Step toward unraveling Alzheimer's disease

ScienceDaily (Oct. 27, 2011) — Scientists outline new methods for better understanding links between specific proteins and the risks associated with Alzheimer's disease in an article co-authored by University of Alabama researchers and publishing in Science Express.

In experiments using a series of model organisms, including yeast, microscopic roundworms and rats, the researchers show how basic mechanisms inside cells are disrupted when a specific human protein, known as the amyloid beta peptide, fails to properly fold. This study also shows the role a second protein, referred to by the scientists as PICALM, can play in modifying the problem.

"By using these yeast models, in combination with worms, we really are hopeful of finding a way by which we can understand and maybe combat Alzheimer's disease more rapidly," said Dr. Guy Caldwell, professor of biological sciences at The University of Alabama and one of three UA-authors on the Science article.

The research involved scientists from several universities and research institutes, including the Whitehead Institute and Massachusetts Institute of Technology, where the lead author, Dr. Sebastian Treusch, is affiliated. Treusch works in the lab of Dr. Susan Lindquist, a renowned expert in cell biology and collaborator with Caldwell on a grant from the Howard Hughes Medical Institute that funded part of this research.

While the repeated misfoldings of amyloid beta peptides within the human brain were previously known to trigger the death of neurons, resulting in Alzheimer's, Caldwell says the underlying mechanisms of toxicity weren't as well understood.

Properly functioning cells must efficiently deliver proteins and chemicals to other parts of the cell, Caldwell said. This research shows how the amyloid beta peptide interrupts a specific cellular pathway called endocytosis, preventing the delivery of other needed proteins to other parts of the cell.

"Understanding what is going wrong inside a cell, or what pathways or proteins might be directly linked to the mechanisms that are involved in Alzheimer's, is really a much more fruitful strategy for drug development."

Information drawn from the brains of deceased Alzheimer's patients, who previously donated their bodies to science, was also significant in the effort, Caldwell said.

Rapid advances in DNA sequencing methods and human genetic population studies are generating an overwhelming number of leads for researchers; those genetic studies, taken in combination with advantageous attributes of simple organisms, can reveal basic functions of genes and proteins and can be an insightful combination, Caldwell says.

"What this paper shows is that simple systems, like yeast and worms, can be engineered to discern mechanisms that might be associated with complex human diseases, and, by that, we may accelerate the path of discovery for advancing therapeutics for those diseases."

UA's lead author is Dr. Shusei Hamamichi, a former post-doctoral researcher in the Caldwell lab who earned his doctorate at UA while working alongside Caldwell and Dr. Kim Caldwell, also a co-author of the paper and an associate professor of biological sciences at UA.

In the paper's conclusion, the researchers describe the potential significance of the development in light of the challenges faced in understanding and treating Alzheimer's disease.

"The treatments available for AD are few and their efficacy limited," the scientists wrote. "Determining how best to rescue neuronal function in the context of the whole brain is a problem of staggering proportions."

"On a personal level," Caldwell said, "so many of us have been affected by family or loved ones who have suffered from Alzheimer's. It's a great privilege for us to be able to contribute to the respective avenues of our understanding of the disease. It's a devastating disorder. The societal cost of Alzheimer's disease is tremendous."

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Sebastian Treusch, Shusei Hamamichi, Jessica L. Goodman, Kent E. S. Matlack, Chee Yeun Chung, Valeriya Baru, Joshua M. Shulman, Antonio Parrado, Brooke J. Bevis, Julie S. Valastyan, Haesun Han, Malin Lindhagen-Persson, Eric M. Reiman, Denis A. Evans, David A. Bennett, Anders Olofsson, Philip L. Dejager, Rudolph E. Tanzi, Kim A. Caldwell, Guy A. Caldwell, Susan Lindquist. Functional Links Between Aß Toxicity, Endocytic Trafficking, and Alzheimer’s Disease Risk Factors in Yeast. Science, 2011; DOI: 10.1126/science.1213210

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NASA launches multi-talented Earth-observing satellite

ScienceDaily (Oct. 28, 2011) — NASA's newest Earth-observing satellite soared into space early Oct. 28, 2011 aboard a Delta II rocket after liftoff at 5:48 a.m. EDT from Space Launch Complex 2 at Vandenberg Air Force Base in California.

