Friday, September 3, 2010

WHAT THE LOCALS ATE 10,000 YEARS AGO

0 comentarios

If you had a dinner invitation in Utah’s Escalante Valley almost 10,000 years ago, you would have come just in time to try a new menu item: mush cooked from the flour of milled sage brush seeds.

After five summers of meticulous excavation, Brigham Young University archaeologists are beginning to publish what they’ve learned from the “North Creek Shelter.” It’s the oldest known site occupied by humans in the southern half of Utah and one of only three such archaeological sites state-wide that date so far back in time.

BYU anthropologist Joel Janetski led a group of students that earned a National Science Foundation grant to “get to the bottom” of a site occupied on and off for the past 11,000 years, according to multiple radiocarbon estimates.

“The student excavators worked morning till night in their bare feet,” Janetski said. “They knew it was really important and took their shoes off to avoid contaminating the old dirt with the new.”

In the upcoming issue of the journal Kiva, Janetski and his former students describe the stone tools used to grind sage, salt bush and grass seeds into flour. Because those seeds are so tiny, a single serving would have required quite a bit of seed gathering. But that doesn’t mean whoever inhabited North Creek Shelter had no other choice.

Prior to the appearance of grinding stones, the menu contained duck, beaver and turkey. Sheep became more common later on. And deer was a staple at all levels of the dig.

“Ten thousand years ago, there was a change in the technology with grinding stones appearing for the first time,” Janetski said. “People started to use these tools to process small seeds into flour.”

BYU graduates David Yoder, Mark Bodily and Brad Newbold are also authors on the new study. Though they have moved on in their careers, the group members continue to work with Janetski to investigate the animal bones, projectile points and signs of climate change influencing human diet.

The North Creek Shelter is located at the base of a sheer sandstone cliff on the same property as the Slot Canyons Inn, which now contains an exhibit about the researchers’ findings. Janetski notes the generous support received from the property owners, Joette Rex and her late husband Jeff Rex.

BYU geology professor Tom Morris and his student Tanner Hicks have also contributed their expertise to the project.

(Photo: BYU)

Brigham Young University

VITAMIN D FOUND TO INFLUENCE OVER 200 GENES, HIGHLIGHTING LINKS TO DISEASE

0 comentarios
The extent to which vitamin D deficiency may increase susceptibility to a wide range of diseases is dramatically highlighted in research published recently. Scientists have mapped the points at which vitamin D interacts with our DNA – and identified over two hundred genes that it directly influences. The results are published in the journal Genome Research.

It is estimated that one billion people worldwide do not have sufficient vitamin D. This deficiency is thought to be largely due to insufficient exposure to the sun and in some cases to poor diet. As well as being a well-known risk factor for rickets, there is a growing body of evidence that vitamin D deficiency also increases an individual's susceptibility to autoimmune conditions such as multiple sclerosis (MS), rheumatoid arthritis and type 1 diabetes, as well as certain cancers and even dementia.

Now, in a study whose funders include the Medical Research Council (MRC), the MS Society, the Wellcome Trust and the MS Society of Canada, researchers at the University of Oxford have shown the extent to which vitamin D interacts with our DNA. They used new DNA sequencing technology to create a map of vitamin D receptor binding across the genome. The vitamin D receptor is a protein activated by vitamin D, which attaches itself to DNA and thus influences what proteins are made from our genetic code.

The researchers found 2,776 binding sites for the vitamin D receptor along the length of the genome. These were unusually concentrated near a number of genes associated with susceptibility to autoimmune conditions such as MS, Crohn's disease, systemic lupus erythematosus (or 'lupus') and rheumatoid arthritis, and to cancers such as chronic lymphocytic leukaemia and colorectal cancer.

They also showed that vitamin D had a significant effect on the activity of 229 genes including IRF8, previously associated with MS, and PTPN2, associated with Crohn's disease and type 1 diabetes.

"Our study shows quite dramatically the wide-ranging influence that vitamin D exerts over our health," says Dr Andreas Heger from the MRC Functional Genomics Unit at Oxford, one of the lead authors of the study.

The first author of the paper, Dr Sreeram Ramagopalan from the Wellcome Trust Centre for Human Genetics, adds: "There is now evidence supporting a role for vitamin D in susceptibility to a host of diseases. Vitamin D supplements during pregnancy and the early years could have a beneficial effect on a child's health in later life. Some countries such as France have instituted this as a routine public health measure."

