Archive for February, 2012

05-02-2012 05:11 Dr. Martin of MetroMD performs a bone marrow extraction procedure to harvest stem cells. The extracted bone marrow will be centrifuged to separate targeted stem cells and re-injected into the patient's injured joints. Questions? Please call the MetroMD Institute of Regenerative Medicine at (323) 285-5300 or email us at info@MetroMD.net. MetroMD.net

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Bone Marrow Extraction Procedure to Harvest Stem Cells | MetroMD Los Angeles - Video

05-02-2012 11:27 MetroMD.net Dr. Martin explains why bone marrow is a better source than fat tissue for viable stem cells in your own body. Questions? Please call the MetroMD Institute of Regenerative Medicine at (323) 285-5300 or email us at info@MetroMD.net. Los Angeles

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What Is The Best Source for Stem Cells- Bone Marrow or Fat Tissue? | MetroMD Los Angeles - Video

18-01-2012 23:09 NewHopeForAging.info - Beverly Hills Plastic Surgeon, Dr. Nathan Newman reveals the truth about the Adult Stem Cell Technology...and the ONLY product on the market with it Luminesce, by Jeunesse. Order it at: NewHope.JeunesseGlobal.com or call 561.779.0000

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Dr Newman Exposes The Truth about Adult Stem Cells - Video

26-01-2012 05:32 Buy Ventolin now - pillsrx24.com albuterol adverse effects Ventorlin inhaler View an audio slide show of “The Mother of Thanksgiving.” See images of Godey’s Lady’s Book, presidential Thanksgiving Day proclamations, and penitant puritans. Be sure and click on...

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albuterol adverse effects - Video

20-12-2011 08:50 If you would like more information please call us Toll Free at 877-578-7908. Or visit our website at http://www.usastemcells.com Or click here to have a Free Phone Constultation with Dr. Matthew Burks usastemcells.com Real patient testimonials for USA Stem Cells. Adult stem cell therapy for COPD, Emphysema, and Pulmonary fibrosis.

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Adult Stem Cell Treatments for COPD - Real patient results, USA Stem Cells - Marian H. Testimonial - Video

29-11-2011 03:32 The MiSeq system is a fully integrated sequencing ecosystem, in a compact and economical instrument. For results in hours, not days, MiSeq uses TruSeq, Illumina's reversible terminator-based sequencing by synthesis chemistry to deliver the fastest time to answer. Perform the widest breadth of sequencing applications, including highly multiplexed PCR amplicon sequencing, small genome resequencing and de novo sequencing, small RNA sequencing, library quality control, and 16S metagenomics, with automated, on-instrument data analysis workflows to take your research further. The widest breadth of applications As the only personal sequencer capable of producing paired-end reads, the MiSeq system puts the largest portfolio of sequencing applications at your fingertips. Optimized sample preparation kits, push-button sequencing, and automated data analysis, create the first truly end-to-end sequencing solution. View the full list of Illumina supported applications See what's possible View the Application Notes: Nextera sample prep for the MiSeq system Sequencing's fastest sample prep delivers quality de novo assembly of small genomes. Sequencing Library QC on the MiSeq system Pre-configured, automated QC workflows prior to a large-scale sequencing study. Amplicon sequencing from FFPE tissues on the MiSeq system Simple and fast workflow for accurate detection of rare variants even from degraded DNA. High-speed, multiplexed microbial sequencing on the MiSeq System Researchers at the ...

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MiSeq Personal Sequencing System - Video

12-01-2012 14:59 Scientists at Westmead Millennium Institute for Medical Research were amazed to see a cell literally laughing at them. Scientists were researching how a cancer-causing protein called Beta Catenin (green) moves into the cell nucleus (the round "face" shape). "Sometimes you feel like diseases really are laughing at your attempts to destroy them, and here it is under our microscope!" says Beric Henderson, head of WMI's gene expression laboratory. Please credit Westmead Millennium Institute for Medical Research if using this.

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smiley face.avi - Video

24-01-2012 16:27 X inactivation is a vital process that occurs in all DNA-containing cells of the female body. It is also an important research model and tool for studying epigenetics. Epigenetics refers to processes that tell our cells how, and when, to read the DNA blueprint. The epigenetic regulation of DNA is critical in both normal development and disease. X inactivation is a type of gene dosage compensation. In humans, the sex chromosomes X and Y determine the sex of an individual - females have two X chromosomes (XX), males have one X and one Y chromosome (XY). All of the genes on the Y chromosome are required in male development, while the genes on the X chromosome are needed for both male and female development. Because females receive two X chromosomes, they inherit two copies of many of the genes that are needed for normal function. Extra copies of genes or chromosomes can affect normal development. An example is Down's syndrome, which is caused by an extra copy of part or all of chromosome 21. In female mammals, a process called X inactivation has evolved to compensate for the extra X chromosome. In X inactivation, each cell 'switches off' one of its X chromosomes, chosen at random, to ensure the correct number of genes are expressed, and to prevent abnormal development.

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X Inactivation and Epigenetics - Video

01-02-2012 09:24 Please Subscribe To The EvolutionDocumentary YouTube Channel: http://www.youtube.com Broadcast (2005) In 1973, two scientists, Herb Boyer and Stan Cohen, became the first genetic engineers when they transferred the DNA from one species to another. Their experiment triggered a wave of controversy about the dangers of genetic manipulation, but it also generated a multi billion dollar industry. Was altering the genetic makeup of plants and animals a threat to humanity or the key to alleviating a host of health problems? Biologists, along with lawyers and journalists from all over the world, were called to a meeting in California to decide the future of DNA research. Biotechnology would soon transform the pharmaceutical industry and genetically modified food was to herald the biggest revolution in agriculture since the industrialization of farming. Yet the public was skeptical, and so were certain scientists. Some feared that a cancer causing gene stitched into the DNA of a bacterium might be accidentally absorbed in the human gut, enabling cancer to be passed on like an infectious disease. Biologists from all over the world were called to a meeting in to draw up a strict set of safety guidelines. When the panic subsided the stage was set for a biotechnology bonanza. A race began to produce genetically engineered insulin. A couple of years later a young researcher called Rob Horsch, who worked for the chemical giant Monsanto, produced the first genetically engineered plant. The ...

