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4G network 'will create GPS dead zones across the US'

WHAT would you rather have - a superfast data connection on your cellphone, or a reliable GPS signal to pinpoint your location? If a plan to install a network of base stations for the new 4G mobile wireless protocol goes ahead, it may mean you can have one but not the other.

GPS satellites transmit their navigation signals in the range 1559 to 1610 megahertz. Telecoms firm LightSquared of Reston, Virginia, has long communicated with its satellites using low-power signals in the adjacent frequency band, from 1525 to 1559 MHz, part of the "L band". Despite the closeness of the frequencies, satnav receivers have so far operated without any interference problems.

But in January, the US Federal Communications Commission (FCC) gave preliminary approval to a plan by LightSquared to build 40,000 new 4G base stations on the ground. These stations would broadcast much stronger signals in the 1525 to 1559 MHz range, to link to cellphones.

Based on lab simulations of the new transmissions, Scott Burgett and Bronson Hokuf, engineers with satnav manufacturer Garmin International in Olathe, Kansas, say this will seriously damage GPS reception. In a report to the FCC last month, they say that overlaps between the two systems are inevitable, and that this "will result in widespread, severe GPS jamming [and] will deny GPS service over vast areas of the United States".

Jeff Carlisle of LightSquared says it is the GPS receivers, not his company's base stations, that are at fault. "The issue is that some GPS receivers may be able to see into the L band where we operate," he told New Scientist.

The stakes are high. By 2015, LightSquared expects to spend $6 to $8 billion to complete the network, which promises to bring download speeds of 5 to 10 megabits per second to cellphone users. Meanwhile, over a billion GPS receivers are in use worldwide.

LightSquared has until 25 February to submit a plan to the FCC for working with the GPS industry and federal agencies to analyse interference issues; a final report detailing a solution is due by 15 June. LightSquared wants all future tests to be performed with real transmitters rather than simulators.

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The Pill to Increase Brain Capability

For so many years the pill has been used by millions of women to prevent pregnancy. It is known that the pill reduces the risk of certain diseases. However, in a recent study it was found that using birth control pills could actually have a beneficial effect on the brain as well. It was discovered that those that used it resulted in a three percent increase of brain size.

Dr. Jennifer Wu, an obstetrician at Lenox Hill Hospital (New York) states that MRIs of women using the pill display certain regions of the brain to be larger than in women who do not use the pill. The areas in the brain were found to be larger had to do with speech, memory, and communication.
Having a larger brain does not necessarily mean it is better. It is suggested though that the areas of the brain that grow in a women due to the pill will result in greater brain power. For example, a woman may find that her memory is improving.
There are many theories that explain how the pill could improve the capability of the brain, however, it is not known for sure and has not been proven. As a result of this study much more research is being done in regards to how hormones can affect the brain and how the pill could possibly increase brain size.
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Low sperm count? Your bones might be to blame

Sex hormones are already known to play an important role in maintaining healthy bones – but the relationship may be a two-way street. New evidence suggests that bones are important for controlling testosterone levels.

Gerard Karsenty at Columbia University in New York City and his colleagues applied osteoblasts – bone cells involved in building new bone – to cultures of cells taken from either the testes or ovaries of mice. They found that testis cells treated with bone cells increased their production of the hormone testosterone threefold. The cells from the ovaries, on the other hand, showed no change in their production of the hormones progesterone and oestradiol.

Karsenty's team then focused in closer by looking at osteocalcin – a hormone produced by osteoblasts. They found that testis cells treated with an active form of the hormone released testosterone – and the more of the hormone they got, the more testosterone they produced. Injecting live mice with the hormone similarly boosted levels of testosterone in their bloodstream.

To find out if this effect on testosterone production might affect mice's fertility, the team knocked out the gene for osteocalcin in a group of the rodents. These modified mice had significantly smaller testes and lower sperm counts than their normal counterparts – and when the group bred them with normal females, they found that the litter size was around half normal.

Mice and men

Rebecca Sokol at the University of Southern California in Los Angeles is intrigued by the findings. "I am particularly surprised by the absence of effects in female mice," she says.

Karsenty is stumped too. "We were flabbergasted," he says. "Don't ask me why it only affects males because I don't know."

He thinks the hormone might also boost fertility in men, as many hormones have been found to have the same effects in mice and humans. His team are currently exploring the possibility of osteocalcin as a treatment option for infertile men.

Bone is already known to release hormones. A few years ago, the same group found that osteocalcin plays a role in maintaining the body's glucose levels (Cell DOI: 10.1016/j.cell.2007.05.047).