The main source of vitamin D in the body comes from exposing the skin to sunlight, although a diet of oily fish can provide some of the vitamin. Research has previously suggested that lighter skin colour and hair colour evolved in populations moving to parts of the globe with less sun to optimise production of vitamin D in the body. A lack of vitamin D can affect bone development, leading to rickets; in pregnant mothers, poor bone health can be fatal to both mother and child at birth, hence there are selective pressures in favour of people who are able to produce adequate vitamin D.

This new study supports this hypothesis, having found a significant number of vitamin D receptor binding sites in regions of the genome with genetic changes more commonly found in people of European and Asian descent. It is probable that skin lightening as we migrated out of Africa resulted from the necessity to be able to make more vitamin D and prevent rickets: vitamin D deficiency led to pelvic contraction resulting in increased risk of fatality of both mother and unborn child, effectively ending maternal lineages unable to find ways of increasing availability of the vitamin.

"Vitamin D status is potentially one of the most powerful selective pressures on the genome in relatively recent times," says Professor George Ebers, Action Medical Research Professor of Clinical Neurology and one of the senior authors of the paper. "Our study appears to support this interpretation and it may be we have not had enough time to make all the adaptations we have needed to cope with our northern circumstances."

Wellcome Trust

200-FOLD BOOST IN FUEL CELL EFFICIENCY ADVANCES 'PERSONALIZED ENERGY SYSTEMS'

0 comentarios

The era of personalized energy systems — in which individual homes and small businesses produce their own energy for heating, cooling and powering cars — took another step toward reality today as scientists reported discovery of a powerful new catalyst that is a key element in such a system. They described the advance, which could help free homes and businesses from dependence on the electric company and the corner gasoline station, at the 240th National Meeting of the American Chemical Society.

"Our goal is to make each home its own power station," said study leader Daniel Nocera, Ph.D. "We're working toward development of 'personalized' energy units that can be manufactured, distributed and installed inexpensively. There certainly are major obstacles to be overcome — existing fuel cells and solar cells must be improved, for instance. Nevertheless, one can envision villages in India and Africa not long from now purchasing an affordable basic system."

Such a system would consist of rooftop solar energy panels to produce electricity for heating, cooking, lighting, and to charge the batteries on the homeowners' electric cars. Surplus electricity would go to an "electrolyzer," a device that breaks down ordinary water into its two components, hydrogen and oxygen. Both would be stored in tanks. In the dark of night, when the solar panels cease production, the system would shift gears, feeding the stored hydrogen and oxygen into a fuel cell that produces electricity (and clean drinking water as a byproduct). Such a system would produce clean electricity 24 hours a day, seven days a week — even when the sun isn't shining.

Nocera's report focused on the electrolyzer, which needs catalysts — materials that jumpstart chemical reactions like the ones that break water up into hydrogen and oxygen. He is with the Massachusetts Institute of Technology in Cambridge, Mass. Good catalysts already are available for the part of the electrolyzer that produces hydrogen. Lacking, however, have been inexpensive, long-lasting catalysts for the production of oxygen. The new catalyst fills that gap and boosts oxygen production by 200-fold. It eliminates the need for expensive platinum catalysts and potentially toxic chemicals used in making them.

The new catalyst has been licensed to Sun Catalytix, which envisions developing safe, super-efficient versions of the electrolyzer, suitable for homes and small businesses, within two years.

The National Science Foundation and the Chesonis Family Foundation provided funding for this study. Nocera did the research with post-doctoral researcher Mircea Dinca and doctoral candidate Yogesh Surendranath. The U.S. Department of Energy's Advanced Research Projects Agency has recently awarded the team with a grant, which it plans to use to search for related compounds that can further increase the efficiency of its electrolyzer technology. The team hopes that nickel-borate belongs to a family of compounds that can be optimized for super-efficient, long-term energy storage technologies.

(Photo: Patrick Gillooly/MIT)

American Chemical Society

UT SOUTHWESTERN RESEARCHERS FIND KEY STEP IN BODY'S ABILITY TO MAKE RED BLOOD CELLS

0 comentarios

Researchers at UT Southwestern Medical Center have uncovered a key step in the creation of new red blood cells in an animal study.