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DNA Episode 2 Playing God (PBS) - Video

22-01-2012 17:29 There is no difference between natural foods and genetically modified foods? That's not what research says. This documentary discusses those who have spoken out against the scientific government scam of genetically modified foods and have been fired, harassed and other things as well as the results of their research.

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Scientists Under Attack: Genetic Engineering in the Magnetic Field of Money - Video

24-12-2011 12:55 Research interests include cellular neuroscience, developmental biology and genetics, immunology, microbiology and lipid transport, in both plants and animals. Molecular mechanisms that control cell structure and function as well as the organization of cells into complex organs or organ systems within single organisms. How do the cells respond to stress? How is the expression of key proteins regulated? How do cells use energy ? How do cells make your heart beat - your brain think - your eyes see? How does the action of individual cells translate into working organs and systems? How do the cells organize themselves into complex organs or organ systems in such a way that the whole is greater than the sum of its parts? How can certain organisms survive in an extreme environment? Further career and educational opportunities: The Cells, Molecules and Physiology stream prepares students for careers in Medicine, Diagnostics, Biotechnology and Pharmaceuticals, Cancer Research, Bioengineering, Forensics, Science Writing, Science Education, Genetic Counseling, Dentistry, Veterinary Medicine, consulting in the areas of toxicology, fisheries, and more. Practical knowledge Learn about the science behind the headlines: understand the new developments in how we identify and treat illnesses, modify crops for drought tolerance and higher nutrition, clone cells and organisms. This video includes interviews with graduate students and professors in Biological Sciences at SFU.

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Program in Cellular and Molecular Biology at Simon Fraser University - Video

08-12-2011 08:35 In 1865 Augustinian monk Gregor Mendel discovered the basic laws of heredity.

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Milestones of Science - Gregor Mendel and Classical Genetics - Video

08-02-2012 12:15 Joan shares her family story of bipolar disorder and her journey as a mental health advocate. This workshop is part of a genomics curriculum for practicing healthcare providers developed by the Genomic Medicine Institute at El Camino Hospital, Genetic Alliance, and the National Coalition for Health Professional Education in Genetics. This workshop, the fifth in a 10-part series, covered understanding genetic contribution to schizophrenia, major depression, hypertension, and diabetes; risk assessment for complex conditions; establishing diagnosis; pharmacogenomics; gene-environment interaction; and management.

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Workshop 5: Genetics of Complex Disease - Joan Esnayra - Video

Dr. Renato Dulbecco, an Italian American virologist who shared the 1975 Nobel Prize in physiology or medicine for demonstrating how certain types of viruses invade mammalian cells to cause cancer, died of natural causes Sunday at his home in La Jolla. He was 97.

Dulbecco developed a method for measuring the quantity of virus in animal cells in tissue culture, a finding that greatly facilitated the study of such viruses and paved the way for the development of the Sabin polio vaccine. He was a faculty member at Caltech from 1949 to 1963 before moving to the Salk Institute for Biological Studies in La Jolla. He later served as president of the institute.

Dulbecco was also one of the first proponents of the human genome project, which many researchers initially thought would be both excessively expensive and relatively useless but which has since proved invaluable in biological research.

"Renato was one of the most brilliant scientific minds of our generation," current Salk Institute President William R. Brody said in a statement. "His contributions have truly made this a better world for all of us."

It has been known since the early 1900s that certain viruses can cause tumors in animals. The best-known example was the Rous sarcoma virus, which causes cancer in chickens. But it was not clear how the viruses produced this effect and what proportion of human cancers might be attributed to them.

In experiments carried out at Caltech in the 1950s, Dulbecco showed that a viral infection can have two outcomes: the virus can multiply inside the cell, killing the cell and releasing thousands of new viruses into the host animal; or it could alter the cell so that the cell would continue to divide and grow indefinitely, a process called transformation.

In the latter case, no new virus particles appear and the infecting virus seemingly disappears.

Through an elegant series of experiments, Dulbecco showed that the DNA from the polyoma virus became integrated into the DNA of the host cell, where it was replicated intact every time the cell replicated. Moreover, the viral DNA served as the blueprint for a small number of proteins that subverted cellular machinery, causing the cells to reproduce repeatedly — the hallmark of tumor formation.

Additionally, this feat was achieved before it was possible to sequence the DNA of either viruses or animal cells.

For his achievement, Dulbecco shared the 1975 Nobel Prize with Howard Temin and David Baltimore, who demonstrated the existence of an enzyme — reverse transcriptase — that allowed RNA viruses to integrate their genes into a host cell in the same fashion as the DNA viruses studied by Dulbecco. Both were former students of his.

In his Nobel address, Dulbecco called for increased restrictions on tobacco use because of its carcinogenic potential and urged governments to make greater efforts to limit the introduction of dangerous chemicals.

"While we spend our life asking questions about the nature of cancer and ways to prevent or cure it," he said, "society merrily produces oncogenic substances and permeates the environment with them."

Renato Dulbecco was born Feb. 22, 1914, in Catanzaro, Italy, the son of a civil engineer. He enrolled at the University of Turin, where he had meant to study physics and chemistry but soon became interested in biology instead.

He received his medical degree in 1936 and during World War II served in France and Russia, where he was injured in 1942 during a major Russian offensive along the Don River.

After several months of hospitalization, he returned home, hiding out in a small village near Turin when German forces occupied Italy after Mussolini's fall. He served as a medical officer for partisan forces resisting the occupation.

In medical school, Dulbecco had worked in the laboratory of noted anatomist Giuseppi Levi, along with fellow students Salvador Luria and Rita Levi-Montalcini, both of whom also became Nobel laureates. In 1946, Luria invited Dulbecco to join his small laboratory at the Indiana University and Dulbecco immigrated the following year, becoming a U.S. citizen in 1953. At IU, he shared bench space with James Watson, another eventual Nobel laureate.

