New Stem Cell Found in the Brain

GRAND RAPIDS, Mich., April 19, 2012 /PRNewswire/ --Researchers at Lund University in Sweden have discovered a new stem cell in the adult brain. These cells can proliferate and form several different cell types -- most importantly, they can form new brain cells. Scientists hope to take advantage of the finding to develop methods to heal and repair disease and injury in the brain.

Analyzing brain tissue from biopsies, the researchers for the first time found stem cells located around small blood vessels in the brain. The cell's specific function is still unclear, but its plastic properties suggest great potential.

"A similar cell type has been identified in several other organs where it can promote regeneration of muscle, bone, cartilage and adipose tissue," said Patrik Brundin, M.D., Ph.D., Jay Van Andel Endowed Chair in Parkinson's Research at Van Andel Research Institute (VARI), Head of the Neuronal Survival Unit at Lund University and senior author of the study.

In other organs, researchers have shown clear evidence that these types of cells contribute to repair and wound healing. Scientists suggest that the curative properties may also apply to the brain. The next step is to try to control and enhance stem cell self-healing properties with the aim of carrying out targeted therapies to a specific area of the brain.

"Our findings show that the cell capacity is much larger than we originally thought, and that these cells are very versatile," said Gesine Paul-Visse, Ph.D., Associate Professor of Neuroscience at Lund University and the study's primary author. "Most interesting is their ability to form neuronal cells, but they can also be developed for other cell types. The results contribute to better understanding of how brain cell plasticity works and opens up new opportunities to exploit these very features."

The study, published in the journal PLoS ONE, is of interest to a broad spectrum of brain research. Future possible therapeutic targets range from neurodegenerative diseases to stroke.

"We hope that our findings may lead to a new and better understanding of the brain's own repair mechanisms," said Dr. Paul-Visse. "Ultimately the goal is to strengthen these mechanisms and develop new treatments that can repair the diseased brain."

Link to the study here:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0035577

About the Neuronal Survival Unit, Faculty of Medicine, Lund University

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New Stem Cell Found in the Brain

UI freshman physiology major starts clothing line

UI freshman physiology major starts clothing line

BY JULIA JESSEN | APRIL 19, 2012 6:30 AM

The design on Androu De Vera's black T-shirt is striking. The graphic letters in pure white boldly stand out in stylized script against the dark background of the shirt.

De Vera created the design himself. It was the first image he came up with for the clothing line he started last fall, Fresh to Death Society.

"It's very simple. It's to the point," he said. "I always like simplicity; that's how the whole design came out it wasn't too extravagant."

Failing a chemistry test spurred the 19-year-old to an activity he found comfort in: drawing. He created the first design on paper, showed his friends and decided to start his own clothing company, something he had thought about for a while before the fateful test.

"I just love the fashion," De Vera said. "I always liked to dress different from everyone else I don't like to look the same as everyone else."

The human physiology major started the line with his own savings and a loan from his parents, who would prefer that he stay focused on his medical studies.

"At first they thought it was really silly, like what are you doing, you're wasting your time," he said.

But De Vera's parents did start to feel a little better about his extracurricular pursuits when he showed them the growing following forFresh to Death Society.

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UI freshman physiology major starts clothing line

More exciting comparative physiology sessions at EB 2012! [Life Lines]

In looking through the online program for this years' EB, I came across additional comparative physiology seminars that I am very much looking forward to attending (to see the prior list of must-see seminars, click here):

Monday April 23rd: 8:00am-10:00am: "Hypoxia Inducible Factors in Health and Disease," chaired by B. Rees, CG Wilson, and M Watanabe.

10:30-12:30: "Sodium and water homeostasis: Genetic and comparative models," chaired by T Pannabecker and K Hyndman.

12:45-3:15pm: Don't forget to attend the Scholander poster session to meet the future scientists in comparative physiology and hear about their research. (posters: D522-D551) Also be sure to stop by the other comparative physiology posters listed in the program!

Tuesday April 24th: 12:45-3:15: More comparative physiology posters!

Wednesday April 25th: 8:00-10:00am: "Gastrointestinal physiology and the microbiome," chaired by RT Worrel and APS Past-President, HV Carey. There are some really neat comparative physiology seminars in this session!

I look forward to seeing everyone at the APS 125th Anniversary opening and closing ceremonies as well!

