US biologist suggests sending DNA sequencing machine to Mars

By: Boris Pavlishchev, Vitaly Radnayev, Prominent US biologist Craig Venter, decoderof the human genome, has suggested sending a DNA sequencing machine to Mars to search for ancient microorganisms. If the machine finds anything there it will decode the genome and send its DNA sequence back to Earth where bioengineers would reconstruct a synthetic Martian gene. Russian experts welcome the idea and consider it to be a good alternative to costly projects requiring the delivery of soil samples from Mars to our planet. Mr. Venter believes that searching for life on Mars relying on DNA is much more reliable than using chemical experiments like the one currently carried out by Curiosity rover. He says that his method would help to find even the most exotic forms of life which cannot be searched with the use of traditional methods. DNA is the key to success of the project. This is the way new bacteria are discovered on Earth. Many forms can be detected only by analyzing its DNA. One of the most complicated tasks is to place a laboratory that would decode genes inside a Martian rover. The process of synthesizing a gene will be even a more challenging task to do as scientists have not yet learned how to get partially synthesized bacteria using genetic chains provided by donor microorganisms. But scientists have been working hard on this lately which means that if any bacteria arrive from Mars on our planet they will be synthesized. It was recently discovered that it takes a gene about 1.5 million years to break up after an organism’s death. Scientists, however, expect that due to its cold and dry climate conditions the Red Planet could contain ancient genomes aged billions of years since the time when Mars was covered with water and life existed there. If genomes found on Mars and on Earth turn out to be alike this will prove a theory that life originated somewhere in the solar system and was brought to Mars and to Earth by comets. Scientists hope to invent a machine already dubbed as ‘biological transmitter’ by 2018, when the second stage of the joint Russian-European ExoMars mission is due to begin. The transmitter will be then placed inside a Mars rover. Source: Voice of Russia
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Scientists to build ' Artificial human brain'; useful to cure brain disease

The human brain’s power could rival any machine. And now scientists are trying to build one using the world’s most powerful computer. It is intended to combine all the information so far uncovered about its mysterious workings - and replicate them on a screen, right down to the level ofindividual cells and molecules. Supercomputer will simulate the entire mind and will help fight against brain diseases If it works it could be revolutionary for understanding devastating neurological diseases such as Alzheimer’s and Parkinson’s, and even shedding light into how we think, and make decisions. Leading the project is Professor Henry Markram based in Switzerland, who will be working with scientists from across Europe including the Wellcome Trust Sanger Institute at Cambridge. They hope to complete it within 12 years. He said: ‘The complexity of the brain, with its billions of interconnected neurons, makes it hard for neuroscientists to truly understand how it works. ‘Simulating it will make it much easier – allowing them
to manipulate and measure any aspect of the brain.’Housed at a facility in Dusseldorf in Germany, the ‘brain’ will feature thousands of three-dimensional images built around a semi-circular ‘cockpit’ so scientists can virtually ‘fly’ around different areas and watch how they communicate with each other. It aims to integrate all the neuroscience research being carried out all over the world – an estimated 60,000 scientific papers every year - into one platform. The project has received some funding from the EU and has been shortlisted for a 1 billion euro (£825million) EU grant which will be decided next month. When complete it could be used to test new drugs, which could dramatically shorten the time required for licencing them than human trials, and pave the way for more intelligent robots and computers. But Prof Markram said: ‘This will, when successful, help two billion people annually who suffer from some type of brain impairment. They have also simulated part of a rat’s brain using a computer. But the human brain is a totally different proposition. Our brains have 100 billion neurons. Each one performs billions of ‘calculations’ per second – roughly similar to a desktop computer. So the brain computer will need to be able to do a billion billion calculations which will require the output of a nuclear power station. Finding a way to power the supercomputer will be one of the researchers’ major challenges. The brain is still largely an unknown quantity for researchers and unravelling its mysteries - which have evolved over millions of years - is widely considered the final frontier of science. Richard Walker, who works with Professor Markram, said: ‘Our brains consume tiny amounts of energy but they last for 90 or more years. ‘At the moment we cannot even afford to run the biggest computers we could build, so if we can find out how the brain works, it could bring huge advances.’ Disorders of the brain, from depression and mental illness to the diseases of old age such as Alzheimer’s – which affects 800,000 people in Britain– are also a growing problem. David Cameron recently pledged £66million to fund research into the ‘national crisis’ of dementia. Source: Ananta-Tech
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Biophysicists unravel secrets of genetic switch