NASA's National Polar-orbiting Operational Environmental Satellite System Preparatory Project, or NPP, successfully separated from the Delta II 58 minutes after launch, and the first signal was acquired by the Tracking and Data Relay Satellite System. NPP's solar array deployed 67 minutes after launch to provide the satellite with electrical power. NPP is on course to reach its sun-synchronous polar orbit 512 miles (824 km) above Earth.

"NPP is critical to our understanding of Earth's processes and changes," said NASA Deputy Administrator Lori Garver. "Its impact will be global and builds on 40 years of work to understand our complex planet from space. NPP is part of an extremely strong slate of current and future innovative NASA science missions that will help us win the future as we make new discoveries."

NPP carries five science instruments, including four new state-of-the-art sensors, which will provide critical data to help scientists understand the dynamics of long-term climate patterns and help meteorologists improve short-term weather forecasts. The mission will extend more than 30 key long-term datasets NASA has been tracking, including measurements of the ozone layer, land cover, and ice cover.

NPP serves as a bridge mission between NASA's Earth Observing System (EOS) of satellites and the next-generation Joint Polar Satellite System, a National Oceanic and Atmospheric Administration (NOAA) program that will also collect weather and climate data.

Scientists will use NPP data to extend and improve upon EOS data records. These satellites have provided critical insights into the dynamics of the entire Earth system, including clouds, oceans, vegetation, ice, solid Earth and atmosphere. NPP will allow scientists to extend the continuous satellite record needed to detect and quantify global environmental changes.

"The measurements from NPP will benefit science and society for many years to come," said Michael Freilich, director of NASA's Earth Science Division. "NPP will help improve weather forecasts, enable unique scientific insights, and allow more accurate global environmental predictions. I'm confident that the strong partnerships forged in the NPP program between NASA and NOAA, industry, and the research and applications communities will ensure the success of the mission."

The satellite will be operated from the NOAA Satellite Operations Facility in Suitland, Md. NASA will operate NPP for the first three months after launch while the satellite and instrument are checked out. NPP operations will then be turned over to NOAA and the JPSS program for the remainder of the mission.

NPP data will be transmitted once every orbit to a ground station in Svalbard, Norway, and to direct broadcast receivers around the world. The data will be sent back to the United States via fiber optic cable to the NOAA Suitland facility. NPP data is then processed into data records that NASA and NOAA will make available through various data archives.

The Delta II launch vehicle that delivered NPP into orbit also deployed auxiliary payloads within 98 minutes after launch. The five small "CubeSat" research payloads are the third in a series of NASA Educational Launch of Nanosatellite missions, known as ELaNa missions.

The NPP mission is managed by NASA's Goddard Space Flight Center in Greenbelt, Md., for the Earth Science Division of the Science Mission Directorate at NASA Headquarters in Washington. The Joint Polar Satellite System program provides the NPP ground system. NOAA will provide operational support for the mission. Launch management is the responsibility of the NASA Launch Services Program at the Kennedy Space Center in Florida.

For more information about NPP, visit: http://www.nasa.gov/npp

For more information about the ELaNa III mission, visit: http://go.nasa.gov/tgbuVn

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New oncolytic virus shows improved effectiveness in preclinical testing

ScienceDaily (Oct. 27, 2011) — A new fourth-generation oncolytic virus designed to both kill cancer cells and inhibit blood-vessel growth has shown greater effectiveness than earlier versions when tested in animal models of human brain cancer.

Researchers at the Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC -- James) are developing the oncolytic virus as a treatment for glioblastoma, the most common and deadly form of brain cancer (average survival: 15 months after diagnosis).

The new oncolytic virus, called 34.5ENVE, improved survival of mice with transplanted human glioblastoma tumors by 50 percent in a majority of cases compared with the previous-generation oncolytic virus.

The study was published online in the journal Molecular Therapy.

"These findings show the amazing therapeutic efficacy of this new oncolytic virus against four different glioblastoma models in animals," says cancer researcher Dr. Balveen Kaur, associate professor of neurological surgery, and a member of the OSUCCC -- James viral oncology research program.

The new oncolytic virus is engineered to replicate in cells that express the protein nestin. First identified as a marker for neuronal stem cells, nestin is also expressed in glioblastoma and other malignancies including gastrointestinal, pancreatic, prostate and breast cancer.

"We believe that nestin-driven oncolytic viruses will prove valuable for the treatment of many types of cancer," Kaur says.