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More exciting comparative physiology sessions at EB 2012! [Life Lines]

Nutrition and you: Sugar in the news…

By Peggy Korody, RD, CLT

Sugar and our health has been in the news a lot lately. Perhaps you saw the CBS 60 Minutes segment titled Is sugar toxic? Dr. Lustig, a pediatric endocrinologist at the University of California, San Francisco, concluded that sugar, more than any other substance, is to blame for obesity, type 2 diabetes, hypertension, and heart disease. Bonnie Liebman, director of Nutrition at Center for Science in the Public Interest, recently wrote that for years researchers have found a higher risk of type 2 diabetes, heart disease, high blood pressure, high triglycerides, gout, and weight gain in people who consume more sugar-sweetened beverages. And a flurry of new studies suggests that our out-of-control sweet tooth is connected to our out-of-control belly fat.

The average American consumes 22 to 28 teaspoons of added sugar a day mostly in the form of high-fructose corn syrup (HFCS) or ordinary table sugar (sucrose). Since its peak in 1999, intake from total sugars is down 8% and HFCS is down approximately 9% for the same time period, yet our obesity rates continue to rise dramatically during this same time period.

Since the 1970s, we have been warned to lower our fat consumption to reduce our risks of heart disease. I remember the explosion of fat-free or low-fat products in the cookie and snack aisle. Consumers bought these items freely thinking they were being healthy, but our obesity rates continued to rise. How could this be? When you take the fat out of products they dont taste very good, so the food manufacturers simply replaced the fat with sugar, and over time sugar was replaced with HFCS. A slice of Starbucks Reduced-Fat Cinnamon Swirl Coffee Cake has 10 teaspoons of added sugars!

First I would like to remind everyone that sugar from any source in non-nutritive, in other words its just calories. With few exceptions (like agave and corn syrup), most sweeteners and naturally occurring sugars in fruit break down into roughly half fructose and half glucose in the body (see the chart below).

Sweetener %Glucose % Fructose

Glucose or Dextrose 100% 0% Corn syrup 100% 0% Maple syrup 51.5% 48.5% Brown sugar 49.5% 49.5% Molasses 47.5% 49.5% Raw sugar (sucrose) 50% 50% Table sugar (sucrose) 50% 50% Honey 44.5% 50.5% Orange juice concentrate 49% 51% HFCS 45% 55% Apple juice concentrate 33.5% 66.5% Agave 12% 88% Fructose 0% 100%

Source: USDA Nutrient Database.

In three different studies, scientists randomly assigned people sugary beverages (made with sugar or HFCS) versus diet beverages for three to 10 weeks. No surprise, the people who consumed the sugar or HFCS drinks gained weight. So why does HFCS get such a bad rap? Sweeteners high in fructose do not affect blood sugar because fructose is metabolized in the liver very quickly. Research shows that when there is more sugar than the liver can process, it converts the sugar to fat. Some of the fat goes into the bloodstream, and thats why we get elevated triglycerides and increase ones risk for heart disease. It may also increase the risk of metabolic syndrome/insulin resistance, which leads to type 2 diabetes.

The bottom line:

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Nutrition and you: Sugar in the news…

Nutrition Society honours Liow

HEALTH Minister Datuk Seri Liow Tiong Lai was recently conferred honorary member of the Nutrition Society of Malaysia.

The societys president Dr Tee E. Siong said Liow was recognised as an honorary member of the society because of his many years of contributions to the field of nutrition.

Liow received the membership certificate from Dr Tee during the launch of Nutrition Month Malaysia and NutriFun Land Carnival recently.

Id like to thank the society for conferring the honorary membership to me, said Liow, adding that it was meaningful to him as he himself was a nutritionist.

Dr Tee said Liow had helped establish the Health Ministrys Nutrition division in 2009 and increased the number of nutritionists to the current 300.

Liow also launched the National Strategic Plan for non-communicable disease (2010-2014) to strengthen the cardiovascular and diabetes prevention and control programme and to combat obesity as the main risk factor, he said.

As part of Liows plans, 300 nutritionists were placed at the clinic level for a four-year period from Aug 14, 2009 to guide patients on good nutrition.

He also made extensive revisions to the 1999 edition of the Malaysian Dietary Guidelines, said Dr Tee.

The publication of the 2010 guideline is timely in view of the Governments effort to ensure that all Malaysians have adequate access to practical and accurate information on nutrition and health, he said.