"I hope this kind of experiment will lead to better understanding of how our own DNA is compacted into chromosomes, and how it unravels locally to become expressed," says biophysicist Laura Finzi.
By Carol Clark: When an invading bacterium or virus starts rummaging through the contents of a cell nucleus, using proteins like tiny hands to rearrange the host’s DNA strands, it can alter the host’s biological course. The invading proteins use specific binding, firmly grabbing onto particular sequences of DNA, to bend, kink and twist the DNA strands. The invaders also use non-specific binding to grasp any part of a DNA strand, but these seemingly random bonds are weak. Emory University biophysicists have experimentally demonstrated, for the fist time, how the nonspecific binding of a protein known as the lambda repressor, or C1 protein, bends DNA and helps it close a loop that switches off virulence. The researchers also captured the first measurements of that compaction. Their results, published in Physical Review E, support the idea that nonspecific binding is not so random after all, and plays a critical role in whether a pathogen remains dormant or turns virulent. “Our findings are the first direct and quantitative determination of non-specific binding and compaction of DNA,” says Laura Finzi, an Emory professor of biophysics whose lab led the study. “The data are relevant for the understanding of DNA physiology, and
Lysis plaques of lambda phage on E. coli bacteria.
the dynamic characteristics of an on-off switch for the expression of genes.”C1 is the repressor protein of the lambda bacteriophage, a virus that infects the bacterial species E. coli, and a common laboratory model for the study of gene transcription.The virus infects E. coli by injecting its DNA into the host cell. The viral DNA is then incorporated in the bacterium’s chromosome. Shortly afterwards, binding of the C1 protein to specific sequences on the viral DNA induces the formation of a loop. As long as the loop is closed, the virus remains dormant. If the loop opens, however, the machinery of the bacteria gets hi-jacked: The virus switches off the bacteria’s genes and switches on its own, turning virulent.“The loop basically acts as a molecular switch, and is very stable during quiescence, yet it is highly sensitive to the external environment,” Finzi says. “If the bacteria is starved or poisoned, for instance, the viral DNA receives a signal that it’s time to get off the boat and spread to a new host, and the loop is opened. We wanted to understand how this C1-mediated, loop-based mechanism can be so stable during quiescence,Transient-loop formation, left, occurs due to non-specific binding of proteins (small orange disks) to DNA (black line). DNA is attached at one end to the glass surface of a microscope flow-chamber and at the other end to a magnetic bead (large gray disk) that reacts to the pulling force of a pair of magnets. The weak, non-specific DNA-protein interactions are disrupted as the force increases. (Graphic by Monica Fernandez.) 
and yet so responsive to switching to virulence when it receives the signal to do so.” Finzi runs one of a handful of physics labs using single-molecule techniques to study the mechanics of gene expression. In 2009, her lab proved the formation of the C1 loop. “We then analyzed the kinetics of loop formation and gained evidence that non-specific binding played a role,” Finzi says. “We wanted to build on that work by precisely characterizing that role.” Emory undergraduate student Chandler Fountain led the experimental part of the study. He used magnetic tweezers, which can pull on DNA molecules labeled with miniscule magnetic beads, to stretch DNA in a microscope flow chamber. Gradually, the magnets are moved closer to the DNA, pulling it further, so the length of the DNA extension can be plotted against the applied force. “You get a curve,” Finzi explains. “It’s not linear, because DNA is a spring. Then you put the same DNA in the presence of C1 protein and see how the curve changes. Now, you need more force to get toSpecifically-bound proteins are shown as orange ovals on a thicker part of the DNA sequence and non-specifically bound proteins are portrayed as gray ovals on regular DNA. Non-specific, transient loops facilitate the coming together of the specifically-bound proteins that mediate formation of the “switch loop”. Once this loop is formed, non-specifically bound protein further stabilize it by increasing the length of the closure in a zipper-like effect. (Graphic by Monica Fernandez.)
the same extension because the protein holds onto the DNA and bends it.” An analysis of the data suggests that, while the specific binding of the C1 protein forms the loop, the non-specific binding acts like a kind of zipper, facilitating the closure of the loop, and keeping it stable until the signal comes to open it. “The zipper-like effect of the weaker binding sites also allows the genetic switch to be more responsive to the environment, providing small openings that allow it to breathe, in a sense,” Finzi explains. “So the loop is never permanently closed.” The information about how the C1 genetic switch works may provide insights into the workings of other genetic switches. “Single-molecule techniques have opened a new era in the mechanics of biological processes,” Finzi says. “I hope this kind of experiment will lead to better understanding of how our own DNA is compacted into chromosomes, and how it unravels locally to become expressed.” Other authors on the paper include Sachin Goyal, formerly a post-doc in the Finzi lab; Emory cell biologist David Dunlap; and Emory theoretical physicistFereydoon Family. The research was funded by the National Institutes of Health. Source: eScienceCommons
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'Blade Runner' blows past our ideas of 'disability'

