Posted by: dnanewstoday | May 30, 2009

Can taking a multivitamin extend life?

3:22 PM, May 29, 2009

Multivitamins Among the keys to longevity are telomeres, DNA sequences at the end of chromosomes that shorten as we age. When cells replicate, telomeres shorten. Thus, preserving the length of telomeres is thought to be a possible key to living longer.

A study in the new issue of the American Journal of Clinical Nutrition found that people who take multivitamins daily had telomeres that were 5.1% longer, on average, than non-vitamin users. The researchers, from the National Institutes of Health, looked at multivitamin use and nutrient intake, as well as telomere length, in 586 women ages 35 to 74. They also found a link between telomere length and intake of vitamins C and E.

How multivitamins may affect telomeres is unknown. But studies have shown that telomeres are vulnerable to oxidative stress, and some vitamins are antioxidants. But since the study is epidemiology, not a cause-and-effect study, it will take more research to know whether multivitamins really impact telomere length.

“To our knowledge, this was the first epidemiological study of multivitamin use and telomere length,” Dr. Honglei Chen, of the National Institute of Environmental Health Sciences, wrote in the report. “Regular multivitamin users tend to follow a healthy lifestyle and have a higher intake of micronutrients, which sometimes makes it difficult to interpret epidemiological observations in multivitamin use.” But, they added, “the results are consistent with experimental findings that vitamins C and E protect telomeres in vitro.”

— Shari Roan

Photo credit: Los Angeles Times

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Posted by: dnanewstoday | May 9, 2009

The Genetic Dimension of Height and Health

It may be no tall tale: A few inches taller or shorter could signal a risk for some diseases

THE GENETIC DIMENSION OF HEIGHT AND HEALTHView Larger Version The long and short of it is that height genes might affect health as well as height, although scientists don’t completely understand how.From left: Jennifer Pottheiser/Getty Images; Terry Schmitt/UPI Photo; Photo Illustration by J. Korenblat

From Danny Devito to Yao Ming, the world is filled with short people and tall people and everyone in between. While factors such as nutrition influence height differences, much of that variation depends on genes. After all, both of Ming’s parents were basketball stars, and Devito’s were not.

But the genes that made Ming grow to 7 feet 6 inches and Devito stop growing several feet shorter could be important for more than sports. Changes in how height genes work could not only add or subtract a few centimeters from leg length, but could also affect underlying cell biology in ways that can lead to disease, recent research suggests.

Statistical studies find that shorter people are more likely to get heart disease, diabetes and osteoarthritis. Other studies show that the same genes that make healthy cells multiply to make a person grow taller can also make cancer cells proliferate in tumors. On the other hand, genes that make bones grow longer can form extra cartilage in joints, protecting them from the ravages of osteoarthritis.

The long and short of it is that height genes might affect health as well as height — although scientists don’t completely understand how.

Some genes that have been implicated in determining height have been well-studied for their connections to particular diseases, but not as well-studied for how they affect height. And while statistical links between height and disease are robustly documented, scientists don’t completely understand if or how the same genes could set the foundation for both height and disease.

Pinning down that connection could have payoffs for treating disease and ensuring health.

“When you take a kid to the pediatrician, the first thing they do is measure the child’s height,” says geneticist Guillaume Lettre of Children’s Hospital Boston and of the Broad Institute, in Cambridge, Mass. He is coauthor of a study that identified several genes associated with height.

Growing too fast or too slow could be a sign of health problems such as hormone imbalances. But if the genes controlling height were well known, pediatricians could easily determine whether a short-for-their-age child simply inherited the gene variants that denote a more diminutive stature, or actually has a more serious condition, Lettre says.

Linking height genes to health is difficult, though, because details of the genetic pathway to height are complex. Many genes work together to create normal variations in height. So far, the suspicion that height genes affect health is supported mostly by statistical studies.

In 2001, for instance, epidemiologist David Gunnell of the University of Bristol in England and colleagues found that taller people can face a 20 to 60 percent greater risk for various cancers, including of the breast, prostate and colon.