Liows other contributions included supporting the implementation of the National Plan of Action for Nutrition of Malaysia, (2006-2015), the drive for infant and young child feeding, especially breastfeeding and spearheading the Food Basket Programme which focused on the rehabilitation for malnourished children in the country, he said.

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Nutrition Society honours Liow

New estimates show black men gain, women lose in longevity race

Black men in South Florida have made tremendous strides in longevity, according to new estimates released Thursday. Those born in 2009 could expect to live 7 years longer than those born two decades earlier.

But researchers with the Institute of Health Metrics and Evaluation who calculated lifespans in every U.S. county in 1989, 1999 and 2009 also said there was troubling news. The numbers show women's lifespan gains have slowed to a crawl nationwide. Also, how long one might live varies hugely among counties in the same state, hinting at differences in healthcare access.

Florida, for example, claims the nation's highest life expectancy: the 85.9-year lifespan projected for white females in Collier County, which includes Naples. Then there's rural Baker County, up in the state's upper northeast corner, where black men are estimated to live 62.4 years 23.5 years less than Naples' white women.

In four Florida counties, all in the Panhandle, women's longevity estimates dropped by several months from 1989 to 2009 a trend echoed in hundreds of counties nationwide. Dr. Ali Mokdad, the head of the institute's U.S. County Peformance Research Team, said this means girls born in these places three years ago will live shorter lives than their mothers.

"This should be a wake-up call for all of us, and should rally people in their communities. These are disparities we should not ignore," Mokdad said from Atlanta, where the data were released at a health care journalists' conference.

The biggest culprit? The institute team, based at the University of Washington in Seattle, blamed health risks stemming from poor lifestyle choices: smoking, alcohol abuse, obesity, poor diet and lack of exercise.

South Florida public health experts agreed. "Unfortunately in our healthcare delivery system today, we focus more on medical intervention than health promotion," said Cecilia Rokusek, executive director of education, planning and research for Nova Southeastern University's College of Osteopathic Medicine. People need to begin working on healthy aging in midlife or younger, not in their 80s and 90s, she said.

Rokusek thinks the increase in healthcare education targeting minorities over the past decade helped boost black male longevity. Those alive in 2009 are now projected to have an average life expectancy of around 73 years in Broward, Miami-Dade and Palm Beach counties, above the state average.

Dr. Richard C. Palmer, of the College of Public Health & Social Work at Florida International University in Miami, said black men also benefitted tremendously from better blood pressure drugs, as they are more likely to be hypertensive. But he noted that many minorities and people living in rural areas continue to have shorter lives than their white or urban counterparts, an observation born out in the new estimates.

In his own research, Palmer found rural doctors were less likely to discuss health prevention with their patients. And life experiences can affect health habits: "One black man, who remembered segregation as a child, told me he wouldn't go to doctors as an adult because he didn't trust them," Palmer said.

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New estimates show black men gain, women lose in longevity race

SAGE® Labs Creates the First Tissue-Specific Gene Deletion in Rats

ST. LOUIS, April 19, 2012 /PRNewswire/ --Sigma-Aldrich Corporation (Nasdaq: SIAL - News) today announced that Sigma Advanced Genetic Engineering (SAGE) Labs, an initiative of Sigma Life Science, extended CompoZr Zinc Finger Nuclease (ZFN) technology to achieve the first tissue-specific conditional knockout of an endogenous gene in rats. For two decades this approach for generating sophisticated disease models could be performed only in mice. Rats, however, are preferred by drug discovery and basic researchers because the animal's physiology, neurobiology and other features are more predictive of human conditions. Rats engineered to contain tissue-specific conditional gene knockouts are available exclusively through the SAGEspeed Custom Model Development Service. Details are available at http://www.sageresearchmodels.com/conditional-KO.

(Logo: http://photos.prnewswire.com/prnh/20050215/CGSIGMAALLOGO)

Conventional gene knockout eliminates a gene throughout an entire animal. In contrast, conditional gene knockout can eliminate a gene solely in the relevant tissue or organ, leading to a more accurate understanding of the gene's function. Conditional gene knockout can also knock out genes at certain points in development, enabling studies of genes whose absence in embryos is lethal, but whose loss of function in adulthood is critical to investigate for many human diseases.

"Almost 89% of drug candidates fail to achieve approval," said Edward Weinstein, Director of SAGE Labs. "Basic and drug discovery researchers need access to more predictive animal models whose physiology, biology, and genetics more closely reflect specific human conditions. SAGE Labs is applying ZFN technology to achieve previously impossible genetic manipulations, such as tissue-specific gene deletion in rats."