They found that a tiny fragment of ribonucleic acid (RNA), a chemical cousin of DNA, prompts stem cells to mature into red blood cells. The researchers also created an artificial RNA inhibitor to block this process.

Such interventions, if fruitful in humans, might be useful against some cancers and other diseases, such as polycythemia vera, in which the body produces a life-threatening excess of blood cells. Conversely, a drug that boosts red blood cell production might be useful against anemia, blood loss or altitude sickness.

“The important finding is that this microRNA, miR-451, is a powerful natural regulator of red blood cell production,” said Dr. Eric Olson, chairman of molecular biology at UT Southwestern and senior author of the study, which appears in the Aug. 1 issue of Genes & Development.

“We also showed that a man-made miR-451 inhibitor can reduce miR-451 levels in a mouse and block blood-cell production. We hope that this inhibitor and similarly functioning molecules might lead to new drugs against the fatal disease polycythemia vera, which currently has no therapies,” said Dr. Olson, who directs the Nancy B. and Jake L. Hamon Center for Basic Research in Cancer and the Nearburg Family Center for Basic and Clinical Research in Pediatric Oncology.

Red blood cells, which carry oxygen throughout the body, are created in bone marrow from stem cells. The body steps up its production of red blood cells in response to stresses such as anemia, blood loss or low oxygen, but overproduction of the cells increases the risk of stroke and blood clots.

RNA molecules, found throughout cells, perform several jobs. MicroRNAs often bind to and disable other types of RNA, preventing them from carrying out their functions.

Dr. Olson and his colleagues study many different types of microRNAs to determine their functions and to find therapeutic uses of artificial microRNAs.

“miR-451 is found in great abundance in mature red blood cells, but its function was not known,” said lead author David Patrick, a graduate student in molecular biology.

In the new study, the scientists created genetically engineered mice that could not make miR-451. The mice had a lowered red blood cell count and also had difficulty creating more red blood cells under conditions that usually stimulate production.

miR-451 works by interacting with another RNA involved in producing a protein called 14-3-3-zeta, which plays a role in the maturation of many types of cells, the researchers found.

The team also treated blood stem cells with an artificial RNA designed to inhibit miR-451. As a result, the number of red blood cells decreased.

Dr. Olson and his colleagues are pursuing a patent on miR-451 inhibitors and studying whether a microRNA-based drug might be useful in treating several blood-related disorders.

(Photo: UTSW)

University of Texas Southwestern Medical Center

‘WHITE GRAPHENE’ TO THE RESCUE

0 comentarios
What researchers might call "white graphene" may be the perfect sidekick for the real thing as a new era unfolds in nanoscale electronics.

But single-atom-thick layers of hexagonal boron nitride (h-BN), the material under intense study at Rice University's world-class Department of Mechanical Engineering and Materials Science, are likely to find some macro applications as well.

Researchers in the lab of Pulickel Ajayan, Rice's Benjamin M. and Mary Greenwood Anderson Professor in Mechanical Engineering and Materials Science and of chemistry, have figured out how to make sheets of h-BN, which could turn out to be the complementary apple to graphene's orange.

The results were reported in the online journal Nano Letters.

Graphene, touted as a possible successor to silicon in microelectronics applications, is the new darling of research labs that hope to take advantage of its superb electronic properties.

Hexagonal boron nitride, on the other hand, is an insulator. Earlier this year, Rice postdoctoral researchers in Ajayan's group found a way to implant islands of h-BN into sheets of graphene, a unique way to exert a level of control over the sheet's electronic character.

Now the team, led by primary author Li Song, has figured out how to deposit sheets of pure h-BN, which is naturally white in bulk form, anywhere from one to five atoms thick on a copper substrate. The material can then be transferred to other substrates.

They used a chemical vapor deposition process to grow the h-BN sheets on a 5-by-5 centimeter copper backing at temperatures around 1,000 degrees Celsius. The sheets could then be stripped from the copper and placed on a variety of substrates.

Ultimately, Song sees h-BN sheets finding wide use as a highly effective insulator in graphene-based electronics, another stride on the quick-step march toward the replacement of silicon with materials that could push beyond the boundaries of Moore's Law, which states the number of transistors that can be placed on an integrated circuit doubles about every two years.