Last year, epidemiologist Luisa Zuccolo, also of Bristol, followed up on Gunnell’s work with a study focused on the link between height and prostate cancer. The risk of developing prostate cancer increased by 6 percent for every 10 centimeters over the median height of the 1,357 men in the study, Zuccolo and colleagues reported in Cancer Epidemiology, Biomarkers & Prevention. Despite the link, height was still less of a risk factor than age and family history, but “understanding why height is associated with prostate cancer could help us to understand its causes,” Zuccolo says.

One molecule that taller people have in abundance compared with shorter people is insulin-like growth factor 1, or IGF-1. The insulin-like molecule stimulates the growth of cells and tissues, and higher levels of the molecule have also been linked to the incidence and progression of several different types of cancer. IGF-1 can bind to the tumors of cancers of the breast, prostate and bladder, stimulating the growth of tumor cells. Zuccolo speculates that the IGF-1 gene could link height and prostate cancer.

Stimulating growth

IGF-1 is a protein that binds to receptor molecules on other cells, triggering a cascade of events that eventually stimulate cell growth.


HEIGHT AND DISEASE RISKView Larger Version | Statistical studies among large populations suggest links between height and the chances of certain diseases. Genes are the likely connectors, but the mechanisms remain unclear.

A study reported in 2007 in Science found that variations in the IGF-1 gene were one reason that Chihuahuas don’t grow as large as Great Danes. Geneticist Nathan Sutter, then at the National Human Genome Research Institute in Bethesda, Md., and colleagues found that small dog breeds had one particular variant of the gene for IGF-1, but almost all giant breeds had a different version of the gene.

A 1993 study by Michael Ranke and colleagues at University Children’s Hospital in Tübingen, Germany, found that shorter children had lower levels of IGF-1. Ranke and his colleagues speculate that lower levels of IGF-1 could cause a reduction in growth in early childhood.

In 2001, Gunnell and colleagues reported that leg length is the height component most strongly associated with coronary heart disease and with insulin resistance, a condition that can lead to type 2 diabetes. After measuring leg length and trunk length in 2,429 men and tracking coronary heart disease over 15 years, the team found that insulin resistance and heart disease were more frequent in men with shorter legs, while trunk length showed less association.

But it’s not height itself that makes people sick, researchers say. The ratio of leg length to trunk length could signal IGF-1 levels and thus, possibly, a likelihood for certain diseases. Small variations in the amount of IGF-1 produced can affect growth during childhood, and also alter the incidence of disease later in life.

Lower levels of IGF-1 may have other effects. One study found that individuals with the lowest IGF-1 levels had a twofold increase in heart disease incidence, epidemiologist Torben Jørgensen of the University of Copenhagen and colleagues reported in 2002 in Circulation.

In a 2004 study of IGF-1, height and disease, Gunnell and his colleagues found that shorter stature is linked to heart disease and to insulin resistance.

Researchers aren’t sure why, but large amounts of the IGF-1 protein increase insulin sensitivity, which can reduce a person’s risk for heart problems. Insensitivity to insulin, or insulin resistance, associated with type 2 diabetes is linked to the inflammation that leads to heart disease, but the mechanism of this link is not known.

More evidence of an IGF-1–heart disease link comes from a 2007 finding that IGF-1 injections lowered the incidence of heart disease in mice fed a high-fat diet. The study, by Patrice Delafontaine of Tulane University School of Medicine in New Orleans and colleagues, was published in Arteriosclerosis, Thrombosis, and Vascular Biology. The researchers think that increased IGF-1 reduces the inflammation that can cause heart disease.

But while IGF-1 is known to function in both disease and height, it’s not yet known exactly how the two intersect.

A height and cancer suspect

Genome-wide association studies offer one way to sift through the human genome by comparing genomes of thousands of people for variations associated with a specific trait. To hunt for height genes, researchers try to identify genetic variations that crop up more often in shorter people or taller people.

So far, several studies have related about 40 different genes to height. But more genes are likely to be found, says Gonçalo Abecasis, a statistical geneticist at the University of Michigan in Ann Arbor who collaborated on two of the studies. “There are lots of different genes that each only make a small contribution to height,” he says.

The researchers expect that the list of height genes will run into the hundreds. “We’re making progress, but there are many more height genes to find,” says geneticist Michael Weedon of the Peninsula Medical School in Exeter, England.