Using the conditional knockout methodology, scientists at SAGE Labs have generated a pair of rat lines in which two important neuronal genes, Crhr1 and Grin1, were removed in specific neuronal populations. Crhr1 and Grin1 have been implicated as playing a role in depression and schizophrenia, respectively. The rat lines were developed through the SAGEspeed model creation process, which uses Sigma's CompoZr ZFN technology to create sophisticated genetic modifications in rats, mice, rabbits, and other organisms. CompoZr ZFN technology is the first to enable highly efficient, targeted editing of the genome of any species.

For more information and to request pricing, visit http://www.sageresearchmodels.com.

Cautionary Statement: The foregoing release contains forward-looking statements that can be identified by terminology such as "enable," "enabling," "leading to," "achieve," "predictive" or similar expressions, or by expressed or implied discussions regarding potential future revenues from products derived there from. You should not place undue reliance on these statements. Such forward-looking statements reflect the current views of management regarding future events, and involve known and unknown risks, uncertainties and other factors that may cause actual results to be materially different from any future results, performance or achievements expressed or implied by such statements. There can be no guarantee that iPS cells, iPS-cell derived primary cell lines, novel assays, or related custom services will assist the Company to achieve any particular levels of revenue in the future. In particular, management's expectations regarding products associated iPS cells, iPS-cell derived primary cell lines, novel assays, or related custom services could be affected by, among other things, unexpected regulatory actions or delays or government regulation generally; the Company's ability to obtain or maintain patent or other proprietary intellectual property protection; competition in general; government, industry and general public pricing pressures; the impact that the foregoing factors could have on the values attributed to the Company's assets and liabilities as recorded in its consolidated balance sheet, and other risks and factors referred to in Sigma-Aldrich's current Form 10-K on file with the US Securities and Exchange Commission. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those anticipated, believed, estimated or expected. Sigma-Aldrich is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

About Sigma Life Science: Sigma Life Science is a Sigma-Aldrich business that represents the Company's leadership in innovative biological products and services for the global life science market and offers an array of biologically-rich products and reagents that researchers use in scientific investigation. Product areas include biomolecules, genomics and functional genomics, cells and cell-based assays, transgenics, protein assays, stem cell research, epigenetics and custom services/oligonucleotides. Sigma Life Science also provides an extensive range critical bioessentials like biochemicals, antibiotics, buffers, carbohydrates, enzymes, forensic tools, hematology and histology, nucleotides, amino acids and their derivatives, and cell culture media.

About Sigma-Aldrich: Sigma-Aldrich is a leading Life Science and High Technology company whose biochemical, organic chemical products, kits and services are used in scientific research, including genomic and proteomic research, biotechnology, pharmaceutical development, the diagnosis of disease and as key components in pharmaceutical, diagnostics and high technology manufacturing. Sigma-Aldrich customers include more than 1.3 million scientists and technologists in life science companies, university and government institutions, hospitals and industry. The Company operates in 40 countries and has nearly 9,000 employees whose objective is to provide excellent service worldwide. Sigma-Aldrich is committed to accelerating customer success through innovation and leadership in Life Science and High Technology. For more information about Sigma-Aldrich, please visit its website at http://www.sigma-aldrich.com.

Sigma-Aldrich and Sigma are trademarks of Sigma-Aldrich Co, LLC registered in the US and other countries. SAGE and CompoZr are registered trademarks of Sigma-Aldrich Co. LLC. SAGEspeed is a trademark of Sigma-Aldrich Co. LLC.

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UCLA researchers develop genetically engineered stem cells to fight HIV in mice

A team of UCLA researchers has found a genetic engineering technique that suppresses the HIV virus in mice, an encouraging step toward potentially fighting the disease in humans, researchers said.

The study, led by Scott Kitchen, a member of the UCLA AIDS Institute and assistant professor at the David Geffen School of Medicine, draws upon previous UCLA research findings. It was published last week in the epidemiology journal PLoS Pathogens and funded in part by the UCLA Center for AIDS Research.

Researchers examined the effectiveness of genetically engineered killer T cells, which are capable of fighting off disease, at combating the HIV virus in a mouse. The team used a humanized mouse engineered to have a human immune system. In the humanized mouse, the disease progressed similarly to its progression in humans, making it a reliable tool for the study and providing powerful predictive value for the therapy in humans, Kitchen said. Its a major advance and a step closer in demonstrating the potential use of this in people, he said.

