Archive for the ‘Gene Therapy Research’ Category

By RTT News, February 04, 2014, 06:24:00 PM EDT

(RTTNews.com) - Myriad Genetics Inc. ( MYGN ), the molecular diagnostic company, Tuesday reported a better-than-expected increase in second-quarter profit, led by a 37 percent jump in revenues.

Myriad also announced a deal to buy molecular diagnostic laboratory Crescendo Bioscience Inc. for $270 million, subject to adjustments including a reduction of $25 million for debt repayments. Myriad expects to close the deal before the end of its fiscal 2014.

Looking ahead, Myriad again lifted its outlook for fiscal year 2014, citing the Crescendo acquisition and growth in core markets. The news boosted investor sentiment, with Myriad shares surging about 14 percent in after-hours trade on the Nasdaq.

For the fourth quarter, the Salt Lake City, Utah-based company posted net income of $50 million or $0.66 per share, compared with $35 million or $0.42 per share last year.

On average, 19 Analysts polled by Thomson Reuters estimated earnings of $0.46 per share for the quarter. Analysts' estimates typically exclude special items.

Revenues for the second quarter climbed to $204 million from $149 million in the prior year. Analysts estimated revenues of $176 million for the quarter.

Among segments, Molecular diagnostic testing revenue jumped 39 percent year-over-year, on strong growth in oncology and women's health businesses.

For fiscal 2014, Myriad now projects earnings of $2.09 to $2.12 per share on revenues of $740 million to $750 million. The company earlier estimated earnings of $1.92 to $1.97 per share on revenues of $700 million to $715 million. Analysts currently expect earnings of $1.97 per share on revenues of $705.62 million.

CEO Peter Meldrum said, "We plan to continue to execute upon our strategic plan of transitioning our hereditary cancer market, expanding our business internationally, and diversifying our revenue base with new product launches."

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Myriad Genetics Profit Up, To Acquire Crescendo Bioscience; Stock Jumps 14%

Gene Therapy May Treat Rare Form of Blindness1348

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Gene Therapy May Treat Rare Form of Blindness1348 - Video

Researchers used blood platelets and bone marrow cells to deliver potentially curative gene therapy to mouse models of the human genetic disorder Hurler syndrome -- an often fatal condition that causes organ damage and other medical complications.

Scientists from Cincinnati Children's Hospital Medical Center and the National Institute of Neurological Disorders and Stroke (NINDS) report their unique strategy for treating the disease the week of Feb. 3-7 in Proceedings of the National Academy of Sciences (PNAS).

Researchers were able to genetically insert into the cells a gene that produces a critical lysosomal enzyme (called IDUA) and then inject the engineered cells into mice to treat the disorder. Follow up tests showed the treatment resulted in a complete metabolic correction of the disease, according to the authors.

"Our findings demonstrate a unique and somewhat surprising delivery pathway for lysosomal enzymes," said Dao Pan, PhD, corresponding author and researcher in the Division of Experimental Hematology and Cancer Biology at Cincinnati Children's. "We show proof of concept that platelets and megakaryocytes are capable of generating and storing fully functional lysosomal enzymes, which can lead to their targeted and efficient delivery to vital tissues where they are needed."

The mice tested in the study modeled human Hurler syndrome, a subset of disease known as mucopolysaccharidosis type I (MPS I), one of the most common types of lysosomal storage diseases. MPS I is a lysosomal storage disease in which people do not make an enzyme called lysosomal alpha-L-iduronidase (IDUA).

IDUA helps break down sugar molecules found throughout the body, often in mucus and fluids around joints, according to the National Library of Medicine/National Institutes of Health. Without IDUA, sugar molecules build up and cause organ damage. Depending on severity, the syndrome can also cause deafness, abnormal bone growth, heart valve problems, joint disease, intellectual disabilities and death.

Enzyme replacement therapy can be used to treat the disease, but it is only temporary and not curative. Bone marrow transplant using hematopoietic stem cells also has been tested on some patients with mixed results. The transplant procedure can carry severe risks and does not always work.

Pan and her colleagues -- including Roscoe O. Brady, MD, a researcher at NINDS -- report that using platelets and megakaryocytes for gene therapy is effective and could reduce the risk of activating cancer-causing oncogenes in hematopoietic stem cells.