Dulbecco was working with bacteriophage, small viruses that invade only bacteria cells. He showed that bacteriophage that had been disabled by exposure to ultraviolet light could be reactivated by exposing them to bursts of white light.

That work attracted the attention of microbiologist Max Delbruck, who invited Dulbecco to join him at Caltech. In the summer of 1949, Dulbecco and his then-wife, the former Giuseppina Salvo, drove an old car cross-country. He wrote in his Nobel autobiography that he was struck by "the beauty and immensity of the U.S.A. and the kindness of its people" and vowed to continue to live here forever.

While at Caltech, Dulbecco adapted a technique he had used with bacteriophage to count the number of virus particles that are present in a tissue sample. Dubbed the plaque assay technique, the assay relies on the fact that viruses added to a culture of cells kill small areas of cells, producing clear circles that can be counted.

This technique enabled researchers for the first time to measure the concentrations of virus in a sample and was crucial to Albert Sabin's work in inventing an attenuated virus polio vaccine. Dulbecco, in fact, originally isolated the mutant polio virus used by Sabin in his vaccine.

In 1962, Dulbecco became a founding member of the Salk Institute, where he remained for the rest of his career. He also spent time at the Imperial Cancer Fund Research Laboratories in London, where he worked on human cancer viruses, although he remained on the staff at Salk. In his later years, he researched breast cancer and concluded that breast cancer stem cells gone awry might be responsible for certain types of breast tumors.

In 1988, he became interim president at Salk, a position that soon became permanent. He held the post until he returned to his laboratory research in 1992.

During the 1980s, Dulbecco had argued passionately in favor of a human genome project. After his retirement as Salk president he was asked by the Italian National Research Council to develop an Italian human genome project, and he spent about half his time each year in that country. The project was abandoned after five years, however, because of lack of funding and facilities.

Dulbecco was a classically trained pianist who was passionate about music and performed opera. He was also a dedicated do-it-yourself handyman and once told The Times, "If I can get a week off to work on the house, that's the best vacation I can get." He remodeled his kitchen and added about 1,000 square feet of space to his home in La Jolla, performing all the work — including plumbing and electrical — himself.

Dulbecco is survived by his second wife, Maureen, whom he married in 1962; a brother, two daughters and four grandchildren. A son predeceased him.

Maugh is a former Los Angeles Times staff writer.

news.obits@latimes.com

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Renato Dulbecco dies at 97; 1975 Nobel Prize winner in medicine

20-12-2011 08:50 If you would like more information please call us Toll Free at 877-578-7908. Or visit our website at http://www.usastemcells.com Or click here to have a Free Phone Constultation with Dr. Matthew Burks usastemcells.com Real patient testimonials for USA Stem Cells. Adult stem cell therapy for COPD, Emphysema, and Pulmonary fibrosis.

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Adult Stem Cell Treatments for COPD - Real patient results, USA Stem Cells - Marian H. Testimonial - Video

EDMOND, OK--(Marketwire -02/19/12)- The team of veterinarians at White Oaks Veterinary Clinic in Edmond announced that the animal hospital is now offering pet stem cell therapy. This new regenerative medicine for pets helps animals suffering from degenerative joint disease or arthritis. Based on the research and technology provided by a company called Stemlogix, White Oaks Veterinary Clinic can now offer affordable, same-day stem cell therapy to dogs suffering from these debilitating conditions. The Stemlogix technology enables the Edmond veterinarians to extract adult stem cells from a pet's own body fat, virtually eliminating the risk of rejection or negative reaction.

"I see far too many otherwise healthy pets at our veterinary clinic that have been hobbled by the effects of arthritis," Dr. Jennifer Bianchi said. "We're thrilled to be able to offer this holistic solution which harnesses the pet's own healing power to aid in the pain relief process. Our main goal with stem cell therapy is to reduce long-term inflammation and slow the progression of cartilage damage. The motto at our veterinary hospital is, 'Quality service at a great value.' Being able to provide stem cell transplants in about two hours at an affordable rate helps us live up to that promise and makes me happy to think of the pets we'll be able to help move freely again."

The veterinary hospital now has an on-site stem cell laboratory for producing stem cells. The on-site lab allows for immediate processing after extraction as the stem cells have a limited lifespan outside of the pet's body. Once the fat cells have been procured from the pet, the stem cells are isolated and returned back to the host body within ninety minutes. Stemlogix promotes this therapy as being able to relieve pain and increase range of motion in pets suffering with joint pain, arthritis, tendon and ligament damage, hip dysplasia and cartilage damage.

Once implanted, stem cells have the ability to stimulate regeneration, reduce pain and inflammation, and assist in the repair of damaged tissue. They can also differentiate into other cell types such as tendon, cartilage, bone, and ligament, which may further aid the repair process. The Edmond veterinarian says that pain relief can be expected within a few days to a few weeks. Pet owners are cautioned to gradually allow their pets to experience increased activity so as not to interfere with the healing process.

As a holistic veterinarian, White Oaks Veterinary Clinic combines natural healing techniques, such as pet acupuncture, with traditional veterinary medical services. The animal hospital was founded in 1997 and is currently practicing out of a 6500 square foot facility. Equine vet, Dr. Mark Bianchi, offers general and advanced services such as surgery, equine dentistry, lameness evaluations and reproduction consultations.

White Oaks Veterinary Clinic is located at 131 W. Waterloo Rd. Further information on the animal hospital or pet stem cell therapy may be obtained by visiting the website at http://www.whiteoaksvet.com.

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Edmond Veterinary Hospital Offers Pet Stem Cell Therapy for Arthritis

SUNDAY, Feb. 19 (HealthDay News) -- A new animal study suggests that a genetic mutation could put certain people at higher risk for becoming obese if they eat high-fat diets.

At the moment, the practical uses of the research seem to be limited, but physicians could conceivably test people for the mutation and recommend that they avoid certain kinds of diets, said study co-author Dr. Gozoh Tsujimoto, a professor at Kyoto University's department of genomic drug discovery science in Japan. It may also be possible, Tsujimoto said, to eventually give people drugs to combat the effects of the mutation.