The new oncolytic virus also carries a gene to inhibit tumor blood-vessel growth. That gene, called Vstat120, was added to increase its anti-tumor effectiveness and prolong the virus's presence within tumors.

In this study of eight animals with intracranial tumors, six lived longer than 80 days, and these were later found to be tumor free. By comparison, control mice survived a median of 20 days, and mice treated with a first-, a second-, and a third-generation oncolytic virus survived 33, 34 and 53 days, respectively.

"Magnetic resonance imaging and histological analyses revealed extensive tumor destruction in animals treated with 34.5 ENVE," says Kaur, who is also chief of Ohio State's Dardinger Laboratory of Neurosciences. "We hope that we can soon evaluate the safety of this virus in patients with cancer."

Funding from the National Institute for Neurological Disorders and Stroke, National Cancer Institute and National Research Foundation of Korea supported this research.

Other researchers involved in this study were Ji Young Yoo, Amy Haseley, Anna Bratasz, E. Antonio Chiocca, Jianying Zhang and Kimerly Powell of The Ohio State University.

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Ji Young Yoo, Amy Haseley, Anna Bratasz, E Antonio Chiocca, Jianying Zhang, Kimerly Powell, Balveen Kaur. Antitumor Efficacy of 34.5ENVE: A Transcriptionally Retargeted and “Vstat120”-expressing Oncolytic Virus. Molecular Therapy, 2011; DOI: 10.1038/mt.2011.208

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Do bacteria age? Biologists discover the answer follows simple economics

ScienceDaily (Oct. 27, 2011) — When a bacterial cell divides into two daughter cells and those two cells divide into four more daughters, then 8, then 16 and so on, the result, biologists have long assumed, is an eternally youthful population of bacteria. Bacteria, in other words, don't age -- at least not in the same way all other organisms do.

But a study conducted by evolutionary biologists at the University of California, San Diego questions that longstanding paradigm. In a paper published in the November 8 issue of the journal Current Biology, they conclude that not only do bacteria age, but that their ability to age allows bacteria to improve the evolutionary fitness of their population by diversifying their reproductive investment between older and more youthful daughters. An advance copy of the study appears this week in the journal's early online edition.

"Aging in organisms is often caused by the accumulation of non-genetic damage, such as proteins that become oxidized over time," said Lin Chao, a professor of biology at UC San Diego who headed the study. "So for a single celled organism that has acquired damage that cannot be repaired, which of the two alternatives is better -- to split the cellular damage in equal amounts between the two daughters or to give one daughter all of the damage and the other none?"

The UC San Diego biologists' answer -- that bacteria appear to give more of the cellular damage to one daughter, the one that has "aged," and less to the other, which the biologists term "rejuvenation" -- resulted from a computer analysis Chao and colleagues Camilla Rang and Annie Peng conducted on two experimental studies. Those studies, published in 2005 and 2010, attempted unsuccessfully to resolve the question of whether bacteria aged. While the 2005 study showed evidence of aging in bacteria, the 2010 study, which used a more sophisticated experimental apparatus and acquired more data than the previous one, suggested that they did not age.

"We analyzed the data from both papers with our computer models and discovered that they were really demonstrating the same thing," said Chao. "In a bacterial population, aging and rejuvenation goes on simultaneously, so depending on how you measure it, you can be misled to believe that there is no aging."

In a separate study, the UC San Diego biologists filmed populations of E. coli bacteria dividing over hundreds of generations and confirmed that the sausage-shaped bacteria divided each time into daughter cells that grew elongated at different rates -- suggesting that one daughter cell was getting all or most of the cellular damage from its mother while the other was getting little or none. Click this link to watch the time-lapse film of one bacterium dividing over 10 generations into 1,000 bacteria in a period of five hours and see if you can see any differences.

"We ran computer models and found that giving one daughter more the damage and the other less always wins from an evolutionary perspective," said Chao. "It's analogous to diversifying your portfolio. If you could invest $1 million at 8 percent, would that provide you with more money than splitting the money and investing $500,000 at 6 percent and $500,000 at 10 percent?"

"After one year it makes no difference," he added. "But after two years, splitting the money into the two accounts earns you more and more money because of the compounding effect of the 10 percent. It turns out that bacteria do the same thing. They give one daughter a fresh start, which is the higher interest-bearing account and the other daughter gets more of the damage."

