, Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN.

Audio-Digest Foundation, the largest independent publisher of Continuing Medical Education in the world, records over 10,000 hours of lectures every year in anesthesiology, emergency medicine, family practice, gastroenterology, general surgery, internal medicine, neurology, obstetrics/gynecology, oncology, ophthalmology, orthopaedics, otolaryngology, pediatrics, psychology, and urology, by the leading medical researchers at the top laboratories, universities, and institutions.

Recent researchers have hailed from Harvard, Cedars-Sinai, Mayo Clinic, UCSF, The University of Chicago Pritzker School of Medicine, The University of Kansas Medical Center, The University of California, San Diego, The University of Wisconsin School of Medicine, The University of California, San Francisco, School of Medicine, Johns Hopkins University School of Medicine, and many others.

Out of these cutting-edge programs, Audio-Digest then chooses the most clinically relevant, edits them for clarity, and publishes them either every week or every two weeks.

In addition, Audio-Digest publishes subscription series in conjunction with leading medical societies: DiabetesInsight with The American Diabetes Association, ACCEL with The American College of Cardiology, Continuum Audio with The American Academy of Neurology, and Journal Watch Audio General Medicine with Massachusetts Medical Society.

For 60 years, the global medical community of doctors, nurses, physician assistants, and other medical professionals around the world has subscribed to Audio-Digest specialty series in order to remain current in their specialties as well as to maintain their Continuing Education requirements with the most cutting-edge, independent, and unbiased continuing medical education (CME).

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Audio-Digest Foundation Announces the Release of Gastroenterology Volume 27, Issue 11: Celiac Disease

Genetics problems 2 (dihybrid cross)
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Genet...

By: Suman Bhattacharjee

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Genetics problems 2 (dihybrid cross) - Video

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The first private Medical Genetics Center in Romania, an investment worth more than two million Euros, was launched in Bucharest yesterday, during the conference entitled Personalized Medicine New Prospects for the Romanian Patien, Agerpres informs. The Center is part of the World Map of Next Generation Sequencers, a world network including the centers that use high-capacity genomic sequencer platforms, it has four floors totalling 650 square meters and offers integrated services of examination and genetic testing. The Microarray NimbleGen platform equipping the Personal Genetics medical genetics center is yet another unique initiative in the Romanian private medical sector, with major use in the prenatal and postnatal diagnosis, said Dr Bogdanka Militescu, the Genetics Center managing director. The Center is structured by two departments, molecular biology and cyto-genetics respectively and it also offers genetic and psychological counselling. The expertise of the molecular biology department is divided into three categories of tests: diagnosis tests, genetic predisposition tests and pharma-genetic tests. The cyto-genetics department provides complex cyto-genetic diagnosis both for the prenatal diagnosis based on tests taken from chorionic villus, amniotic liquid, fetal blood, conceptive product as well as for the postnatal diagnosis from peripheral blood tests for the newborn babies, children or adults and from the haematogenous bone marrow in order to identify various types of leukemia. Also conducted at the Center are tests for identifying lung cancer, colon cancer, the hereditary breast- and ovary cancer risk, among others. Studies show that if the women having a breast cancer diagnosis made a genetic test before beginning treatment, there would be 34 percent less chemotherapy. Moreover, some 17,000 strokes could be prevented every year if a genetic test were made to assess the patients response to anti-coagulant therapy.

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First private medical genetics Center, launched in Bucharest

Let #39;s Play The Sims 3 - Perfect Genetics Challenge - Episode 26
My Sims 3 Page: http://mypage.thesims3.com/mypage/Llandros2012 My Blog: http://Llandros09.blogspot.com My Facebook: https://www.facebook.com/Llandros09?ref=t...

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Let's Play The Sims 3 - Perfect Genetics Challenge - Episode 26 - Video

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

Vybion will present data on how its drug, INT41, alters a critical event in the development of Huntingtons disease at the 7th Neurodegenerative Conditions Research & Development Conference in Boston on September 9-10, 2013. INT41 is an Intrabody drug delivered by Gene Therapy that blocks gene dysregulation in Huntingtons Disease by neutralizing a toxic fragment of the Huntingtin mutant protein in the nucleus of the cell preventing gene dysregulation.

We are extremely excited by these data linking INT41 results to specific molecular events in Huntingtons pathology. INT41 provides a surgical approach to inactivate the event for which a growing body of evidence indicates occurs prior to symptoms and may be the driver of disease progression said Lee Henderson, Ph.D., the CEO of Vybion and a coauthor on the presentation. Vybion is pursuing the completion of preclinical development and expects to begin human clinical trials in the next 18 months.

About Vybion, Inc. Vybion is a development stage Company with proprietary technologies that form the core of our business strategy. Vybion uses proprietary technologies for Intrabody development to treat neurodegenerative diseases such as Huntington's, SBMA and SCA, and for target validation in signal transduction pathways and in multiple therapeutic areas. Vybion is advancing its novel research therapy for Huntingtons disease, INT41, through preclinical development with the aim of initiating clinical studies in the near future.

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Vybion’s Huntington Drug Neutralizes Critical Disease Driver

Cell Therapy Live - GOODIE MOB - AGE AGAINST THE MACHINE TO
I was so close for the stage monitors so the sound not as good in this video...BUT TRUST THE SHOW WAS INCREDIBLEEEEEE!!!!

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