If that happens, there would be "a new avenue for personalized health care," Tsujimoto said.

Scientists have been busy studying genetic links to obesity that could make some people more prone to gain extra weight. Two-thirds of Americans are either overweight or obese, the U.S. Centers for Disease Control and Prevention estimates. Excess pounds contribute to a variety of diseases, including heart disease and cancer.

In the new study, researchers looked at the component of the body's internal communication system that plays a role in the regulation of appetite and the production of fat cells.

The investigators found that mice that didn't have the component were 10 percent fatter than other mice when all were fed a high-fat diet. Mice without the component also developed higher intolerance to glucose.

Research conducted in animals does not always translate into humans, and much more research is needed. However, the researchers found that Europeans with the genetic mutation, known as GPR120, were more likely to be obese.

"Our study for the first time demonstrated the gene responsible for diet-induced obesity," Tsujimoto said.

According to Tsujimoto, more than 3 percent of Europeans have the trait. The next step for researchers is to study its prevalence in Japanese, Korean and Chinese people.

What can be done with the knowledge from the study?

Tsujimoto said physicians could advise people with the trait to avoid high-fat diets. A test is available to detect the trait and it costs about $200 in Japan, Tsujimoto said.

While medications could potentially be developed that would reverse the effects of the genetic trait, there are no such drugs now, Tsujimoto added.

Ruth Loos, director of Genetics of Obesity and Related Metabolic Traits at Mount Sinai School of Medicine in New York City, said "these findings provide another piece of what turns out to be the very large puzzle that describes the causes of obesity."

Consistent findings in mice and humans have put the trait "more firmly on the obesity map and provides a new starting point for more research into the function of this gene," said Loos.

"This is only the beginning of likely many years of research to disentangle the physiological mechanisms that lie behind the link between this gene and obesity risk," she said. "It is only when we understand the physiology and biology better that one can start thinking of developing a drug."

The study appears online Feb. 19 in the journal Nature.

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For more on obesity, visit the U.S. National Library of Medicine.

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Gene Might Boost Risk for Obesity

ScienceDaily (Feb. 19, 2012) — Global warming has forced alpine chipmunks in Yosemite to higher ground, prompting a startling decline in the species' genetic diversity, according to a new study by researchers at the University of California, Berkeley.

The study, appearing Feb. 19, in the advance online publication of the journal Nature Climate Change, is one of the first to show a hit to the genetic diversity of a species because of a recent climate-induced change in the animals' geographic range. What's more, the genetic erosion occurred in the relatively short span of 90 years, highlighting the rapid threat changing climate can pose to a species.

With low genetic diversity a species can be more vulnerable to the effects of inbreeding, disease and other problems that threaten species survival, the researchers said.

"Climate change is implicated as the cause of geographic shifts observed among birds, small mammals and plants, but this new work shows that, particularly for mountain species like the alpine chipmunk, such shifts can result in increasingly fragmented and genetically impoverished populations," said study lead author Emily Rubidge, who conducted the research while a Ph.D. student at UC Berkeley's Museum of Vertebrate Zoology and the Department of Environmental Science, Policy and Management. "Under continued warming, the alpine chipmunk could be on the trajectory towards becoming threatened or even extinct."

Rubidge worked with Craig Moritz, professor of integrative biology and director of the Museum of Vertebrate Zoology; James Patton, professor emeritus of integrative biology and curator of the Museum of Vertebrate Zoology; and Justin Brashares, associate professor in the Department of Environmental Science, Policy and Management.

The new findings build upon previous research that found major shifts in the range of small mammals in Yosemite National Park since the early 1900s. In 2003, biologists at UC Berkeley began an ambitious resurvey of Yosemite's birds, mammals, reptiles and amphibians, retracing the steps originally taken between 1914 and 1920 by Joseph Grinnell, founder and former director of the Museum of Vertebrate Zoology.

The Grinnell Resurvey Project, led by Moritz and museum colleagues, found that many small mammals in Yosemite moved or retracted their ranges to higher, cooler elevations over the past century, a period when the average temperature in the park increased by 3 degrees Celsius, or about 5.4 degrees Fahrenheit.

It is no surprise that the alpine chipmunk (Tamias alpinus) would be more sensitive to the temperature change, since it is a high-elevation species endemic to California's Sierra Nevada, the researchers said. In the early 1900s, Grinnell and colleagues sighted alpine chipmunks at elevations of 7,800 feet. Now, the alpine chipmunk appears to be sticking to even higher elevations, retracting its range by about 1,640 feet upslope.

To test the genetic impact from that loss of geographic range, researchers compared genetic markers from 146 modern-day alpine chipmunks with those from 88 of their historical counterparts. Samples were collected from seven paired sites throughout Yosemite.

As a control, the researchers also looked at the genetics -- both historic and modern -- of lodgepole chipmunks (Tamias speciosus), a lower elevation species that had not changed its range over the past century.

The analysis of genetic markers revealed a significant decline in "allele richness" among the recently sampled alpine chipmunk populations compared with their historic counterparts. Moreover, the researchers noted that the modern chipmunks were more genetically differentiated across sites than in the past, a sign of increased fragmentation in the alpine chipmunk population.

In comparison, there were no significant changes in genetic diversity detected among the lodgepole chipmunks, a species found at elevations from 4,900 to 9,800 feet.

"Much of what we read and hear about the effects of climate change on biodiversity is based on model projections and simulations, and these models typically involve many moving parts and lots of uncertainty," said Brashares. "Thanks to the baseline provided by Joseph Grinnell's pioneering efforts in the early 20th century, we are able to go beyond projections to document how climate is altering life in California. The research led by Emily is novel and important because it shows empirically that climate change has led to the loss of genetic diversity in a wild mammal over the last several decades."

Moritz added that this study exemplifies how patterns of change in California's ecosystems can be uncovered through analyses of fossil, historic and modern records.