Although E. coli bacteria appear to divide precisely down the middle into two daughter cells, the discovery that the two daughters eventually grow to different lengths suggests that bacteria do not divide as symmetrically as most biologists have come to believe, but that their division is really "asymmetrical" within the cell.

"There must be an active transport system within the bacterial cell that puts the non-genetic damage into one of the daughter cells," said Chao. "We think evolution drove this asymmetry. If bacteria were symmetrical, there would be no aging. But because you have this asymmetry, one daughter by having more damage has aged, while the other daughter gets a rejuvenated start with less damage."

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The above story is reprinted from materials provided by University of California - San Diego. The original article was written by Kim McDonald.

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Camilla U. Rang, Annie Y. Peng, Lin Chao. Temporal Dynamics of Bacterial Aging and Rejuvenation. Current Biology, 27 October 2011 DOI: 10.1016/j.cub.2011.09.018

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NASA in final preparations for Nov. 8 asteroid flyby

ScienceDaily (Oct. 28, 2011) — NASA scientists will be tracking asteroid 2005 YU55 with antennas of the agency's Deep Space Network at Goldstone, Calif., as the space rock safely flies past Earth slightly closer than the moon's orbit on Nov. 8. Scientists are treating the flyby of the 1,300-foot-wide (400-meter) asteroid as a science target of opportunity -- allowing instruments on "spacecraft Earth" to scan it during the close pass.

Tracking of the aircraft carrier-sized asteroid will begin at 9:30 a.m. local time (PDT) on Nov. 4, using the massive 70-meter (230-foot) Deep Space Network antenna, and last for about two hours. The asteroid will continue to be tracked by Goldstone for at least four hours each day from Nov. 6 through Nov. 10. Radar observations from the Arecibo Planetary Radar Facility in Puerto Rico will begin on Nov. 8, the same day the asteroid will make its closest approach to Earth at 3:28 p.m. PST.

The trajectory of asteroid 2005 YU55 is well understood. At the point of closest approach, it will be no closer than 201,700 miles (324,600 kilometers) or 0.85 the distance from the moon to Earth. The gravitational influence of the asteroid will have no detectable effect on anything here on Earth, including our planet's tides or tectonic plates. Although 2005 YU55 is in an orbit that regularly brings it to the vicinity of Earth (and Venus and Mars), the 2011 encounter with Earth is the closest this space rock has come for at least the last 200 years.

During tracking, scientists will use the Goldstone and Arecibo antennas to bounce radio waves off the space rock. Radar echoes returned from 2005 YU55 will be collected and analyzed. NASA scientists hope to obtain images of the asteroid from Goldstone as fine as about 7 feet (2 meters) per pixel. This should reveal a wealth of detail about the asteroid's surface features, shape, dimensions and other physical properties (see "Radar Love" -- http://www.jpl.nasa.gov/news/news.cfm?release=2006-00a ).

Arecibo radar observations of asteroid 2005 YU55 made in 2010 show it to be approximately spherical in shape. It is slowly spinning, with a rotation period of about 18 hours. The asteroid's surface is darker than charcoal at optical wavelengths. Amateur astronomers who want to get a glimpse at YU55 will need a telescope with an aperture of 6 inches (15 centimeters) or larger.

The last time a space rock as big came as close to Earth was in 1976, although astronomers did not know about the flyby at the time. The next known approach of an asteroid this large will be in 2028. NASA detects, tracks and characterizes asteroids and comets passing close to Earth using both ground- and space-based telescopes. The Near-Earth Object Observations Program, commonly called "Spaceguard," discovers these objects, characterizes a subset of them, and plots their orbits to determine if any could be potentially hazardous to our planet.

NASA's Jet Propulsion Laboratory manages the Near-Earth Object Program Office for NASA's Science Mission Directorate in Washington. JPL is a division of the California Institute of Technology in Pasadena.

More information about asteroids and near-Earth objects is at: http://www.jpl.nasa.gov/asteroidwatch .

More information about asteroid radar research is at: http://echo.jpl.nasa.gov/ .

More information about the Deep Space Network is at: http://deepspace.jpl.nasa.gov/dsn .

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High tech detection of breast cancer using nanoprobes and SQUID

ScienceDaily (Oct. 28, 2011) — Mammography saves lives by detecting very small tumors. However, it fails to find 10-25% of tumors and is unable to distinguish between benign and malignant disease. New research published in BioMed Central's open access journal Breast Cancer Research provides a new and potentially more sensitive method using tumor-targeted magnetic nanoprobes and superconducting quantum interference device (SQUID) sensors.