He said it should be also possible to draw microscopic patterns of graphene and h-BN, which could be useful in creating nanoscale field-effect transistors, quantum capacitors or biosensors.

Strength tests using the tip of an atomic force microscope to push h-BN into holes in a silicon substrate showed it to be highly elastic and nearly as strong as graphene, the single-atom form of pure carbon.

Song said the size of h-BN sheets is limited only by the size of the copper foil and furnace used to grow it. The process should be adaptable to the same kind of roll-to-roll technique recently used to form 30-inch sheets of graphene. "If you have a huge furnace, you can go large," he said.

Rice University

BAD BACTERIA AND THEIR HARMLESS KIN SHARE, SWAP GENES

0 comentarios

In the bacterial world, good guys can potentially turn into bad guys and vice versa - just by swapping genes, microbiologists at the University of Arizona have discovered.

The researchers studied bacteria belonging to the genus Neisseria. These bacteria colonize the mucous membranes of humans.

Intrigued by the question of why some species of Neisseria are commensals - harmless colonizers whose presence in the body goes unnoticed - while others cause disease, the team identified the complete genetic codes of eight species of commensal Neisseria and compared them to the published genomes of the two known pathogenic species that cause gonorrhea and meningitis.

"The gene content of Neisseria species is fluid and not etched in stone," said team leader Magdalene So, who is a professor in the UA's department of immunobiology, where she directs the Microbial Pathogenesis Program. She also is a member of the UA's BIO5 Institute.

"These bacteria have the capacity to acquire new genes and drop others frequently," So said.

The study marks the first time scientists have determined the total gene content of a large group of related commensal bacteria and systematically compared it with the genomes of related pathogens. So's team reports its findings in Public Library of Science Online, or PLoS One.

To their surprise, the researchers found no clear genetic demarcation between commensal and pathogenic Neisseria. In fact, many commensals have the same genes known to promote virulence (the capacity to cause disease) in the two pathogens.

"Not only have the commensals most of the genes that make their cousins pathogenic, they also have other genes that may contribute to virulence," said Pradeep Marri, assistant research scientist at BIO5 and lead author of the paper.

The researchers also found evidence that many genes, including virulence genes, have been exchanged between commensals and pathogens. Like the pathogens, the commensals have the machinery to acquire genetic information at high frequency. This leads the researchers to suspect that the Neisseria species exchange genes with each other quite often.

"More than a third of the virulence genes shared among pathogenic and commensal bacteria show signs of genetic exchange, much more than anticipated," Marri added.

"We know that the ability of pathogenic Neisseria to cause disease requires multiple virulence genes," said So. "If a commensal Neisseria by chance acquires the right combination of virulence genes, it would become pathogenic."

"What that combination is, we don't know yet. We have a good guess, and the huge data set we developed in this study will allow us to make much better guesses."

Neisseria use so-called pili, highly specialized structures made of proteins arranged like a spring, to take up large snippets of DNA - usually DNA from other Neisseria species. This process occurs frequently - about one in 10 bacteria take up DNA. The newly acquired DNA is then inserted in the genome. In this way, the bacteria acquire new molecular tools that are advantageous for their survival in a rapidly changing environment.

In previous work, So's group discovered that the bacteria also use pili to make contact with and communicate with their hosts' cells.

Bacteria even use their pili to crawl around: pili filaments grow from the bacterial body, tether to the cell, then are retracted into the bacterial body. This is analogous to the action of a fishing rod. Retraction of the pili allows the bacterial cell to move forward.

Pili are also used by the bacteria to congregate and form micro-colonies, which is an important part of the infection process.

"In the past, medical microbiology has focused on microbes that directly cause diseases," So said. "But there is a whole world of microbes living on and inside of us that we don't know a whole lot about."

While most of these commensals simply use our bodies as living space, others are necessary for us to survive. They help digest food, provide vitamins that our bodies can't make or ward off harmful microbes.

Given how successful commensal bacteria are in colonizing the human body, it may not be too far fetched to suspect these relationships could be beneficial to humans, in ways yet to be understood.

Recently, researchers were surprised to discover that bacteria also play roles in illness not usually associated with microbes, such as heart disease and diabetes.