Weedon and his colleagues used genome-wide association studies to identify height gene candidates and found that the gene at the top of their list is also a well-known cancer gene. Variants of the high-mobility group A2 gene, called HMGA2, correlated with small variations in height within a population of just over 19,000 people, the researchers reported in Nature Genetics in 2007. That study was the first evidence that small variations in the gene could produce normal height differences among people.

“Sometimes it’s hard to link the gene you find to a height-related function — but this one was easy,” says Lettre, a coauthor on the study.

Scientists already knew that rare HMGA2 mutations could have severe effects on body size. Take 13-year-old Brenden Adams of Ellensburg, Wash., for example. An average-sized newborn, Adams began growing faster than anyone could explain and now stands 7 feet and 3 inches.

At first, doctors couldn’t figure out why. Then they took a look at his chromosomes. A portion of one copy of Adams’ chromosome 12 is inverted, as if a piece of the chromosome had broken off, flipped around and then reattached. The genes on this inverted section seemed to be undamaged — except for where the chromosome broke, which turned out to be at HMGA2.

Azra Ligon and Brad Quade of Brigham and Women’s Hospital and Harvard Medical School in Boston studied Adams’ case. They aren’t sure exactly how the change to HMGA2 is making Adams grow so much, but they speculate that the chromosome inversion disrupted the normal regulation of the gene.

The HMGA2 gene encodes a protein that activates other genes by rearranging how DNA is stored. To package huge amounts of DNA inside each cell, the DNA is twisted and coiled into the chromosomes, then compacted in an orderly fashion so that the correct section is easily available when needed. The HMGA2 protein recognizes and binds to specific twists in chromosomes in order to activate the genes needed for a wide array of biological processes, including the growth and proliferation of cells.

Weedon and colleagues speculate that mutations in the HMGA2 gene can affect how much of the protein is produced.

Previous work also showed that the HMGA2 gene is active only during embryo development in both mice and people. In mature tissues, gene 
activity was almost undetectable, a sign that the gene may not have much effect on the later stages of growth and 

“It seems that the contribution of this gene is laid down early in life,” says geneticist Peter Visscher of the Queensland Institute of Medical Research in Brisbane, Australia.

But the gene does get turned on at later stages in cancerous cells. HMGA2 proteins are found in the tumors of several different types of cancer, including those of the breast, pancreas and lung, suggesting that the gene may help cancer cells grow and proliferate. But scientists don’t know whether the increased risk of cancer in taller people has anything to do with differences in the HMGA2 gene. While HMGA2 is implicated in both cancer and height, “the mechanistic dots have not yet been connected,” says Lettre.

“Right now, we fall short of explaining exactly how HMGA2 controls height,” he says. “We don’t know exactly how variations in HMGA2 that correlate with height could affect how the gene works.”

And while genes such as HMGA2 are already well-characterized because of their roles in disease or development, little is known about many of the height genes that the statistical studies turn up.

Figuring out what these genes do could explain the links between height and disease. “We’re not there yet,” says Abecasis. “But when you start looking at all these different genes, you find that they are linked to lots of different things.”

Adds Lettre: “We’re interested in learning more about how genes control height. But we’re hoping that some of the height genes will have other effects on health too.” That would help the scientists gain insights into the biological processes of growth. “Time will tell, but that is certainly a hope.”

The short path to osteoarthritis

Taller people may be at a higher statistical risk of cancer, but short people face height-related disease risks too.

A gene called growth differentiation factor 5, or GDF5, is related to height; it encodes a protein important for bone and cartilage growth and skeletal development. Geneticist Karen Mohlke of the University of North Carolina at Chapel Hill and her colleagues found that slight differences in the GDF5 gene caused differences of about 0.3 to 0.7 centimeters in height. The people on the shorter end of these differences were more likely to have the particular GDF5 variant associated with osteoarthritis, a type of arthritis caused by the breakdown of cartilage in joints.

People with lower levels of the GDF5 protein have shorter bones and less cartilage in their joints. Shorter people are more susceptible to osteoarthritis because they have less cartilage to wear down.