"At the heart of this whole enterprise is the incredibly dense historic record and specimens we have at UC Berkeley from 100 years ago," said Moritz. "These collections allow us to conduct sophisticated analyses to better understand how ecosystems are reacting to environmental changes, and to create more detailed models of future changes."

Other study co-authors are Marisa Lim, a UC Berkeley undergraduate student in integrative biology; and Cole Burton, former UC Berkeley graduate student in environmental science, policy and management (now a research associate at the University of Alberta in Canada).

Funding for this research was provided by the Natural Sciences and Engineering Research Council of Canada, UC Berkeley's Museum of Vertebrate Zoology, the Yosemite Fund, the National Geographic Society and the National Science Foundation.

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Journal Reference:

Emily M. Rubidge, James L. Patton, Marisa Lim, A. Cole Burton, Justin S. Brashares, Craig Moritz. Climate-induced range contraction drives genetic erosion in an alpine mammal. Nature Climate Change, 2012; DOI: 10.1038/nclimate1415

Note: If no author is given, the source is cited instead.

Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

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Yosemite's alpine chipmunks take genetic hit from climate change

Dr. Elizabeth Berry-Kravis has spent much of her career focused on Fragile X, a genetic condition involving a mutation on the X chromosome that causes cognitive disabilities, behavioral issues and other problems.

New medications and therapeutic interventions have revolutionized life for people with the syndrome over the past 20 years, but Berry-Kravis, who runs the Fragile X Clinic and Research Program at Rush University in Chicago, said the most exciting discoveries are being explored now.

She was in Houston recently for a meeting of the Fragile X Clinical and Research Consortium at Texas Children's Hospital and spoke with Chronicle reporter Jeannie Kever.

Q. Tell me a little about Fragile X. How many people does it affect, and how does it manifest?

A. The description everyone uses is, it's the most common inherited form of intellectual disability. It's also the most common known genetic cause of autism. Children will seem pretty normal as young babies, but then they'll present to their pediatrician with a delay in walking or acquiring other motor milestones. A delay in talking is common. They'll have ongoing learning difficulties.

In elementary school, most of the guys with Fragile X will be in special education and have occupational therapy, speech therapy. Fragile X patients have a lot of behavioral difficulties, hyperactivity, problems paying attention, sometimes more aggressive behaviors.

It occurs in about 1 in 4,000 people. The gene that causes Fragile X is on the X chromosome. Men have only one copy of the X chromosome; girls have two. In girls, the normal gene on the other X chromosome tends to make the condition milder.

Q. What are researchers looking at?

A. The research that is particularly exciting, we have a mouse that has Fragile X. The mouse brain looks very similar to the human brain (of someone with Fragile X), so we can study the mechanisms of disease in the mouse.

Now we are working on treatments to target those pathways ... to try to improve the brain cell connections. We can show that certain agents actually work in the mouse to impact different behaviors.

Some of those are being translated into humans. Now, if a patient has attention problems, we would treat it with medicine. But these new medications are targeted to the actual (behavior-causing) mechanisms.

Q. Is that a new approach?

A. It hasn't been done before in a developmental disorder, so Fragile X has become very hot in the research world. What's happening here will become a model for developing treatments for Down syndrome and autism.

Currently, three drugs are in clinical trials. We don't know really how well the drugs are going to work in people yet. We're very hopeful, but we have to remind ourselves the human is not the mouse.

If these drugs do produce improvements, and particularly if they produce cognitive improvements, which has never been done, it would be pretty earth-shaking.

Q. What does that mean for people with Fragile X and their families?

A. In the past, patients with Fragile X were very difficult. They couldn't be handled in the schools. There weren't good medications to help with their symptoms. They would be excluded from society.

They also tended to acquire very few academic skills, because people believed they weren't teachable. Now we've seen a revolution in teaching these patients. Even without the new drugs, the advances in the past 10 or 20 years about early intervention, molding education to the child ... has made a big improvement.

With the advance of behavioral drugs, we can manage the behavior with medications and therapy and educational strategies. More of my patients now are getting out of high school and getting into a job.

If we could treat the biology at least a little bit with these new medications, we would see an added bonus.

jeannie.kever@chron.com

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Research helps demystify a genetic disorder

By Joe Schneider - Mon Feb 20 03:12:04 GMT 2012

Myriad Genetics Inc. (MYGN) and other biotechnology companies can’t monopolize treatment for diseases by patenting human genetic material, an Australian trial was told in the first challenge in the country over the ownership of DNA molecules.

Cancer Voices Australia, a national organization representing people diagnosed with cancer, and Yvonne D’Arcy, a Brisbane resident diagnosed with breast cancer, sued Myriad Genetics and Genetic Technologies Ltd. (GTG) in 2010 over a patent the companies have on a gene mutation associated with an increased risk of breast and ovarian cancers.

“Patents protect inventions, not discoveries,” Rebecca Gilsenan, a partner at Maurice Blackburn Lawyers, who represents the plaintiffs, said before the trial. “No Australian court has considered the question of whether isolated human genes are patentable.”

Gene-sequencing breakthroughs are spawning a multibillion- dollar market for drugs and medical tests. In the U.S., health regulators are developing rules for bolstering oversight of laboratory-developed tests and the U.S. Supreme Court may decide tomorrow whether to hear two cases involving patents over genetic material, including a review of an appeals court decision that upheld Myriad Genetics’ patents.

Myriad Genetics, based in Salt Lake City, contends in the Australian case that it’s not seeking to patent a gene but an artifically-created screening process aimed at identifying a mutation that makes people more susceptible to breast and ovarian cancers.

“You can’t use this to build another human being,” David Shavin, Myriad Genetics’ lawyer, told Federal Court Justice John Nicholas today in his opening statement at the start of the trial in Sydney, referring to the patented screening process. “All you can use it for is to compare” and identify the mutated genes.

Australian law allows for patents on artificially created products with economic benefits, including computer programs and business methods, Shavin said.

“The position in the United States is similar to, but not the same as, in Australia,” he said.

The trial is scheduled to take as long as eight days.