"Commensals have many genes that are known to promote virulence in the pathogens," So said. "So we asked ourselves, what prevents them from becoming pathogenic?"

For example, Neisseria meningitidis, one of the most common causes of bacterial meningitis, makes a capsule that protects it from phagocytes, specialized cells of the immune system that gobble up intruders.

"The capsule, one would think, is key to a pathogen's ability to avoid being eliminated by the host," So said, "but surprisingly, not all Neisseria meningitidis strains have capsule genes."

"This study is a great example of what is possible in a setting like BIO5, with different scientists contributing their expertise to solve a complex problem," So pointed out. We could not have done without the expertise in bioinformatics and comparative genomics provided by Pradeep Marri and Steve Rounsley."

The findings should prompt a renewed interest in the relationships between humans and microbes, she added, and help find targets for vaccines and antibiotics.

"For example, when you are trying to make an antibiotic targeting one of the Neisseria proteins, you want to make sure you choose one only the pathogen has. Otherwise you'll wipe out the commensals as well, which could open a niche for other, potentially harmful, microbes."

(Photo: Dustin Higashi)

University of Arizona

STUDY OF ELECTRON ORBITS IN MULTILAYER GRAPHENE FINDS ENERGY GAPS

0 comentarios

Researchers have taken one more step toward understanding the unique and often unexpected properties of graphene, a two-dimensional carbon material that has attracted interest because of its potential applications in future generations of electronic devices.

In the Aug. 8 advance online edition of the journal Nature Physics, researchers from the Georgia Institute of Technology and the National Institute of Standards and Technology (NIST) describe for the first time how the orbits of electrons are distributed spatially by magnetic fields applied to layers of epitaxial graphene.

The research team also found that these electron orbits can interact with the substrate on which the graphene is grown, creating energy gaps that affect how electron waves move through the multilayer material. These energy gaps could have implications for the designers of certain graphene-based electronic devices.

"The regular pattern of energy gaps in the graphene surface creates regions where electron transport is not allowed," said Phillip N. First, a professor in the Georgia Tech School of Physics and one of the paper’s co-authors. "Electron waves would have to go around these regions, requiring new patterns of electron wave interference. Understanding such interference will be important for bi-layer graphene devices that have been proposed, and may be important for other lattice-matched substrates used to support graphene and graphene devices."

In a magnetic field, an electron moves in a circular trajectory -- known as a cyclotron orbit -- whose radius depends on the size of the magnetic field and the energy of electron. For a constant magnetic field, that's a little like rolling a marble around in a large bowl, First said.

"At high energy, the marble orbits high in the bowl, while for lower energies, the orbit size is smaller and lower in the bowl," he explained. "The cyclotron orbits in graphene also depend on the electron energy and the local electron potential -- corresponding to the bowl -- but until now, the orbits hadn’t been imaged directly."

Placed in a magnetic field, these orbits normally drift along lines of nearly constant electric potential. But when a graphene sample has small fluctuations in the potential, these "drift states" can become trapped at a hill or valley in the material that has closed constant potential contours. Such trapping of charge carriers is important for the quantum Hall effect, in which precisely quantized resistance results from charge conduction solely through the orbits that skip along the edges of the material.

The study focused on one particular electron orbit: a zero-energy orbit that is unique to graphene. Because electrons are matter waves, interference within a material affects how their energy relates to the velocity of the wave -- and reflected waves added to an incoming wave can combine to produce a slower composite wave. Electrons moving through the unique "chicken-wire" arrangement of carbon-carbon bonds in the graphene interfere in a way that leaves the wave velocity the same for all energy levels.

In addition to finding that energy states follow contours of constant electric potential, the researchers discovered specific areas on the graphene surface where the orbital energy of the electrons changes from one atom to the next. That creates an energy gap within isolated patches on the surface.

"By examining their distribution over the surface for different magnetic fields, we determined that the energy gap is due to a subtle interaction with the substrate, which consists of multilayer graphene grown on a silicon carbide wafer," First explained.
In multilayer epitaxial graphene, each layer's symmetrical sublattice is rotated slightly with respect to the next. In prior studies, researchers found that the rotations served to decouple the electronic properties of each graphene layer.

"Our findings hold the first indications of a small position-dependent interaction between the layers," said David L. Miller, the paper's first author and a graduate student in First's laboratory. "This interaction occurs only when the size of a cyclotron orbit -- which shrinks as the magnetic field is increased -- becomes smaller than the size of the observed patches."