The authors said tests showed that human megakaryocytic cells were capable of overexpressing IDUA, revealing their capacity for potential therapeutic benefit. While engineering megakaryocytes and platelets for infusion into their mouse models of Hurler, the scientists report they were able to release IDUA directly into amply sized extracellular spaces or inside micro-particles as the cells matured or activated. The cells were able to produce and package large amounts of functional IDUA and retained the capacity to cross-correct patient cells.

After infusing mouse models of Hurler with the genetically modified cells, researchers said this led to long-term normalization of IDUA levels in the animal's blood with versatile delivery routes and on-target preferential distribution to the liver and spleen. The treatment led to a complete metabolic correction of MPS I in most peripheral organs of the mice.

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Gene therapy may be possible cure for Hurler syndrome: Mouse Study

Gene therapy defeats muscle disease in tests
Scientists studying myotubular myopathy, a devastating disorder, say a new therapy appears to rescue mice and dogs from the disease. The findings demonstrate...

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Gene therapy defeats muscle disease in tests - Video

PUBLIC RELEASE DATE:

4-Feb-2014

Contact: Nick Miller nicholas.miller@cchmc.org 513-803-6035 Cincinnati Children's Hospital Medical Center

CINCINNATI Researchers used blood platelets and bone marrow cells to deliver potentially curative gene therapy to mouse models of the human genetic disorder Hurler syndrome an often fatal condition that causes organ damage and other medical complications.

Scientists from Cincinnati Children's Hospital Medical Center and the National Institute of Neurological Disorders and Stroke (NINDS) report their unique strategy for treating the disease the week of Feb. 3-7 in Proceedings of the National Academy of Sciences (PNAS).

Researchers were able to genetically insert into the cells a gene that produces a critical lysosomal enzyme (called IDUA) and then inject the engineered cells into mice to treat the disorder. Follow up tests showed the treatment resulted in a complete metabolic correction of the disease, according to the authors.

"Our findings demonstrate a unique and somewhat surprising delivery pathway for lysosomal enzymes," said Dao Pan, PhD, corresponding author and researcher in the Division of Experimental Hematology and Cancer Biology at Cincinnati Children's. "We show proof of concept that platelets and megakaryocytes are capable of generating and storing fully functional lysosomal enzymes, which can lead to their targeted and efficient delivery to vital tissues where they are needed."

The mice tested in the study modeled human Hurler syndrome, a subset of disease known as mucopolysaccharidosis type I (MPS I), one of the most common types of lysosomal storage diseases. MPS I is a lysosomal storage disease in which people do not make an enzyme called lysosomal alpha-L-iduronidase (IDUA).

IDUA helps break down sugar molecules found throughout the body, often in mucus and fluids around joints, according to the National Library of Medicine/National Institutes of Health. Without IDUA, sugar molecules build up and cause organ damage. Depending on severity, the syndrome can also cause deafness, abnormal bone growth, heart valve problems, joint disease, intellectual disabilities and death.

Enzyme replacement therapy can be used to treat the disease, but it is only temporary and not curative. Bone marrow transplant using hematopoietic stem cells also has been tested on some patients with mixed results. The transplant procedure can carry severe risks and does not always work.

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Mouse study shows gene therapy may be possible cure for Hurler syndrome

5 hours ago by Dan Krotz One protein complex, two very different shapes and functions: In the top image, the scientists created an Mre11-Rad50 mutation that speeds up hydrolysis, yielding an open state that favors a high-fidelity way to repair DNA. In the bottom image, the scientists slowed down hydrolysis, resulting in a closed ATP-bound state that favors low-fidelity DNA repair. Credit: Tainer lab

(Phys.org) Maybe you've seen the movies or played with toy Transformers, those shape-shifting machines that morph in response to whatever challenge they face. It turns out that DNA-repair machines in your cells use a similar approach to fight cancer and other diseases, according to research led by scientists from the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab).

As reported in a pair of new studies, the scientists gained new insights into how a protein complex called Mre11-Rad50 reshapes itself to take on different DNA-repair tasks.