A few months ago, the team introduced a population of the engineered T cells into a mouse so they could develop and grow into a human immune system, Kitchen said. The researchers then conducted blood and organ tests at the second and sixth weeks, finding a decrease in the HIV levels and an increase in the cells HIV typically kills, according to the journal article.

The findings could theoretically be used to support a clinical trial in humans, said Jerome Zack, associate director at the UCLA AIDS Institute and co-author of the study.

A benefit genetic engineering is that it opens the field to therapeutic HIV treatments, and that it can be extended to potentially treat other diseases such as cancer, said co-author Arumugam Balamurugan.

In 2009, the lead scientists from the most recent study showed that human blood stem cells in mice could be genetically engineered to grow large quantities of killer T cells, As a result of their genetic engineering, these T cells grew to a large population and targeted HIV-infected cells in the mice.

We had the idea that we could take the elements of immune response (the T cells) that are successful in suppressing HIV in infected people to see if it was possible to identify a receptor specific to HIV, Kitchen said, referring to the teams research in 2009.

Though advances have been made in the fight against HIV, an estimated 50,000 new cases are diagnosed in the United States each year, and there are more than 33 million people living with the disease worldwide, according to the National Institutes of Health. Factors that make the disease difficult to fight include its rapid rate of spread and lack of preventative measures. The findings could lead to more comprehensive methods of fighting the disease and eventually to a clinical trial in humans, Kitchen said.

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UCLA researchers develop genetically engineered stem cells to fight HIV in mice

DNA origami puts a smart lid on solid-state nanopore sensors

This illustration shows how a DNA origami nanoplate with a central aperture can serve as a smart lid or "gatekeeper" for a solid-state nanopore sensor. Researchers at the Technische Universitaet Muenchen have demonstrated that this arrangement can be used to filter biomolecules by size or to "fish" for specific target molecules by placing single-strand DNA receptors inside the aperture as "bait." With further research, they suggest, it might be possible to use such single-molecule sensors as the basis of a novel DNA sequencing system. Credit: TU Muenchen

The latest advance in solid-state nanopore sensors devices that are made with standard tools of the semiconductor industry yet can offer single-molecule sensitivity for label-free protein screening expands their bag of tricks through bionanotechnology. Researchers at the Technische Universitaet Muenchen have enhanced the capabilities of solid-state nanopores by fitting them with cover plates made of DNA. These nanoscale cover plates, with central apertures tailored to various "gatekeeper" functions, are formed by so-called DNA origami the art of programming strands of DNA to fold into custom-designed structures with specified chemical properties.

The results are published in Angewandte Chemie International Edition.

Over the past few years, Prof. Hendrik Dietz's research group at TUM has been refining control over DNA origami techniques and demonstrating how structures made in this way can enable scientific investigations in diverse fields. Meanwhile, Dr. Ulrich Rant's research group has been doing the same for solid-state nanopore sensors, where the basic working principle is to urge biomolecules of interest, one at a time, through a nanometer-scale hole in a thin slab of semiconductor material. When biomolecules pass through or linger in such a sensor, minute changes in electrical current flowing through the nanopore translate into information about their identity and physical properties. Now Dietz and Rant, who are both Fellows of the TUM Institute for Advanced Study, have begun to explore what these two technologies can accomplish together.

The new device concept purely hypothetical before this series of experiments begins with the placement of a DNA origami "nanoplate" over the narrow end of a conically tapered solid-state nanopore. "Tuning" the size of the central aperture in the DNA nanoplate should allow filtering of molecules by size. A further refinement, placing single-stranded DNA receptors in the aperture as "bait," should allow sequence-specific detection of "prey" molecules. Conceivable applications include biomolecular interaction screens and detection of DNA sequences. In principle, such a device could even serve as the basis of a novel DNA sequencing system.

Step by step, the researchers investigated each of these ideas. They were able to confirm the self-assembly of custom-designed DNA origami nanoplates, and then their placement after being electrically guided into position over solid-state nanopores. They were able to demonstrate both size-based filtering of biomolecules and bait/prey detection of specific target molecules. "We're especially excited about the selective potential of the bait/prey approach to single-molecule sensing," Dietz says, "because many different chemical components beyond DNA could be attached to the appropriate site on a DNA nanoplate."