The origin of the position dependent interaction is believed to be the "moiré pattern" of atomic alignments between two adjacent layers of graphene. In some regions, atoms of one layer lie atop atoms of the layer below, while in other regions, none of the atoms align with the atoms in the layer below. In still other regions, half of the atoms have neighbors in the underlayer, an instance in which the symmetry of the carbon atoms is broken and the Landau level -- discrete energy level of the electrons -- splits into two different energies.

Experimentally, the researchers examined a sample of epitaxial graphene grown at Georgia Tech in the laboratory of Professor Walt de Heer, using techniques developed by his research team over the past several years.

They used the tip of a custom-built scanning-tunneling microscope (STM) to probe the atomic-scale electronic structure of the graphene in a technique known as scanning tunneling spectroscopy. The tip was moved across the surface of a 100-square nanometer section of graphene, and spectroscopic data was acquired every 0.4 nanometers.

The measurements were done at 4.3 degrees Kelvin to take advantage of the fact that energy resolution is proportional to the temperature. The scanning-tunneling microscope, designed and built by Joseph Stroscio at NIST's Center for Nanoscale Science and Technology, used a superconducting magnet to provide the magnetic fields needed to study the orbits.

According to First, the study raises a number of questions for future research, including how the energy gaps will affect electron transport properties, how the observed effects may impact proposed bi-layer graphene coherent devices -- and whether the new phenomenon can be controlled.

"This study is really a stepping stone in long path to understanding the subtleties of graphene's interesting properties," he said. "This material is different from anything we have worked with before in electronics."

(Photo: GIT)

Georgia Institute of Technology

DISCOVERY POINTS TO ANCESTOR 'LUCY' USE OF STONE TOOLS, MEAT CONSUMPTION

0 comentarios

Two Arizona State University researchers conducting zooarchaeological and archaeometric analyses of four fossilized animal bone fragments found by the Dikika Research Project in northeastern Ethiopia – within walking distance of the discovery of the hominin skeleton “Lucy” (Australopithecus afarensis) – confirm that unusual marks on the bones were inflicted by stone tools.

Their conclusion weighs in on findings reported in the Aug. 12 journal Nature, that A. afarensis used sharp-edged stones and a strong striking force to cleave flesh and marrow from large-sized animal carcasses some 3.4 million years ago.

That evidence pushes back the origins of technology – the use of stone tools – and carnivory by some 800,000 years, from 2.6 Myr to 3.4, explained Curtis Marean, a paleoanthropologist at ASU’s Institute of Human Origins and one of the world’s leading experts in the study of animal bones from archaeological sites.

Marean, a professor in the School of Human Evolution and Social Change in ASU’s College of Liberal Arts and Sciences, is a member of the international team made up of experts in paleoanthropology, archeology, geology, paleontology and materials science who reported the findings in the Nature article “Evidence for stone-tool-assisted consumption of animal tissues before 3.39 million years ago at Dikika, Ethiopia.”

The zooarchaeological analysis of the bone fragments, which included a femur shaft from an animal the size of a goat and a rib fragment from a much larger animal the size of a cow, was conducted at Arizona State University. Using a standard binocular microscope in ASU’s zooarchaeology laboratory, Marean was able to provide evidence that sharp-edged stones and a strong striking force were used to remove flesh and marrow from the bones of large-sized animal carcasses.

To further determine that the markings were not modern, he turned to Hamdallah Béarat, a senior research scientist at ASU’s School for Engineering of Matter, Transport and Energy.

“To confirm that the cutmarks on the bones are ‘old’ and verify that they were induced by stone tools, I used the Environmental Cell Scanning Electron Microscope (E-SEM) and the attached Energy Dispersive X-ray Spectrometry (EDX) in ASU’s LeRoy Eyring Center for Solid State Science,” said Béarat, who has degrees in chemistry, archaeometry, material science and engineering.

The E-SEM was used because it has a chamber and stage that can accommodate large bone fragments, Béarat explained.

“And, since the bone material is an insulator and these precious bone samples cannot be coated with a conducting film, such as gold or carbon, this E-SEM allows us to run the analysis in the H2O-vapor mode and thus avoid charging effects, while still using a high accelerating voltage (15-25kV),” Béarat said.