Their research sheds light on how this molecular restructuring leads to different outcomes in a cell. It could also guide the development of better cancer-fighting therapies and more effective gene therapies.

re11-Rad50's job is the same in your cells, your pet's cells, or any organism's. It detects and helps fix the gravest kind of DNA breaks in which both strands of a DNA double helix are cut. The protein complex binds to the broken DNA ends, sends out a signal that stops the cell from dividing, and uses its shape-shifting ability to choose which DNA repair process is launched to fix the broken DNA. If unrepaired, double strand breaks are lethal to the cell. In addition, a repair job gone wrong can lead to the proliferation of cancer cells.

Little is known about how the protein's Transformer-like capabilities relate to its DNA-repair functions, however.

To learn more, the scientists modified the protein complex in ways that were designed to affect just one of the many activities it undertakes. They then used structural biology, biochemistry, and genomic tools to study the impacts of these modifications.

"By targeting a single activity, we can make the protein complex go down a different pathway and learn how its dynamic structure changes," says John Tainer of Berkeley Lab's Life Sciences Division. He conducted the research with fellow Berkeley Lab scientist Gareth Williams and scientists from several other institutions.

Adds Williams, "In some cases, we sped up or slowed down the protein complex's movements, and by doing so we changed its biological outcomes."

Much of the research was conducted at the Advanced Light Source (ALS), a synchrotron located at Berkeley Lab that generates intense X-rays to probe the fundamental properties of substances. They used an ALS beamline called SYBILS, which combines X-ray scattering with X-ray diffraction capabilities. It yields atomic-resolution images of the crystal structures of proteins. It can also watch the transformation of the protein as it undergoes conformational changes.

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How a shape-shifting DNA-repair machine fights cancer

Y. NIU ET AL/CELL 2014

Two female cynomolgus monkeys named Mingming and Ningning are the first primates to have their genes precisely edited by scientists.

The two cynomolgus monkeys, also known as crab-eating macaques, are the first primates to have their genes precisely edited using a gene-snipping tool borrowed from bacteria, a team of Chinese scientistsreports January 30 inCell. The work is part of an effort to genetically engineer monkeys to produce mutations like those seen in human diseases, especially ones involving the brain.

Other researchers have inserted foreign genes into primates (SN: 6/20/09, p. 13), but until now, no one has succeeded in altering the animals own genes, says Guoping Feng, a neurobiologist at the McGovern Institute for Brain Research at MIT who was not involved in the work.

To alter the monkeys genes, Jiahao Sha of Nanjing Medical University and his colleagues wielded molecular scissors first discovered in bacteria. The scissors are a DNA-cutting enzyme called Cas9. In bacteria, Cas9 is part of a primitive immune system known as CRISPRs that defends against viruses by chopping up ones that the bacteria have encountered before and recognize as threats.

The technique has been used to edit the genes of human cells growing in laboratory dishes and in rats, mice and other laboratory organisms, but never before in a living primate.

Sha, along with Xingxu Huang of Nanjing University and Weizhi Ji of the Yunnan Key Laboratory of Primate Biomedical Research and Kunming Biomed International, injected mRNA used to produce Cas9 into single-celled monkey embryos. At the same time, the researchers inserted other small RNA molecules that would guide the enzyme to three genes the scientists wanted to disrupt. Once the enzyme reached the genes, it would snip the DNA, leaving the cell to attempt a repair. In some cases, the cell would be unable to repair the break correctly, leading to disruption of the genes activity.

Researchers hope to use the technique to disrupt genes linked to human diseases so they can study how the disease develops and test treatments. For this study, the researchers chose three genes to disrupt:NrOb1, which is involved in keeping embryonic stem cells flexible and for determining sex;Ppar-gamma, which helps regulate metabolism; andRag1, an immune system gene.

The researchers found that two of the three targeted genes had been simultaneously altered in eight of 15 injected embryos. Those eight embryos were transplanted into surrogate mothers. The researchers delivered the first two female babies, named Mingming and Ningning, from one of the surrogate moms on November 11, 2013. Both infants carry disruptedPpar-gammaandRag1genes. Two of the other surrogates miscarried, and the researchers said in an e-mail that they are awaiting the birth of the remaining baby monkeys.

Only the targeted genes were disrupted, the researchers reported. That fact is encouraging, says Jennifer Doudna, a biochemist and Howard Hughes Medical Institute investigator at the University of California, Berkeley who is a pioneer of CRISPR techniques. It suggests that CRISPRs could be used to repair some human genes without inadvertently damaging others.