Paul Root Wolpe, director of the Emory Center for Ethics, wrote about Oscar Pistorius, the South African amputee who is running in the 2012 Olympics, as a guest blogger for CNN.com. Dubbed the “Blade Runner,” for his high-tech, carbon-fiber “Cheetah” legs, Pistorius assembled his own legal and scientific team to make a successful bid to compete in the Olympics. But, as Wolpe writes, the story is far from over, with no general guidelines about the future use of “adaptive sports equipment.” An excerpt from the article: “The issue will have to be revisited by each new athlete who wants to use artificial mechanisms in competition. “We do not ultimately know the degree to which technology mimics true physiological function. What if an amputee high jumper wants to use Cheetahs; what level of springiness is "fair" against able-bodied athletes? What about a swimmer who wants to use prosthetic hands or legs? Or an archer whose prosthetic arm does not tremble like an arm of flesh and blood? We do not have metrics that can determine true equivalence with able-bodied athletes. “Then there is the issue of fairness. In this year's U.S. Olympic trials, Dathan Ritzenhein, the two-time Olympian and 5k American record holder, was eliminated from the marathon team because of leg cramps. Pistorius cannot get cramps in his calves because he does not have any, and so he can never be eliminated based on this criterion. “The Pistorius case confronts us with two important questions. What is a disability? And what is the rationale for elite sport?” Source: eScienceCommons
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The "Pioneer Anomaly" Solved


The unexpected slowing of NASA's Pioneer 10 and 11 spacecraft - the so-called "Pioneer Anomaly" - turns out to be due to the slight, but detectable effect of heat pushing back on the spacecraft, according to a recent paper. The heat emanates from electrical current flowing through instruments and the thermoelectric power supply. The results were published on June 12 in the journal Physical Review Letters. "The effect is something like when you're driving a car and the photons from your headlights are pushing you backward," said Slava Turyshev, the paper's lead author at NASA's Jet Propulsion Laboratory, Pasadena, California. "It is very subtle." Launched in 1972 and 1973 respectively, Pioneer 10 and 11 are on an outward trajectory from our sun. In the early 1980s, navigators saw a deceleration on the two spacecraft, in the direction back toward the sun, as the spacecraft were approaching Saturn. They dismissed it as the effect of dribbles of leftover propellant still in the fuel lines after controllers had cut off the propellant. But by 1998, as the spacecraft kept traveling on their journey and were over 8 billion miles (13 billion kilometers) away from the sun, a group of scientists led by John Anderson of JPL realized there was an actual deceleration of about 300 inches per day squared (0.9 nanometers per second squared). They raised the possibility that this could be some new type of physics that contradicted Einstein's general theory of relativity. In 2004, Turyshev decided to start gathering records stored all over the country and analyze the data to see if he could definitively figure out the source of the deceleration. In part, he and colleagues were contemplating a deep space physics mission to investigate the anomaly, and he wanted to be sure there was one before asking NASA for a spacecraft. He and colleagues went searching for Doppler data, the pattern of data communicated back to Earth from the spacecraft, and telemetry data, the housekeeping data sent back from the spacecraft. At the time these two Pioneers were launched, data were still being stored on punch cards. But Turyshev and colleagues were able to copy digitized files from the computer of JPL navigators who have helped steer the Pioneer spacecraft since the 1970s. They also found over a dozen of boxes of magnetic tapes stored under a staircase at JPL and received files from the National Space Science Data Center at NASA Goddard Space Flight Center, Greenbelt, Maryland, and worked with NASA Ames Research Center, Moffett Field, California, to save some of their boxes of magnetic optical tapes. He collected more than 43 gigabytes of data, which may not seem like a lot now, but is quite a lot of data for the 1970s. He also managed to save a vintage tape machine that was about to be discarded, so he could play the magnetic tapes. The effort was a labor of love for Turyshev and others. The Planetary Society sent out appeals to its members to help fund the data recovery effort. NASA later also provided funding. In the process, a programmer in Canada, Viktor Toth, heard about the effort and contacted Turyshev. He helped Turyshev create a program that could read the telemetry tapes and clean up the old data. They saw that what was happening to Pioneer wasn't happening to other spacecraft, mostly because of the way the spacecraft were built. For example, the Voyager spacecraft are less sensitive to the effect seen on Pioneer, because its thrusters align it along three axes, whereas the Pioneer spacecraft rely on spinning to stay stable. With all the data newly available, Turyshev and colleagues were able to calculate the heat put out by the electrical subsystems and the decay of plutonium in the Pioneer power sources, which matched the anomalous acceleration seen on both Pioneers. "The story is finding its conclusion because it turns out that standard physics prevail," Turyshev said. "While of course it would've been exciting to discover a new kind of physics, we did solve a mystery." Pioneer 10 and 11 were managed by NASA Ames Research Center, Moffett Field, Calif. Pioneer 10's last signal was received on Earth in January 2003. Pioneer 11's last signal was received in November 1995. Illustration credit: NASA, Source: Minsex
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