“There is a philosophical and ethical issue about the commercialization of the human body,” Gilsenan said. “The patent owner has a right to prevent people from studying and testing for the gene mutation, so gene patents can stifle research.”

The case is: Cancer Voices Australia v. Myriad Genetics. NSD643/2010. Federal Court of Australia (Sydney).

To contact the reporter on this story: Joe Schneider in Sydney at jschneider5@bloomberg.net

To contact the editor responsible for this story: Douglas Wong at dwong19@bloomberg.net

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Myriad Genetics’ Australian Cancer Gene Patents Go on Trial in Sydney

A research team led by UC Davis Health System scientists has developed a novel technique to enhance bone growth by using a molecule which, when injected into the bloodstream, directs the body's stem cells to travel to the surface of bones.

Once these cells are guided to the bone surface by this molecule, the stem cells differentiate into bone-forming cells and synthesize proteins to enhance bone growth. The study, which was published online today in Nature Medicine, used a mouse model of osteoporosis to demonstrate a unique treatment approach that increases bone density and prevents bone loss associated with aging and estrogen deficiency.

"There are many stem cells, even in elderly people, but they do not readily migrate to bone," said Wei Yao, the principal investigator and lead author of the study. "Finding a molecule that attaches to stem cells and guides them to the targets we need is a real breakthrough."

Researchers are exploring stem cells as possible treatments for a wide variety of conditions and injuries, ranging from peripheral artery disease and macular degeneration to blood disorders, skin wounds and diseased organs. Directing stem cells to travel and adhere to the surface of bone for bone formation has been among the elusive goals in regenerative medicine.

The researchers made use of a unique hybrid molecule, LLP2A-alendronate, developed by a research team led by Kit Lam, professor and chair of the UC Davis Department of

Biochemistry and Molecular Medicine. The researchers' hybrid molecule consists of two parts: the LLP2A part that attaches to mesenchymal stem cells in the bone marrow, and a second part that consists of the bone-homing drug alendronate. After the hybrid molecule was injected into the bloodstream, it picked up mesenchymal stem cells in the bone marrow and directed those cells to the surfaces of bone, where the stem cells carried out their natural bone-formation and repair functions.

"Our study confirms that stem-cell-binding molecules can be exploited to direct stem cells to therapeutic sites inside an animal," said Lam, who also is an author of the article. "It represents a very important step in making this type of stem cell therapy a reality."

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Stem cells used to increase bone strength

ScienceDaily (Feb. 16, 2012) — Genetic information provided by a large group of specially-designed mice could pave the way to faster human health discoveries and transform the ways people battle and prevent disease.

In 15 papers published Feb. 16 in the Genetics Society of America journals Genetics and G3:Genes/Genomes/Genetics, researchers from North Carolina State University, the University of North Carolina at Chapel Hill, The Jackson Laboratory and other universities and labs across the globe highlight a new genetic resource that could aid development of more effective treatments for any number of human diseases.

The resource, known as the Collaborative Cross (CC), is a reference manual of genetic variation contained in hundreds of specially-bred mice and their genetic sequences. The CC mice have much more genetic variation than normal lab mice, and thus more closely mirror the genetic complexity found in humans.

Moreover, the mice and their genetic sequences will be publicly available, allowing researchers around the world to work with mice that have particular genetic variations.

"If you can't mimic the genetic variation in people, you can't necessarily use mouse findings to understand more about human disease," says Dr. David Threadgill, professor and department head of genetics at NC State who originally proposed the idea for the CC project a decade ago and who serves as one of the project leaders. Threadgill is also a member of the University of North Carolina's Lineberger Comprehensive Cancer Center.

Threadgill developed the idea for the CC in order to harness the power of so-called whole genome studies that examine all genes at once instead of subsets of genes. Complex interactions between large numbers of genes frequently govern traits and behavior. Learning more about these interactions could help researchers tease out links between certain genes and certain diseases, for example.

In one of the 15 papers, Threadgill and corresponding author Dr. Francis S. Collins, director of the National Institutes of Health, identify key genes involved in red and white blood cell counts and red blood cell volume. These hematological parameters are important indicators of health and disease.

Project leaders include Dr. Fernando Pardo-Manuel de Villena of the UNC Department of Genetics, who is a member of UNC Lineberger Comprehensive Cancer Center, and Dr. Gary Churchill at The Jackson Laboratory. The international consortium participating in the development of the CC project includes NC State, UNC-Chapel Hill, The Jackson Laboratory, Tel Aviv University, Oxford University and Geniad/Australia. The mice are housed and "curated" at UNC-Chapel Hill.

The research was supported by grants from the National Institutes of Health; Ellison Medical Foundation; National Science Foundation; Australian Research Council; and the Wellcome Trust. The University Cancer Research Fund from the state of North Carolina also provided important funding.

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The above story is reprinted from materials provided by North Carolina State University, via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

S. N. P. Kelada, D. L. Aylor, B. C. E. Peck, J. F. Ryan, U. Tavarez, R. J. Buus, D. R. Miller, E. J. Chesler, D. W. Threadgill, G. A. Churchill, F. Pardo-Manuel de Villena, F. S. Collins. Genetic Analysis of Hematological Parameters in Incipient Lines of the Collaborative Cross. G3: Genes|Genomes|Genetics, 2012; 2 (2): 157 DOI: 10.1534/g3.111.001776

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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New mouse reference library should speed gene discoveries

February 17, 2012, 6:33 PM EST

By Kristen Hallam

(Updates with Life, Illumina shares in fifth paragraph.)

Feb. 17 (Bloomberg) -- Oxford Nanopore Technologies Ltd. is entering the gene-sequencing race with a new portable device that will allow people to analyze DNA on the go.

The product, called MinION, is about the size of a USB memory stick, the closely held Oxford, England-based company said today. MinION will be ready for sale in the second half of the year at a cost of less than $900. It’s a smaller version of the GridION device that Oxford Nanopore is developing.