A team of researchers from University of New Mexico School of Medicine and Cancer Research and Treatment Center, Senior Scientific, LLC, and the Center for Integrated Nanotechnologies facility at Sandia National Laboratories created nanoprobes by attaching iron-oxide magnetic particles to antibodies against HER-2, a protein overexpressed in 30% of breast cancer cases. Using these tiny protein-iron particles the team was able to distinguish between cells with HER-2 and those without, and were able to find HER-2 cancer cells in biopsies from mice. In their final test the team used a synthetic breast to determine the potential sensitivity of their system.

Dr Helen Hathaway explained, "We were able to accurately pinpoint 1 million cells at a depth of 4.5 cm. This is about 1000x fewer cells than the size at which a tumor can be felt in the breast and 100x more sensitive than mammographic x-ray imaging. While we do not expect the same level of nanoparticle uptake in the clinic, our system has an advantage in that dense breast tissue, which can mask traditional mammography results, is transparent to the low-frequency magnetic fields detected by the SQUID sensors."

Future refining of the system could allow not only tumor to be found but to be classified according to protein expression (rather than waiting for biopsy results). This in turn could be used to predict disease progression and refine treatment plans and so improve patient survival.

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Helen J Hathaway, Kimberly S Butler, Natalie L Adolphi, Debbie M Lovato, Robert Belfon, Danielle L Fegan, Todd C Monson, Jason E Trujillo, Trace E Tessier, Howard C Bryant, Dale L Huber, Richard S Larson and Edward R Flynn. Detection of breast cancer cells using targeted magnetic nanoparticles and ultra-sensitive magnetic field sensors. Breast Cancer Research, 2011; 13: R108 DOI: 10.1186/bcr3050

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Python study may have implications for human heart health

ScienceDaily (Oct. 27, 2011) — A surprising new University of Colorado Boulder study shows that huge amounts of fatty acids circulating in the bloodstreams of feeding pythons promote healthy heart growth, results that may have implications for treating human heart disease.

CU-Boulder Professor Leslie Leinwand and her research team found the amount of triglycerides -- the main constituent of natural fats and oils -- in the blood of Burmese pythons one day after eating increased by more than fiftyfold. Despite the massive amount of fatty acids in the python bloodstream there was no evidence of fat deposition in the heart, and the researchers also saw an increase in the activity of a key enzyme known to protect the heart from damage.

After identifying the chemical make-up of blood plasma in fed pythons, the CU-Boulder researchers injected fasting pythons with either "fed python" blood plasma or a reconstituted fatty acid mixture they developed to mimic such plasma. In both cases, the pythons showed increased heart growth and indicators of cardiac health. The team took the experiments a step further by injecting mice with either fed python plasma or the fatty acid mixture, with the same results.

"We found that a combination of fatty acids can induce beneficial heart growth in living organisms," said CU-Boulder postdoctoral researcher Cecilia Riquelme, first author on the Science paper. "Now we are trying to understand the molecular mechanisms behind the process in hopes that the results might lead to new therapies to improve heart disease conditions in humans."

The paper is being published in the Oct. 28 issue of the journal Science. In addition to Leinwand and Riquelme, the authors include CU postdoctoral researcher Brooke Harrison, CU graduate student Jason Magida, CU undergraduate Christopher Wall, Hiberna Corp. researcher Thomas Marr and University of Alabama Tuscaloosa Professor Stephen Secor.

Previous studies have shown that the hearts of Burmese pythons can grow in mass by 40 percent within 24 to 72 hours after a large meal, and that metabolism immediately after swallowing prey can shoot up by fortyfold. As big around as telephone poles, adult Burmese pythons can swallow prey as large as deer, have been known to reach a length of 27 feet and are able to fast for up to a year with few ill effects.

There are good and bad types of heart growth, said Leinwand, who is an expert in genetic heart diseases including hypertrophic cardiomyopathy, the leading cause of sudden death in young athletes. While cardiac diseases can cause human heart muscle to thicken and decrease the size of heart chambers and heart function because the organ is working harder to pump blood, heart enlargement from exercise is beneficial.