“Hamdallah is an expert in materials research and keenly interested in archaeology,” noted Marean. “He had the great idea to do X-ray mapping of the surfaces of the bone to see whether minerals that passed from the marks to the surface of the bone were fossilized.”

The geologist on the team, Jonathan Wynn, from the University of South Florida, relied on documented dated volcanic deposits in the Dikika area to estimate the date of the marked bones to 3.4 million years ago.

“This discovery dramatically shifts the known timeframe of a game-changing behavior for our ancestors,” said paleoanthropologist Zeresenay “Zeray” Alemseged, director of the Dikika project and director of anthropology at the California Academy of Sciences.

No hominin remains were found with the animal bone fragments that were uncovered 200 meters away from the site where Alemseged and a team discovered “Selam” (Lucy’s baby) in 2000. Lucy was discovered in 1974 a few miles north, near Hadar, by Donald Johanson, the world renowned ASU paleoanthropologist.

“There is no question that the announcement of stone tool use at 3.4 million years ago will unleash a flurry of controversy and genuine disbelief among some scholars,” said Johanson. “However, I believe the team has presented a convincing case of stone tool use during Lucy’s time. These unexpected results may well generate a new understanding of early hominid behavior and will prompt a reexamination of the tens of thousands of animal bones already collected from this time period at Hadar, Lucy’s home, and other sites in Kenya and Tanzania.

“Very often it is breakthroughs such as this that stimulate new and expanded research strategies that promise to significantly enlarge our understanding of human origins,” Johanson said.

Lead author of the Nature article Shannon McPherron observed: “Now, when we imagine Lucy walking around the east African landscape looking for food, we can for the first time imagine her doing so with a stone tool in her hand.” McPherron is an archeologist with the Dikika project and research scientist at the Max Planck Institute in Leipzig, Germany. He and Alemseged led the Dikika fieldwork.

The last place early humans – like Lucy – wanted to be on the African landscape was in a competitive dangerous situation next to an animal carcass, noted Marean.

Yet, “these marks are unusual compared to other butchery marks I have seen,” he said. “They show a lot of force, a lot of heavy action.”

Marean framed the research findings as “a spectacular and exciting discovery pertaining to early human evolution.” But, while the evidence shows the Australopithecines at Dikika were using sharp-edged stones to crack and strip meat from the bones, it is impossible to tell from the marks alone whether these early hominins were making their tools and carrying them, or simply finding naturally sharp rocks.

Many questions remain about the use of stone tools by human ancestors and the introduction of meat into their diet.

“The subtle implication is that in this instance, it was not hunted but scavenged meat and marrow, since the really large animal was almost certainly outside the ability of hominins to kill. This could be a key tipping point in the origins of human uniqueness,” Marean said. “One of the big steps in human evolution is when males and females pair-bond, and males provided females with meat. This result may suggest this is happening at this early stage in human origins.”

Other co-authors of the Nature paper include paleontologists Denné Reed, University of Texas, Austin; Denis Geraads, Centre National de la Recherche Scientifique, Paris; and René Bobe, University of Georgia.

The interdisciplinary nature of the team exemplifies what collaboration between social sciences and physical sciences can produce, noted ASU’s Béarat.

“I believe that, in the coming few decades, major archaeological discoveries are to be expected in the laboratory rather than in the field,” he said, advocating for more archaeometric studies, which are like forensic investigations. “In both cases, the scientist is investigating a process or an act. In this case from Dikika, our role was to confirm, using physical/engineering methods, that the act of cutting the bones was old and thus corresponded to our remote hominin ancestor.”

(Photo: Dikika Research Project)

Arizona State University

EVOLUTION MAY HAVE PUSHED HUMANS TOWARD GREATER RISK FOR TYPE-1 DIABETES

0 comentarios

Gene variants associated with an increased risk for type-1 diabetes and rheumatoid arthritis may confer previously unknown benefits to their human carriers, say researchers at the Stanford University School of Medicine. As a result, the human race may have been evolving in the recent past to be more susceptible, rather than less, to some complex diseases, they conclude.