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Scientists Genetically Engineered Monkeys To Have Human Diseases

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On average, organic farms support 34% more plant, insect and animal species than conventional farms, say Oxford University scientists.

Researchers looked at data going back thirty years and found that this effect has remained stable over time and shows no signs of decreasing.

'Our study has shown that organic farming, as an alternative to conventional farming, can yield significant long-term benefits for biodiversity,' said Sean Tuck of Oxford University's Department of Plant Sciences, lead author of the study. 'Organic methods could go some way towards halting the continued loss of diversity in industrialised nations.'

For pollinators such as bees, the number of different species was 50% higher on organic farms, although it is important to note that the study only looked at 'species richness'.

'Species richness tells us how many different species there are but does not say anything about the total number of organisms,' said Mr Tuck. 'There are many ways to study biodiversity and species richness is easy to measure, providing a useful starting point. Broadly speaking, high species richness usually indicates a variety of species with different functions. Taking the example of bees, species richness would tell us how many different species of bee were on each farm but not the total number of bees.'

The study, published this week in the Journal of Applied Ecology, looked at data from 94 previous studies covering 184 farm sites dating back to 1989. The researchers re-analysed the data using satellite imagery to estimate the land use in the landscape surrounding each farm site to see if this had an impact on species richness. The study was carried out by scientists at Oxford University and the Swedish University of Agricultural Science, and partly funded by the Natural Environment Research Council (NERC).

Organic farms had a bigger impact on species richness when the land around them was more intensively farmed, particularly when it contained large tracts of arable land. Arable land is defined as land occupied by crops that are sown and harvested in the same agricultural year, such as wheat or barley.

'We found that the impacts of organic farms on species richness were more pronounced when they were located in intensively-farmed regions,' said Dr Lindsay Turnbull of Oxford University's Department of Plant Sciences, senior author of the study. 'This makes sense because the biodiversity benefits of each organic farm will be diluted in clusters of organic farms compared to an organic 'island' providing rich habitats in a sea of pesticide-covered conventional fields. This effect was weakest in pollinators, which may be because pollinators are likely to visit neighbouring farms and could be affected by pesticides there.'

The impact of organic farming on total species richness varied significantly across the data, with the average gain in species richness varying between 26% and 43%. This variation could be down to a number of factors relating to regional variation in farming practices and definitions of 'organic'.

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Organic farms support more species

PUBLIC RELEASE DATE:

3-Feb-2014

Contact: Rachel Seroka rseroka@aan.com 612-928-6129 American Academy of Neurology

MINNEAPOLIS New research shows how pesticides may increase the risk of Parkinson's disease and that people with certain gene variants may be more susceptible to the disease. The research is published in the February 4, 2014, print issue of Neurology, the medical journal of the American Academy of Neurology.

The research shows that certain pesticides that inhibit an enzyme called aldehyde dehydrogenase (ALDH) are related to an increased risk of Parkinson's disease. The enzyme plays a role in detoxifying substances in cells, along with metabolism of alcohol. The study also found that people with a variant of the ALDH2 gene were two to five times more likely to develop Parkinson's disease with exposure to these pesticides than people who did not have that gene variant.

"These results show that ALDH inhibition appears to be an important mechanism through which pesticides may contribute to the development of Parkinson's disease," said study author Jeff M. Bronstein, MD, PhD, of the David Geffen School of Medicine at UCLA and the Greater Los Angeles Veterans Affairs Medical Center and a member of the American Academy of Neurology. "Understanding this mechanism may reveal several potential targets for preventing the disease from occurring or reducing its progression."

The study involved 360 people with Parkinson's disease in three rural California counties who were compared to 816 people in the area who did not have the disease. Researchers looked at participants' exposure to pesticides at work and at home using a geographic computer model based on information from the California Department of Pesticide Regulation.

The researchers developed a test to identify which pesticides inhibited ALDH. The 11 pesticides that inhibited ALDH, all used in farming, fell into four structural classesdithiocarbamates, imidazoles, dicarboxymides and organochlorides. Exposure to an ALDH-inhibiting pesticide at both the workplace and at home was associated with increased risks of developing Parkinson's disease, ranging from 65 percent for the pesticide benomyl to six times the risk for the pesticide dieldrin. People who were exposed to three or more of the pesticides at both work and home were 3.5 times more likely to develop Parkinson's disease as those who were not exposed.