"Well-conditioned athletes like Olympic swimmer Michael Phelps and cyclist Lance Armstrong have huge hearts," said Leinwand, a professor in the molecular, cellular and developmental biology department and chief scientific officer of CU's Biofrontiers Institute. "But there are many people who are unable to exercise because of existing heart disease, so it would be nice to develop some kind of a treatment to promote the beneficial growth of heart cells."

Riquelme said once the CU team confirmed that something in the blood plasma of pythons was inducing positive cardiac growth, they began looking for the right "signal" by analyzing proteins, lipids, nucleic acids and peptides present in the fed plasma. The team used a technique known as gas chromatography to analyze both fasted and fed python plasma blood, eventually identifying a highly complex composition of circulating fatty acids with distinct patterns of abundance over the course of the digestive process.

In the mouse experiments led by Harrison, the animals were hooked up to "mini-pumps" that delivered low doses of the fatty acid mixture over a period of a week. Not only did the mouse hearts show significant growth in the major part of the heart that pumps blood, the heart muscle cell size increased, there was no increase in heart fibrosis -- which makes the heart muscle more stiff and can be a sign of disease -- and there were no alterations in the liver or in the skeletal muscles, he said.

"It was remarkable that the fatty acids identified in the plasma-fed pythons could actually stimulate healthy heart growth in mice," said Harrison. The team also tested the fed python plasma and the fatty acid mixture on cultured rat heart cells, with the same positive results, Harrison said.

The CU-led team also identified the activation of signaling pathways in the cells of fed python plasma, which serve as traffic lights of sorts, said Leinwand. "We are trying to understand how to make those signals tell individual heart cells whether they are going down a road that has pathological consequences, like disease, or beneficial consequences, like exercise," she said.

The prey of Burmese pythons can be up to 100 percent of the constricting snake's body mass, said Leinwand, who holds a Marsico Endowed Chair of Excellence at CU-Boulder. "When a python eats, something extraordinary happens. Its metabolism increases by more than fortyfold and the size of its organs increase significantly in mass by building new tissue, which is broken back down during the digestion process."

The three key fatty acids in the fed python plasma turned out to be myristic acid, palmitic acid and palmitoleic acid. The enzyme that showed increased activity in the python hearts during feeding episodes, known as superoxide dismutase, is a well-known "cardio-protective" enzyme in many organisms, including humans, said Leinwand.

The new Science study grew out of a project Leinwand began in 2006 when she was named a Howard Hughes Medical Institute Professor and awarded a four-year, $1 million undergraduate education grant from the Chevy Chase, Md.-based institute. As part of the award Leinwand initiated the Python Project, an undergraduate laboratory research program designed to focus on the heart biology of constricting snakes like pythons thought to have relevance to human disease.

Undergraduates contributed substantially to the underpinnings of the new python study both by their genetic studies and by caring for the lab pythons, said Leinwand. While scientists know a great deal about the genomes of standard lab animal models like fruit flies, worms and mice, relatively little was known about pythons. "We have had to do a lot of difficult groundwork using molecular genetics tools in order to undertake this research," said Leinwand.

CU-Boulder already had a laboratory snake facility in place, which contributed to the success of the project, she said.

"The fact that the python study involved faculty, postdoctoral researchers, a graduate student and an undergraduate, Christopher Wall, shows the project was a team effort," said Leinwand. "Chris is a good example of how the University of Colorado provides an incredible educational research environment for undergraduates." Wall is now a graduate student at the University of California, San Diego.

Hiberna Corp., a Boulder-based company developing drugs based on natural models of extreme metabolic regulation, signed an exclusive agreement with CU's Technology Transfer Office in 2008, licensing technology developed by Leinwand based on the natural ability of pythons to dramatically increase their heart size and metabolism.

Directed by Nobel laureate and CU Distinguished Professor Tom Cech, the Biofrontiers Institute was formed to advance human health and welfare by exploring critical areas of biology and translating new knowledge into practical applications. The institute is educating a new generation of interdisciplinary scientists to work together on solutions to complex biomedical challenges and to expand Colorado's leadership in biotechnology. For more information on the Biofrontiers Institute visit cimb.colorado.edu .

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Cecilia A. Riquelme, Jason A. Magida, Brooke C. Harrison, Christopher E. Wall, Thomas G. Marr, Stephen M. Secor, Leslie A. Leinwand. Fatty Acids Identified in the Burmese Python Promote Beneficial Cardiac Growth. Science, 2011; 334 (6055): 528-531 DOI: 10.1126/science.1210558

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