“It makes sense that a reduction in GDF5 would decrease bone growth and lead to reduced height,” says Gonçalo Abecasis, a statistical geneticist at the University of Michigan in Ann Arbor and a coauthor of the study, which was published in Nature Genetics in 2008. “And as well as this, there would be less cartilage in the joints, which could increase susceptibility to osteoarthritis,” he says.

Posted by: dnanewstoday | April 27, 2009

Cloning Heats Up as Next Bioresearch Fight

CQ TODAY PRINT EDITION April 27, 2009 – 9:00 p.m.

As the Obama administration prepares to greatly expand the government’s investments in embryonic stem cell research, the next big biomedical research debate in Congress is shaping up: whether to allow government funding of experiments using cloned human embryos.

Two House members who were the chief backers of legislation to expand embryonic stem cell research are working on a new bill that would codify President Obama’s recent executive order allowing greater federal funding for the research. Their legislation will also contain language allowing the National Institutes of Health to invest in other kinds of research into human cell biology, perhaps including what is known as “therapeutic cloning.”

Some scientists were disappointed April 17 when the NIH issued draft guidelines for embryonic stem cell research that excludes from federal funding cell lines developed using a procedure called “somatic cell nuclear transfer,” or SCNT. Synonymous with therapeutic cloning, the procedure could theoretically yield stem cells from human embryos that are genetic copies of adults.

Experts in the field believe that therapeutic cloning could one day lead to advances such as tissue transplants that carry no threat of rejection by a patient’s immune system. SCNT could also be used to reproduce tissue affected by poorly understood diseases like Alzheimer’s or Parkinson’s, allowing scientists to study the genetic underpinnings of the conditions, said Dr. Irving Weissman, director of Stanford University’s stem cell research center.

Weissman issued a statement April 17 blasting the NIH’s proposal to exclude SCNT from funding. “The hope, for me, is to get at diseases that we watch kill people and we can do nothing about,” Weissman said.

Rep. Diana DeGette , D-Colo., who is drafting the new stem cell research legislation with Rep. Michael N. Castle , R-Del., said that she does not seek to order the NIH to fund research based on therapeutic cloning. But she hopes to encourage it.

“I hope the NIH will allow SCNT to move forward with federal funding,” DeGette said. “But if they don’t do that right now, what our bill will do is allow them to change that in the future if research shows it is a necessity and can be done ethically.”

Ethical Questions Arise

But stem cell scientists like Weissman have a much different view of what is ethical than do social conservatives, who liken embryonic stem cell research to abortion because it requires the destruction of embryos. The National Right to Life Committee, an anti-abortion group, sent a letter to Congress March 31 warning that the DeGette-Castle legislation will be a “bait-and-switch,” using obscure language to conceal its intent to authorize funding for cloned embryonic stem cells.

“They know that the American public is strongly against human cloning, so they hope to empower NIH to engage in it through subterfuge,” said Douglas Johnson, legislative director for the committee.

The NIH’s draft guidelines were intended to spell out what kinds of embryonic stem cell research it will support, in the wake of a March 9 executive order by President Obama that ended the George W. Bush administration’s strict limits on funding of the research.

However, the NIH says even now that it will only fund research involving embryonic stem cells derived from embryos discarded by in vitro fertilization clinics, and only in cases where the parents of the embryos consent in writing to their use for science. Embryonic stem cells derived from other means, including somatic cell nuclear transfer, will not be eligible for federal funding.

A law known as Dickey-Wicker, which has been renewed annually as part of the regular appropriations process, forbids federal funding for the creation of embryonic stem cells, including cloned cells, because the process destroys embryos. But both Obama and Bush have interpreted Dickey-Wicker to allow the funding of research using the cells.

NIH’s decision to exclude stem cell lines created using cloning techniques seems to be an attempt to mollify critics on the right, who otherwise might have accused Obama of supporting human cloning.

“There is broad support to use federal funds to conduct human embryonic stem cell research,” said an NIH spokesman, John T. Burklow. “There is not similar broad support for using other sources [for embryonic stem cells] at this time.”

He noted that Obama’s executive order allows NIH to revisit its guidelines in the future. But Weissman said in his April 17 statement that NIH’s guidelines violated Obama’s executive order and his promise that science under his administration would be “based on facts, not ideology.”