Bronstein noted that the relationship between the gene variant and Parkinson's only appeared when people had been exposed to the pesticides. "In other words, having this gene variant alone does not make you more likely to develop Parkinson's," he said. "Parkinson's is a disease that in many cases may require both genetics and environmental factors to arise."

Bronstein said the findings provide several possible targets for lowering Parkinson's risk, including reducing exposure to pesticides and improving the functioning of ALDH.

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Research identifies how pesticides may increase risk of Parkinson's disease

Scientists in China have created two monkeys with customized gene mutations. The successful births of the twin macaques, named Ningning and Mingming, may bring researchers closer to being able to recreate such human diseases as Alzheimers and Parkinsons in primates. This would allow scientists to use primates, rather than rodents, as more realistic models of human illness.

To engineer the monkeys, researchers at Nanjing University and Yunnan Key Laboratory of Primate Biomedical Research in Kunming, China, used a new gene-editing technology called Crispr, which allows scientists to insert, delete, or rewrite a specific gene sequence. The technique, which may help usher in a new era of genetic medicine, has previously been used to manipulate the genomes of rats, mice, and zebrafish. But this is reportedly the first time it has been used successfully in primates.

The Chinese researchers altered genes in several fertilized monkey eggs before implanting them in surrogate mothers. (Several surrogates miscarried and some pregnancies are reportedly ongoing.) Newborn Ningning and Mingming have three modified genes: one that regulates metabolism, another that regulates immune cell development, and a third that regulates stem cells and sex determination, according to the MIT Technology Review.

The infant monkeys are too young for researchers to determine the physiological and behavioral effects of their mutations, but scientists worldwide are already looking to create their own Crispr-modified monkeys. Although mice are giving us tremendous insight into basic brain biology and the biology of the disease, theres still a big gap in between the mouse brain and the monkey brain, Robert Desimone, director of MITs McGovern Brain Institute for Brain Research, told the MIT Technology Review. Not to mention that several drugs that work in mice dont work in humans.

Researchers also hope that the possibility of using genetically-modified monkeys will encourage more companies to boost spending on drugs to treat neurological disorders, reversing a recent trend of large pharmaceutical companies pulling back from such risky research. They also say Crispr may eventually be used for human gene therapy to treat inherited diseases such as cystic fibrosis and sickle-cell anemia. The ability to alter DNA is also being investigated as a way to make people resistant to HIV.

Chinas mutant-monkey breakthrough is controversial among animal rights activists. According to PETA, more than 125,000 primates are kept in U.S. laboratories and used for experiments every year.

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China Creates Monkeys With Custom Gene Mutations

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Newswise BUFFALO, NY New evidence reported by researchers at Roswell Park Cancer Institute (RPCI) lends support to the hypothesis that the SSeCKS/AKAP12 gene is a key inhibitor of prostate cancer metastasis. The data are some of the first to demonstrate this dynamic in transgenic animal models, with promising implications for development of targeted therapies for prostate cancer and perhaps for other solid-tumor cancers.

A team led by Irwin H. Gelman, PhD, noted that aggressive prostate cancers in humans typically turn off or delete two major regulatory genes, SSeCKS/AKAP12 and Rb. To explore this dynamic, the researchers developed a transgenic animal model to study the effects on prostate cancer progression of deleting these two genes. They report in Cancer Research, a peer-reviewed journal published by the American Association for Cancer Research, that the loss of these two genes and associated protein products leads to early prostate cancer. Moreover, more than 80 percent of the transgenic models in their study developed metastatic lesions in lymph nodes near the prostate.

This correlates with our earlier finding that SSeCKS/AKAP12 inhibits the chemotaxis of metastatic prostate tumor cells that is, their ability to move on to another environment in response to chemical attractants, said Dr. Gelman, the John & Santa Palisano Chair in Cancer Genetics at RPCI. Thus, our data suggest that SSeCKS plays a role in preventing the early dissemination of prostate cancer cells to metastatic sites. Importantly, we show that humans whose prostate cancers have turned off or deleted the SSeCKS/AKAP12 gene have significantly higher rates of metastasis formation compared to cases where SSeCKS/AKAP12 levels are sustained.