Oxford Nanopore is relying on the two products to spur demand for machines that can decode the building blocks of life, helping to identify new targets for medicines and illuminate crop science. The company is jumping into a market led by Life Technologies Corp. and Illumina Inc., which last month said they’ve built products that can sequence a genome in a day. GridION is designed so that computing equipment can be clustered to sequence an entire human genome in as little as 15 minutes.

“The USB stick is an absolute game-changer,” Oxford Nanopore Chief Executive Officer Gordon Sanghera in a telephone interview. “It’s plug-and-play, on-the-go DNA sequencing.”

Life Technologies fell 4.3 percent to $47.66 at 1:15 p.m. in Nasdaq Stock Market trading after dropping as much as 7 percent, the biggest intraday decline since Oct. 7. Illumina dropped 2.9 percent to $52.39 after falling as much as 4.5 percent.

Tiny Hole

The company presented data on the two products today at the Advances in Genome Biology and Technology conference in Florida. The devices use a novel technique known as strand sequencing, in which an entire string of DNA is guided by an enzyme and passes intact through a tiny hole in a cell membrane one-billionth of a meter wide, like a child sucking spaghetti through his mouth.

The strand-sequencing technique relies on an engineered protein or nanopore that creates the hole. As DNA bases, or chemical building blocks, pass through the hole, an electronic chip measures changes in electrical current in the membrane and produces data that, when decoded, identifies the sequence of bases that make up a genome.

That’s different from current techniques, in which 200 or 300 continuous bases of DNA are analyzed, Sanghera said. Oxford Nanopore’s machines can read strands of tens of thousands of bases with an accuracy comparable to technology already on the market, he said.

Space Age

“That is some kind of fantastical, space-age thing,” Sanghera said.

The MinION device can only be used once and can’t decode an entire human genome, according to Oxford Nanopore. Users don’t have to amplify DNA to be able to read it, and the sensitivity is about the same as the larger GridION device, Sanghera said.

“This will result in broader adoption of DNA sequencing,” he said. “This allows non-specialist scientists to extract DNA information back in the field. You just need a laptop and software.”

The GridION system, which is about the size of a videocassette recorder, is designed so that researchers who need quick results can add units of cartridges called nodes that speed processing. Using 20 high-end nodes would allow the entire genome to be sequenced in as little as 15 minutes, Oxford Nanopore said.

‘Pregnant Woman’

“Our competitors are like a pregnant woman,” said Zoe McDougall, a company spokeswoman. “It takes nine months to make a baby, and you can’t put nine women on it and get a baby in a month. With our system, you can put nine women on it and make a baby in a month.”

Not all customers want or need such speed, Sanghera said.

“You give flexibility back to the researcher in how they do their experiments,” he said.

Pricing will be “competitive” and will vary, similar to mobile-phone packages tailored to customers’ needs for talk time and data, said Clive Brown, Oxford Nanopore’s chief technology officer.

“There’s no fixed run time on this machine,” Brown said in an interview. “You need pricing elasticity. They all pay same cost per base, but it’s how it’s divided. That’s completely new.”

Life Technologies, based in Carlsbad, California, on Jan. 10 said it is taking orders for its benchtop Ion Proton Sequencer. The machine, available for $149,000, is designed to provide a full transcript of a person’s DNA in a day for $1,000. Illumina, of San Diego, said its HiSeq 2500 will be available in the second half of the year. It didn’t reveal the price.

Potential Buyers

Illumina is the target of a $5.7 billion hostile bid by Roche Holding AG of Basel, Switzerland. Illumina’s board unanimously rejected the offer, calling it “grossly inadequate.” Roche is a sponsor of the conference where Oxford Nanopore presented the data on its machines.

Illumina owns 15 percent of Oxford Nanopore and has a partnership with the U.K. company for a technology called exonuclease sequencing, in which the DNA building blocks are separated by an enzyme and pass individually through a nanopore.

While potential buyers have approached Oxford Nanopore, the company hasn’t pursued any offers, Sanghera said.

“Over the last year, we’ve had various companies express interest in us,” Sanghera said. “We remain focused on our strategy, which is to get this technology to our customers.”

Shareholders

Oxford Nanopore’s shareholders include IP Group Plc, which owns 21.5 percent, hedge-fund manager Lansdowne Partners LP and Invesco Perpetual, the U.K. group of mutual funds. The company also has individual shareholders, including company managers, and employees have stock options.

Oxford Nanopore is valued at about $1 billion, said Charles Weston, a London-based analyst at Numis Securities, which advises IP Group, in a note to investors Feb. 1. Weston based the figures on Oxford Nanopore gaining 25 percent of a market that could grow to $6 billion within five years.

“To get a truly accurate assessment of our valuation, we need to understand what markets we can penetrate,” Sanghera said. “We are not displeased with $1 billion; we feel it could be a lot bigger than that.”

Oxford Nanopore, spun out of University of Oxford in 2005, uses sequencing technologies that were initially based on the research of founder and board member Hagan Bayley, a chemistry professor at the university. The company has built on that science through collaborations with researchers at Harvard University, the University of California Santa Cruz and Boston University, among others, and with internal research, said McDougall, the company spokeswoman.

Early Access

Oxford Nanopore will give early access to a few laboratories to try out the two devices, allowing them to provide feedback and develop applications before the company starts selling the products later this year, Sanghera said.

“The biggest challenge is managing expectations and delivering on the next phase,” Sanghera said. “It feels like you’ve been in a band, and you’ve been doing gigs in grotty little venues, and then you wake up and you’re number one.”

--With assistance from Andrea Gerlin in London. Editors: Phil Serafino, Thomas Mulier

To contact the reporter on this story: Kristen Hallam in London at khallam@bloomberg.net

To contact the editor responsible for this story: Phil Serafino at pserafino@bloomberg.net

Read more:
Oxford Nanopore Plans Portable Gene-Sequencing Device This Year

"The reservoir of genetic diversity contained in the oceans' microbial life is a huge potential source of natural products and genes with applications in medicine, food development and bio-energy," says Curtis Suttle, an expert on marine virology and microbiology at the University or British Columbia and member of the panel.