Scientists distinguish between therapeutic cloning and reproductive cloning — creating a genetic copy of a person, a prospect widely considered unethical. Somatic cell nuclear transfer is the first step in both therapeutic and reproductive cloning.

The nucleus of an unfertilized human egg, which contains the cell’s DNA, is removed and replaced with a nucleus from the somatic tissue — skin or other organs — of a patient. Then the egg is stimulated to divide, becoming an embryo. Stem cells are harvested from the embryo, destroying it. Theoretically, the stem cells — now a genetic match with the patient — can then be developed into whatever tissue the patient needs replaced and implanted with much less risk of rejection than if the cells came from an unrelated embryo.

Conservative groups like Johnson’s, though, warn of a future where cloned embryos are created en masse in “human embryo farms,” strictly to be harvested for stem cells. Or, they say, unscrupulous scientists might bring a cloned embryo to term, raising uncomfortable new legal and moral questions about what it means to be human.

SCNT has been used to create cloned animals. But it has never proved effective in human cells, either for therapeutic or reproductive uses.

DeGette says her legislation will contain language outlawing reproductive cloning. She said that Democratic leaders in the House support her work.

But the prospect of federal funding for human SCNT research looks dicey in the near term. Sen. Tom Harkin , D-Iowa, the sponsor of an embryonic stem cell research bill that Bush vetoed in 2007, says that he is comfortable with the Obama administration’s position.

“His policy strikes a thoughtful balance between respect for human life and the potential to ease suffering through scientific research,” Harkin said in a statement. “Scientists will still be able to study SCNT using private funding. But it’s important to note that no one has yet succeeded in creating a human stem cell line using SCNT. As yet, this is only a theoretical approach.”

Posted by: dnanewstoday | April 27, 2009

Genetics Fuels New Initiatives

The newspaper of The Johns Hopkins University April 27, 2009 | Vol. 38 No. 32

Framework for the future grants seed two programs By Greg Rienzi
The Gazette

A duo of university initiatives seeks to significantly alter the medical landscape in terms of disease research and patient treatment by combining the latest in genetic science with good old-fashioned Johns Hopkins know-how.

Discovery grants seeded both initiatives. A program in computational genomics has already blossomed into a center, while an effort to pioneer individualized medicine has firmly taken root and spawned a steering committee.

The programs were among the 11 inaugural grant winners out of 74 proposals submitted to the Framework for the Future’s Discovery Working Group. Each of the 11 selected initiatives received startup funding of up to $200,000 per year for up to three years. The university hopes that these Discovery grants will ignite new areas and strengthen existing ones where crossdisciplinary interactions make a major difference.

The Discovery Working Group is one part of Framework for the Future, a strategic planning process that then Provost Kristina Johnson and President William R. Brody initiated in May 2008. The other two are Ways and Means, and People.

From their Discovery grant proposal “Nucleating a Discipline: Creating Leadership in Bioinformatics and Computational Biology,” faculty from the schools of Arts and Sciences, Engineering, Medicine and Public Health have recently organized the Johns Hopkins Center for Computational Genomics, which will officially launch its work next month.

The new center looks to extend the work of the university’s Genome Café — a genome biometry laboratory housed in the School of Public Health’s Department of Biostatistics — and the Genomic Integration Across N Technologies (GIANT) working group, which facilitates interactions among people trained in statistics, bioinformatics, computer science, biostatistics and medicine.

Sarah Wheelan, assistant professor of oncology biostatistics and bioinformatics at the School of Medicine and the center’s initiating principal investigator, said that high-throughput technologies such as microarrays generate unprecedented amounts of highly interconnected biological and clinical data, whose interpretation requires pioneering and multidisciplinary approaches. The emergence of these new technologies has made it seemingly impossible, she said, for a single person to conceive, direct, perform and interpret a modern large-scale experiment.

The center looks to bring together the expertise needed to take advantage of these new data sets that promise breakthroughs in disease research. Through training and by facilitating collaboration, the center seeks to enable an investigator to correctly interpret and make use of a much larger fraction of his or her data. Prominent bioinformaticians estimate that out of any given biological or clinical experiment, only a fraction of the potential biological discoveries are made when the data are analyzed with standard techniques by a nonspecialist.