While the SSeCKS/AKAP12 gene is deleted in about a third of metastatic prostate cancers, precluding benefit from targeted therapies exploiting this vulnerability, the remaining two-thirds of such tumors may be treatable with drugs that induce the reactivation of SSeCKS/AKAP12 production. Dr. Gelman and colleagues are now looking to identify the genomic signatures controlled by SSeCKS/AKAP12 in the suppression of metastasis pathways at the level of the tumor cells themselves and in the cells that form the metastatic microenvironment.

At least 93 percent of cancer patients die because of complications due to metastatic cancers, yet the vast majority of pathways studied and therapies developed address the biology of primary cancers, Dr. Gelman noted. This current research is important in that it addresses specific mechanisms of cancer metastasis, with the result that genetic tests and therapies derived from such studies will have a higher chance of affecting cancer patient survival.

The work was supported by National Institutes of Health (NIH)/National Cancer Institute (NCI) grants R01CA70292, R01CA94108 and R01CA116430, by U.S. Department of Defense grants PC074228 and PC101210 and, in part, by RPCIs Cancer Center Support Grant from the NCI (P30CA016056).

The study will be published online ahead of print at cancerres.aacrjournals.org.

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Researchers Advance Findings on Key Gene Related to Cancer Metastasis

"Genetic Engineering" Fan Video
Fan video of "Genetic Engineering" by Acetate. Created using Video Star: http://VideoStarApp.com/FREE.

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PUBLIC RELEASE DATE:

3-Feb-2014

Contact: Vicki Bendure vicki@bendurepr.com 202-374-9259 Society for Maternal-Fetal Medicine

In a study to be presented on Feb. 6 at 2:45 p.m. CST, at the Society for Maternal-Fetal Medicine's annual meeting, The Pregnancy Meeting, in New Orleans, researchers will report that a variant in SERPINE1, a gene involved in inflammation and blood clotting, is associated with cerebral palsy and death in very preterm babies. This gene has been associated with increased risk of cerebral palsy in one previous study of preterm babies.

Previous genetic studies of very preterm babies have suggested several genetic variations that might predispose to brain injury and developmental problems. However, different studies have had different results.

This study, titled Genetic Predisposition to Adverse Neurodevelopmental Outcome After Early Preterm Birth: A Validation Analysis, was a collaborative effort between the Eunice Kennedy Shriver NICHD Maternal-Fetal Medicine Units and Neonatal Research Networks.

Researchers evaluated two different populations of very early preterm births (earlier than 32 weeks) with the goal of confirming the same genetic risk factors in both groups. The first population of preterm births was enrolled in a large Neonatal Research Network study, and the other group was of births that were enrolled in a Maternal Fetal Medicine Units Network study of magnesium sulfate before preterm birth for prevention of cerebral palsy.

Results revealed a variant in the gene SERPINE1, a gene involved in inflammation and blood clotting, was associated with cerebral palsy and death after early preterm birth in both populations of preterm babies.

"Preterm birth is the leading cause of childhood brain injury in otherwise normal children. The earlier a baby is born, the higher the risk of brain injury. However, even among the tiniest preemies, some babies develop quite normally, while others have devastating brain injury and life-long disability," said Erin Clark, M.D., the study's author. "The reason for this difference in outcomes is not well understood. Genetics may allow identification of babies at increased risk so that we can target those babies for prevention and treatment strategies. These results add to the evidence that genes may play a role in risk of brain injury and death in preterm babies."

Clark, assistant professor of Maternal Fetal Medicine, University of Utah School of Medicine's Department of Obstetrics and Gynecology, also noted that additional research is necessary to further evaluate genes that may influence risk and to determine how to apply these results to clinical care.

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Mathematical Models in Population Genetics II
Anand Bhaskar, UC Berkeley Evolutionary Biology Boot Camp http://simons.berkeley.edu/talks/steven-evans-anand-bhaskar-shishi-luo-2014-01-21b.

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Mutants Genetics Gladiator- Bushi Now Hatched
God is amazing because I didnt have to breed a zomborg to get my bushi! Royalty Free Music by: http://www.audiomicro.com My Pages: https://www.facebook.com/j...

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Kirtland Genetics Project Prompt One
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Stretch Goal Cast - Episode #4, Part 1: Jurassic Genetics on Kickstarter
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Genetics at Quixotes Denver CO 02-01-14
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CING-CSMM Herb Garden
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