“At first we were completely shocked because, without insulin treatment, type-1 diabetes will kill you as a child,” said Atul Butte, MD, PhD, assistant professor of pediatric cancer biology and a bioinformatics expert. “Everything we’ve been taught about evolution would indicate that we should be evolving away from developing it. But instead, we’ve been evolving toward it. Why would we have a genetic variant that predisposes us to a deadly condition?”

The researchers speculate that at least some of the risky changes may protect carriers against certain viruses and bacteria — a trade-off that may have made evolutionary sense in the not-too-distant past when infectious diseases were devastating and largely untreatable. It’s not clear, however, whether the beneficial effects arise from the disease-associated mutations themselves, or from neighboring genes that tag along when DNA is divvied up into sperm and eggs.

Butte, who directs the Center for Pediatric Bioinformatics at Lucile Packard Children’s Hospital, is the senior author of the research, published Aug. 17 in Public Library of Science ONE. Graduate student Erik Corona is the first author of the study and conducted the analysis.

The idea that disease-causing genes can be beneficial is not new. The most clear-cut case involves a gene variant that, when present in two copies, causes sickle cell anemia, which can result in severe pain, organ damage and death. Although it seems that natural selection would work to eliminate the disorder, the variant remains prevalent in some areas of Africa because people with just a single copy are less susceptible to malaria. Evolutionarily the trade-off is worth it: Far more people are protected from malaria than ever develop sickle cell anemia even in today’s environment.

Unlike sickle cell anemia, which is caused by a mutation in just one gene, many complex diseases are associated with several variants — specific locations in the DNA where the nucleotide “letters” vary between individuals. These locations are known as SNPs, for single nucleotide polymorphisms. Some of these SNPs are associated with an increased disease risk, while others protect against developing the disease. When calculating an individual’s overall genetic risk, it’s necessary to consider the net effect of all of his or her variants.

Corona picked seven well-known conditions to study: type-1 and type-2 diabetes, rheumatoid arthritis, hypertension, Crohn’s disease, coronary artery disease and bipolar disorder. Previous genome wide association studies have identified several hundred SNPs associated with each disorder. Corona found that of the top SNPs associated with type-1 diabetes, 80 have been recently increasing in prevalence, meaning that they underwent positive selection. Of these, a surprising 58 are associated with an increased risk of the disorder, while 22 appear protective. Similarly, SNPs associated with an increased risk for rheumatoid arthritis were found to be positively selected. In contrast to type-1 diabetes and rheumatoid arthritis, Corona found that we’re evolving away from a tendency to develop Crohn’s disease (that is, more protective SNPs than risky SNPs have been positively selected).

Results for the other three disorders — type-2 diabetes, coronary artery disease and bipolar disorder — showed that protective and risky SNPs were positively selected in about equal proportions. “Now we’re starting to see little hints as to why this might be the case,” said Butte. For example, a recent study in another lab showed that genetic variations in an antiviral response gene called IFIH1 that improve its ability to protect against enterovirus infection (and the resulting severe, potentially deadly, abdominal distress) also increase a carrier’s risk for type-1 diabetes. And scientists who study global disease patterns have long noted that the prevalence of tuberculosis varies inversely with that of rheumatoid arthritis.

“It’s possible that, in areas of the world where associated triggers for some of these complex conditions are lacking, carriers would experience only the protective effect against some types of infectious disease,” said Butte, who pointed out that the cumulative effect of many SNPs in a person’s genome may buffer the effect of any one variant, even if it did raise a person’s risk for a particular condition.

Regardless of the reason, some evolutionary tenets still apply. Healthier people are, presumably, more likely to reproduce and pass those same genes — be they protective or risky — to their offspring. When conditions changed because of differences in diet, exposures or location as populations move around the globe, carriers of the risky SNPs began to develop the conditions we struggle with today.

Corona and Butte are now expanding their investigation to include even more SNPs and diseases. They are also looking at the genetic profile of various types of tumors to see if there’s evidence for positive evolutionary pressure there as well.

“Even though we’ve been finding more and more genetic contributions to disease risk,” said Butte, “that’s not really an appealing answer. There have got to be some other reasons why we have these conditions.”

(Photo: Stanford U.)

Stanford University

Followers

Archive

 

Selected Science News. Copyright 2008 All Rights Reserved Revolution Two Church theme by Brian Gardner Converted into Blogger Template by Bloganol dot com