“The average biologist can’t make a dent analyzing all this complicated information, and the average statistician doesn’t have the biological intuition to follow up on leads presented by the results,” said Wheelan, who has a joint appointment in Biostatistics in the School of Public Health. “There are not enough people who have both biological and statistical knowledge to direct these experiments and clinical trials. The center will provide this hybrid training and foster collaboration that will allow us to more effectively attack biological problems using statistical and computational approaches.”

The Johns Hopkins Center for Computational Genomics will encompass three interacting entities: a research center, a graduate education program and a program in skills development for professionals. The core staff are Wheelan; Rafael Irizarry, a professor of biostatistics at the School of Public Health; Luigi Marchionni, an instructor of oncology at the School of Medicine; and Jonathan Pevsner, an associate professor at the Kennedy Krieger Institute and of neuroscience at the School of Medicine.

It will be housed in the Preclinical Teaching Building on the East Baltimore campus. The center’s Web site,, is currently under construction.

A three-year grant also dealing with genetics was given to a proposal in individualized medicine submitted by faculty and staff from the Applied Physics Laboratory, the Berman Institute of Bioethics and the schools of Arts and Sciences, Medicine and Public Health.

David Valle, director of the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins and a principal member of the newly founded Johns Hopkins Individualized Medicine Program, looks to shake up the one-size-fits-all approach to medicine and usher in a new era where physicians treat a person based on his or her genome and environmental factors.

“Since the earliest days of medicine, physicians have been educated in terms of generalities. In a sense, standard medicine is average medicine; not to say it’s mediocre, but that it’s based on a law of averages,” Valle said. “You’ll learn here is what happens with a patient with pneumonia. But once you get into practice, you don’t see generalities; you see a specific person with pneumonia. When you talk with experienced physicians, very often you come to the realization that no two patients are exactly alike.”

While the genomes of any two people are 99 percent identical, the minute genetic variations in the 3 billion DNA letters can make the difference between a person who needs five times the average amount of a certain drug to someone for whom the average dose would be unsafe.

The Johns Hopkins Individualized Medicine Program looks to take advantage of recent advances in genetics, fueled by the completion of the Human Genome Project in 2003 and the HapMap Project, a multicountry effort to identify and catalog genetic similarities and differences in human beings. To date, HapMap has identified up to 90 percent of the common genetic variation in humans.

Valle said that the evolution of genotype technology has made the process cheaper and the prospect of individualized medicine more practical.

“All of a sudden we can see right before us the possibility of assessing each patient based on his or her genetic individuality,” Valle said. “By the same token, there is an emerging field of exposure biology aimed at understating environmental-experience histories. We have the means to see the differences and similarities among all patients.”

Valle said that JHIMP will help measure and interpret those differences.

“That is a big challenge, but one can certainly argue that the future of health care will be in individualized medicine,” he said. “We have a strong clinical-rich tradition here at Johns Hopkins. We should be the leaders in this area. We should set the pace.”

JHIMP’s initial aim will be to select a small pilot group of patients, collect DNA samples from each, give each an environmental questionnaire, and begin to assess and develop a framework of utilizing genetic and environmental variants in each patient.

Researchers will develop a set of criteria of how and when to use such information. Valle said he realizes that major issues need to be confronted, such as building a secure computational infrastructure for storing and sharing this sensitive information.

“For it to be practical, the information needs to be instantly accessible so that a physician can use it following a diagnosis, but we need to store it in a way that protects the patient’s privacy,” he said. “The transformation from average medicine to individualized medicine will not happen overnight. It will be an evolving process.”

Valle said that the program will initially target 10 biological systems and develop research tools to make use of the genetic information gathered from the pilot group. As part of this effort, the program will partner with the Johns Hopkins Center for Computational Genomics.

“Sarah’s group will be crucial to our activities,” Valle said.

To date, a 16-member JHIMP steering committee, from across JHU divisions, has been formed. Its principals include Kathy Hudson, director of the Genetics and Public Policy Center; Stephanie Reel, the university’s chief information officer; and Alex Szalay, Alumni Centennial Professor in the Krieger School’s Department of Physics and Astronomy.

“Alex is familiar with big-computations issues, so that is where he comes in. What we’re doing also has enormous ethical aspects, and Kathy Hudson will play a vital role so that we can avoid pitfalls,” he said.