High-resolution sensing applications such as DNA sequencing will face some additional hurdles, however, as Rant explains: "By design, the nanopores and their DNA origami gatekeepers allow small ions to pass through. For some conceivable applications, that becomes an unwanted leakage current that would have to be reduced, along with the magnitude of current fluctuations."

More information: DNA Origami Gatekeepers for Solid-State Nanopores, Ruoshan Wei, Thomas G. Martin, Ulrich Rant, and Hendrik Dietz, Angewandte Chemie International Edition online, April 4, 2012. DOI: 10.1002/anie.201200688

Provided by Technische Universitaet Muenchen

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Posted in DNA

Polar bears emerged far earlier than thought, DNA study indicates

Polar bears were previously thought to have split from brown bears some 150,000 years ago. But a study of the bears' mitochondrial DNA indicates that they became a distinct species about 600,000 years ago.

Polar bears have been chilling on the ice far longer than is generally thought, new research suggests, and they probably interbred with brown bears at one point after the two species separated.

The new German study contradicts data from a study published last July in the journal Current Biology that suggested polar bearsseparated from brown bears150,000 years ago. The new study analyzed the bears' mitochondrial DNA, a special "additional genome" that lives in the cell's energy factories and is passed down only from the mother. The new study concludes that the bears became separate species closer to 600,000 years ago.

If the polar bears were only 150,000 years old, as suggested by the previous study, they would have had to evolve many specialized traits in a curiously brief time, the German researchers said.

"I've been long puzzled by the suggestion that the polar bears would have been such a miraculous and rapidly evolving species," Frank Hailer of the Senckenberg Nature Research Society in Frankfurt told LiveScience. "I had this lingering question: Is it really true?"

Hailer and his colleagues looked at the polar bear's nuclear DNA, which comes from both parents and is much larger than the mitochondrial genome. [Fun Facts About Polar Bears]

They compared 9,000 base-pair sequences (the chemicals that make up the "rungs" of DNA's ladderlike molecule) from the nuclear DNA of 45 polar, brown and black bears. This comparison let the researchers build a family tree, with the idea that the greater the genetic differences between the species, the farther they were apart in evolutionary time. They were able to estimate when the polar bears and brown bears separated.

"We found that polar bears are much older than we previously knew from other studies; their appearance dated to about 600,000 years ago," Hailer said. "That would make sense around that time for something like apolar bear to evolve, because Arctic habitats were much larger than they are today, so there would have been much larger habitats that would have been suitable for a species like a polar bear."

The researchers say the mitochondrial DNA data could have come from a hybridization event between polar and brown bears 150,000 years ago during the last warm interglacial period. During that time, sea ice melted and polar bears took to the shores, where they came intocontact with brown bears.

The researchers say this hybridization (similar to the hybrid "grolar" or "pizzly" bears seen in recent years in Canada) would have introduced the brown bear mitochondrial DNA into the polar bear population. If the DNA from the brown bears helped the polar bears survive the warm period, it's possible it could have easily spread throughout the population.

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Polar bears emerged far earlier than thought, DNA study indicates

Posted in DNA

Polar bears emerged far earlier than thought, DNA study indicates (+video)

Polar bears were previously thought to have split from brown bears some 150,000 years ago. But a study of the bears' mitochondrial DNA indicates that they became a distinct species about 600,000 years ago.

Polar bears have been chilling on the ice far longer than is generally thought, new research suggests, and they probably interbred with brown bears at one point after the two species separated.

The new German study contradicts data from a study published last July in the journal Current Biology that suggested polar bearsseparated from brown bears150,000 years ago. The new study analyzed the bears' mitochondrial DNA, a special "additional genome" that lives in the cell's energy factories and is passed down only from the mother. The new study concludes that the bears became separate species closer to 600,000 years ago.

If the polar bears were only 150,000 years old, as suggested by the previous study, they would have had to evolve many specialized traits in a curiously brief time, the German researchers said.

"I've been long puzzled by the suggestion that the polar bears would have been such a miraculous and rapidly evolving species," Frank Hailer of the Senckenberg Nature Research Society in Frankfurt told LiveScience. "I had this lingering question: Is it really true?"

