|
|
|
DNA robot steps forth
THE US chemists have designed the world’s first two-footed molecular robot and taken it for a stroll in a lab dish, New Scientist reveals.
The robot’s legs, which measure just 10 billionths of a metre, are the first nanoscale device to be capable of bipedal movement.
The robot is able to “walk” because it is made out of scraps of DNA, the molecule of life, which comprises a dual strand joined together by mating pairs of chemical rungs, called bases.
A single strand of DNA, like one side of a zip fastener, provides the track along which the robot moves.
The robot itself looks rather like a geometry compass, with two legs comprising 36 DNA bases.
It gets attached to the walkway thanks to tiny anchor strands of DNA that are introduced into the solution and which bind to the track as well as the undersides of the feet.
To get the robot to move forward, another piece of DNA, called an unset strand, is introduced.
It peels the anchor strand away from the track. This causes the foot to move forward and look for the next mating anchor strand along the line.
Repeating the procedure with the backward foot gets the robot to shuffle along.
The biped’s inventors are Nadrian Seeman and William Sherman of New York University, who have published their work in a peer-reviewed journal, Nano Letters.
“Persuading the walker to ferry a load, such as a metal atom, is the team’s next challenge,” New Scientist says.
Molecular gadgets, known as nanotechnology, are an eagerly explored frontier.
Scientists hope these innovations, most of them still at a highly experimental stage, will provide miniaturised but highly-powered and extremely accurate tools for computing, medicine and manufacturing.
Mars scientists find new rocks
Excited Mars mission scientists released spectacular pictures of cliff-like rocks they hope will provide further clues about the extent of water on the red planet.
Scientists at the Mars mission headquarters in Pasadena said the pictures were taken by the robot rover Opportunity from the rim of a football-stadium sized crater reached after a six-week trek across martian flatlands.
The crater, dubbed Endurance, is lined by multiple layers of exposed bedrock resembling cliffs that mission scientists said is completely different from anything they have seen since the ground-breaking Mars mission began in January.
“It’s the most spectacular view we’ve seen of the martian surface, for the scientific value of it but also the sheer beauty,” principal science investigator Steve Squyres told a news conference.
“It looks fundamentally different from anything we’ve seen before. It’s big. It’s massive. It has a story to tell us.”
The Endurance crater is about 500 meters from the Eagle crater where Opportunity landed and where scientists announced in March that they had found geologic evidence of a body of salty water once deep enough to splash in.
Since then they have been trying to fill in the picture of the environment on Mars before the water evaporated.
Eagle Crater “was the last dying gasp of a body of water,” Squyres said. “The question that has intrigued us since we left Eagle Crater is what preceded that. Was there a deep body of water for a long time? Was there a shallow, short-lived playa (beach)? We don’t know.”
Squyres said the team planned to send Opportunity on a traverse lasting several weeks around the rim of the Endurance crater to assess the prospects of the rover descending into it and using its array of geological tools to inspect and take samples from the rocks.
Mission scientists are anxious to balance the geologic discoveries within their grasp with the danger of Opportunity toppling into the crater, thereby ending the mission, if it takes the wrong route.
“The rover could fall off and die if we are not careful,” Squyres said.
Opportunity and its twin rover Spirit, on the other side of the planet, were designed for 90-day missions. That landmark came and went last month but the rovers, controlled from the Jet Propulsion Laboratory in Pasadena, are still in such good health that Nasa has approved funding to extend the missions through September.
Self-renewing insulin cells
The cells in the pancreas that make insulin can create copies of themselves, a finding that shows potential new ways to treat juvenile or type-1 diabetes, US researchers says.
The research, published in this week’s journal Nature, also boosts arguments that controversial research using embryonic stem cells may be the best way to pursue a cure for the disease, experts says.
Dr Douglas Melton of Harvard University and the Howard Hughes Medical Institute and colleagues found the self-renewing pancreatic cells in mice.
These cells, called beta cells, make insulin. But in type-1 diabetes, which affects between 1 million and 2 million people in the US alone, the immune system mistakenly destroys these cells.
Patients must inject themselves with insulin daily to stay alive, and they risk blindness, limb loss and stroke.
Scientists are working to find new sources of these cells. But there are not enough donors for transplants.
Gene linked to heart attack
Scientists have pinpointed a gene which seems to play a crucial role in heart attacks. They found that a particular mutation of the gene occurs more frequently in people who have had a heart attack.
It is thought the gene controls inflammation in the arteries supplying blood to the heart. A blockage here can trigger a heart attack.
The research, by Toyko’s Institute of Physical and Chemical Research, is published in Nature. The Japanese team hope their work will prove to be a crucial step towards a better understanding of the underlying causes of heart attacks. They found that the key mutation is caused by just one tiny change to the chemical components of DNA.
Their work is based on an analysis of DNA samples from more than 2,600 heart attack patients.
These were compared with samples from 2,500 volunteers from the general population. The heart attack patients were significantly more likely to carry a specific mutation in a gene that produces a protein called galectin-2.
Galectin-2 is known to bind to a molecule that assists inflammation — lymphtoxin-alpha (LTA) — and which is released when a coronary artery ruptures. — Sci-Tech World Report
|
|
|
|