Scott Zeger, acting provost and senior vice president for academic affairs, said that important scientific questions often require interdisciplinary teams for significant discovery.

“I am encouraged and pleased to see outstanding Johns Hopkins faculty, like these, working across disciplines, departments and schools to use the new biological measurements to advance our understanding of biologic processes and ultimately to promote health and treat disease,” Zeger said.

Posted by: dnanewstoday | April 26, 2009

DNA ‘ambassadors’ reach out to high school students

Published: Apr 26, 2009 12:30 AM
Modified: Apr 26, 2009 01:27 AM

Young scientists from the University of North Carolina at Chapel Hill and nine other institutions fanned out on Friday to more than 100 high schools across the state for the annual DNA Day commemorations.

DNA Day marks two key scientific breakthroughs — the discovery of DNA’s double helix in 1953 and the completion of the Human Genome Project in 2003. The event aims to engage and excite students about genomics and to inform them about career options available in the numerous scientific fields that deal with DNA, such as forensics, biotechnology and the study of genes and disease.

This year, 160 graduate students and postdoctoral fellows were to visit more than 200 classes in 101 different schools, including East Chapel Hill High School in the Chapel Hill-Carrboro school district and A.L. Stanback Middle School, Gravelly Middle School and Cedar Ridge High School in the Orange County district.

The student volunteers, known as ambassadors, used one of six different presentations depending on their field of expertise.

As well as helping communicate the science of DNA, ambassadors talk about their day-to-day lives working as researchers, and prompt discussions about topics such as the ethical considerations involved in genetic testing and health care decisions.

Along with UNC-Chapel Hill researchers, graduate students and post-doctoral fellows from the University of North Carolina at Charlotte, North Carolina State, Appalachian State, North Carolina A&T State, Wake Forest and Duke universities — as well as scientists from GlaxoSmithKline, the National Institute of Environmental Health Sciences and BioNetwork — were to take part.

Source: The Chapel Hill News

Posted by: dnanewstoday | April 24, 2009

Learn How You’ll Die For Only $68,000

Bid in a one-of-a-kind auction to have your DNA sequenced and interpreted

DNA Strands: Sequencing individual genomes may lead to medical breakthroughs such as specifically tailored medications. iStockphoto

No doubt you have it on your calendars, but in case you forgot, the 25th is National DNA Day. Can’t think how to celebrate it? Well, if you have $68,000 or more lying around, you can bid for a chance to have your entire personal genome sequenced by Knome, a company that does such things.

The proceeds from the ten-day auction will benefit the X-Prize Foundation, whose mission is to “bring about radical breakthroughs for humanity.” They’ve put up a prize of $10 million to anyone who can sequence 100 human genomes in 10 days or less. Considering that the first sequencing of the human genome, back in 2001, took an entire year, this will prove to be a remarkable feat.

According to Dr. Peter H. Diamandis, chairman and CEO of the X-Prize Foundation, “The ability to fully sequence human genomes and use that personal genetic information to predict disease susceptibility and guide proactive care has the power to transform our entire healthcare system. It is that quantum jump in speed and reduction of cost that make this X-Prize so important in accelerating the dawn of personalized medicine,” says Diamandis.

Oh, one more thing… your personal genome will be delivered to you in a silver box containing a brushed steel USB flash drive. Happy bidding!

April 24, 2009

An international team of scientists have published the entire DNA genome of an 8-year-old female Hereford living at an experimental farm in Montana, a major milestone in animal genetics. The project was a six-year effort that involved more than 300 scientists from 25 countries and cost $53 million. In mapping the cattle genome, scientists discovered how certain chromosomal rearrangements affect genes related to immunity, metabolism, digestion, reproduction and lactation.

“We chose to study the cow genome because these animals are of such immense importance to humans,” explained Richard Gibbs from Baylor College of Medicine’s Human Genome Sequencing Center, a leading contributor to the project. Part of the work involved comparing the genome of the cow, Bos taurus, with that of the human, dog, mouse, rat, opossum and platypus. In the way their chromosomes are organized, cows are more like people than mice and rats commonly used as research animals. Cows have about 22,000 genes, and about 80 percent of their genetic material is the same as humans who have 20,000 or so genes. By comparing the results to other sequenced genomes, including that of humans, the researchers discovered how cows could help inform research into human health and disease. Agriculture officials say the research will drastically improve the way cattle are bred and consequently bolster efforts to produce better beef and dairy products.