"The question is whether they fall under a regime of 'freedom of the high seas' which allows the discoverer to keep what they find, or under a regime of 'the common heritage of mankind' which would require benefits from the use of genetic resources to be equitably shared amongst countries."

Marine genetic resources discovered in coastal waters are subject to bilateral 'benefit sharing' under international agreements currently being ratified. But no such agreements govern the patenting and commercialization of proteins and genes harvested from international waters.

"Marine genetic resources within national jurisdiction are subject to requirements for benefit sharing under the Nagoya Protocol, and it is time to consider a parallel agreement for areas beyond national jurisdiction," says panelist Marjo Vierros with the United Nations University (UNU). The UNU is the academic arm of the United Nations system.

"Any agreement should include mechanisms to support marine scientific research and invention through creative tools such as patent pools, open access programs, and gene libraries. It should also include measures for tracing the geographic origin of organisms, conservation and sustainable use."

More than 5,000 genes derived from marine organisms have already been associated with patent claims. Ten countries own more than 90% of those claims, including 'marine genes'. Three countries own approximately 70%, a pattern similar to the one observed for human and plant crop genes, according to panelist Sophie Arnaud-Haond, from the Institut Francais de Reserche sur la Mer.

The panel--which alincludes UBC marine chemist Raymond Andersen and researchers from Spain and Germany--cites the need to enhance the capacity of developing countries to participate in this research and invention through capacity development and technology transfer.

Provided by University of British Columbia (news : web)

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'Wild west' approach to claiming the oceans' genetic resources must end: researchers

Student genetic research projects at Concord High School suddenly meant more last week, when genetics researcher and guest speaker Michele Nikoloff explained how similar tests developed at Roche Molecular Diagnostics are used to improve cancer patient treatment.

CHS honors biology teacher Ellen Fasman said as a research leader, Nikoloff's cutting-edge work dovetails with her curriculum.

"We are studying the targeted therapy genetics approach for certain disease genetic disorders, pedigrees and mutations."

Fasman and Dr. Ernie Liu are among the highly credentialed CHS Science Department teachers who brought their classes to the scientist's PowerPoint presentation where the human stories and images seemed to intrigue students most.

Our students loved Dr. Nikoloff's lectures," Liu said. "The most important thing is that my students found out what they have learned in the classroom they can apply to the real world and make a difference for other people's lives."

Nikoloff said, "The field of genetics is rapidly evolving and it is important to prepare students for future developments. Genetics play a role in how drugs are metabolized and enzyme activity varies among different ethnic populations."

In the area of drug metabolism, she relayed to students the story of the unexpected death of a 13 day-old Canadian baby in 2006. The mother, who was subsequently found to be a genetically ultrarapid metabolizer of codeine, was taking

it for post-labor pain relief and breast-feeding the infant.

Metabolized codeine in the breast milk essentially gave the baby a lethal dose of morphine. Since then, measures have been put in place to prevent such incidents from occurring.

Now, physicians can order a genetic test which reveals how an individual patient metabolizes specific drugs.

Nikoloff said only 80 percent of patients respond to analgesic drugs, while less than 60 percent benefit from asthma medications and less than 15 percent of melanoma cancer patients improve with chemotherapy.

"There is a clear need to identify patients likely to respond to medication based on their genetic makeup," Nikoloff said.

Dylan Parisi, CHS honors biology student said, "I found it interesting how rarely treatments such as chemotherapy actually make a difference for patients."

Targeted therapy is based on testing for a patient's genetic markers to determine who is likely to respond to a particular medication. One benefit of these genetic tests is that physicians will not prescribe drugs that are genetically unsuitable. Nikoloff expects targeted therapy will be part of standard health care in the future.

Nikoloff said that treating melanoma patients with a drug targeted to work only in tumors with a specific mutation led to increased survival.

She showed striking images comparing the appearance of a patient with a deadly case of metastasized melanoma (skin cancer) before and after the targeted therapy treatment with the Zelboraf drug.

"Melanoma is the sixth most common cancer in the United States and amongst the most common fatal cancers in young adults, with 8,000 deaths per year," Nikoloff said.

One student lingered after the lecture with questions such as, "Why does genetically targeted drug therapy work better than chemotherapy?"

Nikoloff explained that targeted medication kills only cancer cells, whereas chemotherapy is designed to kill any dividing cells. The severe side-effects of chemotherapy are evidence of the destruction of the body's other rapidly dividing cells.

"Only 50 percent of patients respond to the average anti-depression drugs and sometimes these medications can be harmful," Nikoloff said. "Personalized health care aims to target the right medicine for the right patient at the right time."

That is just what students are doing, according to Fasman.

"Students are learning to research metabolic disorders and working on 80 to 90 genetic disorders. They look for biological markers which can predict a predisposition to illnesses such as cystic fibrosis, diabetes, asthma and other autoimmune diseases."

Fasman initiated the relationship with Roche in Pleasanton and said she appreciated the company allowing Nikoloff to spend the day addressing CHS biology and biotechnology classes.

Nikoloff is a biochemistry graduate from UC-Berkeley, has a doctoral degree from Carnegie Mellon University, and completed postdoctoral training in plant biology at the Carnegie Institution of Washington at Stanford University. She has developed tests for drug metabolism and cancer treatment.

"(Students) get excited about the possibility of experimenting and coming up with new solutions to diseases and global warming," Fasman said. "Students need to know the approaches being used in the manufacture of medicine."

Constantly on the lookout for experts and equipment to enrich her classes in the rapidly changing field of genetics, Fasman said it is challenging for teachers in the current budget-cutting climate.

"Thirty-two students have to take turns using a limited number of expensive pieces of biotechnology equipment. It can range from $100 for lab equipment, to $30,000 to $40,000 for a PCR (polymerase chain reaction "thermocycler")," Fasman said. "We buy the expensive equipment used when it becomes available through industry upgrades."

Contact Dana Guzzetti at dguzzetti10@gmail.com or call 925-202-9292.

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Concord High School students learn latest in genetics research