Hailer and his colleagues looked at the polar bear's nuclear DNA, which comes from both parents and is much larger than the mitochondrial genome. [Fun Facts About Polar Bears]

They compared 9,000 base-pair sequences (the chemicals that make up the "rungs" of DNA's ladderlike molecule) from the nuclear DNA of 45 polar, brown and black bears. This comparison let the researchers build a family tree, with the idea that the greater the genetic differences between the species, the farther they were apart in evolutionary time. They were able to estimate when the polar bears and brown bears separated.

"We found that polar bears are much older than we previously knew from other studies; their appearance dated to about 600,000 years ago," Hailer said. "That would make sense around that time for something like apolar bear to evolve, because Arctic habitats were much larger than they are today, so there would have been much larger habitats that would have been suitable for a species like a polar bear."

The researchers say the mitochondrial DNA data could have come from a hybridization event between polar and brown bears 150,000 years ago during the last warm interglacial period. During that time, sea ice melted and polar bears took to the shores, where they came intocontact with brown bears.

The researchers say this hybridization (similar to the hybrid "grolar" or "pizzly" bears seen in recent years in Canada) would have introduced the brown bear mitochondrial DNA into the polar bear population. If the DNA from the brown bears helped the polar bears survive the warm period, it's possible it could have easily spread throughout the population.

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Polar bears emerged far earlier than thought, DNA study indicates (+video)

Posted in DNA

Artificial DNA Can Replicate in Lab, Researchers Find

By Robert Langreth - Thu Apr 19 18:00:00 GMT 2012

Scientists moved a step closer to synthesizing new life forms in the laboratory after researchers showed that artificial genetic material called XNA can be replicated in the test tube much like real DNA.

Researchers at the Medical Research Council Laboratory of Molecular Biology in the U.K. demonstrated for the first time a way to extract information from the artificial genetic molecules and mass produce copies of them. The finding, published today in the journal Science, shows that DNA and its sister molecule RNA may not be the only chemical structures upon which a living unit can be based.

Life is based on this amazing ability of DNA and RNA to store and propagate information, said Philipp Holliger, a Medical Research Council molecular biologist and senior author on the study. We have shown that the basic functions of DNA and RNA can be recapitulated with new artificial molecules.

The scientists invented a lab method for making copies of synthetic DNA. They also developed a way to make XNA fragments that evolve with desired properties. In particular, they created XNA fragments that could bind with great specificity to a molecular target in the HIV virus. The discovery could create a new platform for devising targeted drugs to treat a variety of diseases, researchers said.

This brings us one big step closer to artificial life, said Gerald Joyce, a biochemist at Scripps Research Institute in San Diego, in a telephone interview. The heart of what life is, is the replication of genetic information, he said. Joyce wrote a commentary accompanying the study.

DNA, deoxyribonucleic acid, is the hereditary molecule at the center of our cells. It contains code, in the form of chemical letters A, T, C and G, that tells the body how to make proteins that perform numerous bodily functions such as regulating blood sugar or fighting infections.

XNAs, or xeno-nucleic acids, maintain the same four-letter chemical code while altering the backbone of the DNA double helix molecule to add properties such as acid resistance.

While XNAs arent new, chemists have always had to make them one at a time, limiting their utility, Joyce said. With the new work, if I give you a few XNAs in the morning, I can come back in the afternoon and you can give me trillions of copies.

The work may give scientists a new method for creating designer drugs and diagnostic tools. There are a whole host of opportunities in biotechnology which now become possible, Holliger said.

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Artificial DNA Can Replicate in Lab, Researchers Find

Posted in DNA

DNA reveals polar bear's origins

19 April 2012 Last updated at 19:57 ET By Helen Briggs BBC News

The polar bear is much older than previously thought, according to new genetic evidence.

DNA studies suggest the Arctic predator split from its ancestor, the brown bear, about 600,000 years ago.

Previous estimates put the polar bear at about 150,000 years old, suggesting the mammal adapted very rapidly to Arctic life.

Conservationists say the new study, published in Science, has implications for bear conservation.

Polar bears are listed as threatened under the US Endangered Species Act.

Conservationists say their survival is at risk, mainly due to the loss of the Arctic sea ice on which they spend much of their lives.

Dr Frank Hailer of the German Biodiversity and Climate Research Centre in Frankfurt, who led the international study, said the genetic information shed new light on conservation issues.

"It fundamentally changes our understanding of polar bears and their conservation today," he told BBC News.

"They have survived previous warm phases but they carry scars from these times - they must have been close to extinction at times."

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DNA reveals polar bear's origins

Posted in DNA