April 24, 2009

US (ChattahBox) – Researchers at Scripps Research Institute have made a major breakthrough in creating stem cells from adult cells, without the manipulation of genetic materials.

According to the study, the scientists involved used a combination of proteins retrieved from a number of organisms to inject into the cells, transforming them into stems cells that are nearly indistinguishable from embryonic stem cells.

This method is safer then those that previously used genes with specified DNA sequences injected into the cells to create that transformation, which was unstable and gave the risk of cancerous tumors developing within the body’s tissue.

These cells have been marked as ‘pluripotent’, as they can be use to potentially treat a myriad of diseases by replacing damaged cells and tissue in the body. There is also hope that this could allow for safer organ transplants.

The cells have been named “protein-induced pluripotent stem cells”m or piPS for short. This is the first time a viable, safe option has been provided as an alternative to embryonic stem cells, which has sparked an incredible amount of controversy for it’s harvesting from aborted fetuses.

The study has been published in the journal Cell Stem Cell.

Posted by: dnanewstoday | April 18, 2009

New Breakthrough in Aging…Based on Your DNA

Biotech company has launched a brand new breakthrough product all about healthy aging, health performance and skin care.

New research shows that patients would take advantage of DNA testing if their physicians offered the service, and would return to physicians for preventive care based on results.

Carlsbad, CA (PRWEB) April 17, 2009 — A new survey of U.S. patient opinions suggests that wider adoption of DNA testing could increase efficiency and cut costs for both consumers and the healthcare industry. Although this has been a widely held industry view, it now seems that patients would react proactively to adverse test results.

The short-form survey is part of the morefocus group’s on-going health and lifestyle research initiative, designed to study the changing attitudes of U.S. consumers to healthcare, leisure, education and work. The survey was carried out over a four-week period ending on April 15, 2009, and delivered across a mix of 175 health and lifestyle websites reaching some two million consumers.

Of those who participated in the survey, 85.3% said they would have their DNA tested if they didn’t have to pay for it, with only 14.6% reporting that they would not be tested irrespective of cost. With 84.5% indicating that they would get tested if their doctor simply offered the service, it is clear that price has little impact on the decision. With the dramatic reduction and enhanced breadth of DNA testing over the past year, the availability of more effective testing provides a new avenue for a healthcare system that is severely overstretched and facing reduced cost-cutting options.

Dr. Regan Carey, who led the analytics team for the Morefocus Group said, “We have been watching the changing attitudes in healthcare consumer perceptions since 2001. The introduction of commercial full body scans some five years ago, in spite of their relatively low cost, did not attract a high degree of consumer confidence. Wide availability of DNA testing has changed the paradigm. As the costs of DNA analysis have come down, and consumer confidence increased in line with privacy legislation, so have attitudes of both consumers and professionals swung to make testing a viable and effective tool for healthcare providers and consumers alike.”

Cost savings for the healthcare industry is but one potential benefit of DNA testing, however. When asked how participants would react to results that showed a high risk for developing a cancer or disease, 70% indicated that they would consult a physician for information, and 49% indicated that they would take better care of themselves. Proactive physician visits and healthier lifestyles both contribute to a preventive care plan, which has been suggested as a long-term cost-cutting method for the U.S. healthcare industry.

Richar Scuderi MD PhD, a Morefocus consultant, said, “One of the most significant benefits of risk testing is awareness. There are always those who would rather not know. However, as longevity has increased, so a rapidly increasing percentage of the population are proactive in acting on preventative lifestyle changes.”

Overall, 89.8% of participants agreed that DNA testing was a good idea. When asked why respondents would want to have their DNA tested, 48.5% indicated a desire to discover their risk for cancer and disease, and 23.7% responded that they would want to diagnose current health symptoms. Scuderi’s comments were demonstrated through the, 91.6% who agreed with the sentiment, “It would be helpful to know if I’ve inherited a risk for a certain disease so I can try to prevent it.” DNA testing provides this service

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