Botox.(botulinum toxin – a protein )

Beyond erasing wrinkles, Botox can now help people who spend more than half their lives in headache agony. But is there enough evidence to support treating chronic migraine sufferers with regular shots of the toxin around the head and neck? Doctors are divided

What is Botox?

Botox is the trade name for botulinum
 toxin – a protein produced by the Clostridium botulinum bacterium. By blocking the release of a chemical messenger in the brain, the toxin stops muscles from contracting.

Why try preventing migraines with it?
The story starts around 10 years ago, with some of Hollywood's most revered residents – cosmetic surgeons.

"The plastics people suggested that some of their patients had relief from migraine after Botox treatment," says Peter Goadsby, director of the University of California, San Francisco's Headache Centre.

The idea began to spread and clinicians started giving Botox as an "off-label" treatment – that is, in a way not approved by regulators – to people with migraines.

Allergan, the pharmaceutical company that developed Botox, soon cottoned on and started marketing Botox as a migraine treatment. However, with no proof that the treatment worked, last year the company was fined $375 million for unlawful marketing.

Since then, a number of clinical trials have ruled out any significant reduction in normal tension headaches and non-chronic migraine after Botox treatment.

Chronic migraine differs from ordinary migraines and tension headaches, however. In chronic migraine, the
person has a headache on more than 15 days of each month, at least eight of which are migraines.

What is the evidence for using Botox for chronic migraine, then?

Two clinical trials have investigated this. In both, people with chronic migraine received a series of five 12-weekly rounds of injections of either Botox or a placebo. In each round, individuals were given 31 injections at specific sites around the head and neck.

The first trial concluded that the Botox injections had no effect on the number of headaches experienced by those with chronic migraine, but hinted that the number of days affected by migraine might have been reduced.

When the same team looked at the latter outcome in the second trial, they found a 10 per cent reduction in the number of headache days compared with the placebo group.

How is Botox thought to help chronic migraine?
No one knows. The general consensus is that the blocking of muscle contraction isn't involved in headache relief, says Goadsby. Beyond that, researchers are generally stumped.

How solid is the evidence that Botox works?
Solid enough for the US Food and Drug Administration and the UK Medicines and Healthcare products Regulatory Agency: both bodies approved the therapy for chronic migraine last year.

Others remain unconvinced. Jes Olesen, a neurologist at the University of Copenhagen and chief of the Danish Headache Centre at Glostrup University Hospital in Denmark, has identified a number of faults in the trials, listed in a letter to The Lancet in November. His concerns were echoed in an editorial published in Drug and Therapeutics Bu
lletin this month.

Why is there a dispute?
According to Olesen, over half the trial participants overused pain medication, so the researchers wouldn't have been able to tell whether the participants had chronic migraine or medication overuse headache. What's more, it's impossible to hide the fact that people are receiving Botox, he adds – and that would invalidate the double-blind nature of the experiment. "Their facial expressions change," he says.

Even if you were able to get over those issues, the 10 per cent improvement pales in comparison to the usual 20 to 30 per cent required for most approved drugs, he says. "The FDA has committed one of the biggest blunders in regulatory history."

Sheena Aurora, neurologist at the Swedish Pain and Headache Center in Seattle, Washington, and lead researcher in the clinical trials, says the criticisms are "shocking". People with chronic migraine regularly take painkillers, so the trial represents the real-life situation, she argues.

The placebo group saw a 30 per cent response to the injections, compared with a 40 per cent response from the real injection. This indicates that people weren't looking for changes in their appearance to judge pain relief, either, she adds. And as for the 10 per cent improvement of the Botox group over the placebo group: "Who are we to say 10 per cent isn't enough for these patients?"

Goadsby agrees. "People with chronic migraine are highly disabled and have an unmet need for therapy," he says. "Everyone in clinical practice knows that chronic migraine is very difficult to treat."

While academic criticisms of trials are interesting, Goadsby says, they're not helpful to the millions of migraineurs. "Worrying about a little stone on the road is interesting, but we need to look at the bigger picture."

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Protein dose reverses learning problems in Down's mice

LEARNING and memory problems have been reversed in mice with a syndrome that mimics Down's.

Catherine Spong and colleagues at the National Institutes of Health in Bethesda, Maryland, found they could prevent developmental problems in mice engineered to have Down's syndrome by injecting their mothers with two proteins, called NAP and SAL, while they were still in the womb. This treatment would carry many risks for humans, so the team wondered whether the proteins might also help adult mice.

Spong's team engineered mice to have an extra chromosome 16, which causes similar problems to those caused by an extra chromosome 21 in humans, the trigger for Down's (see picture). The mice then had to find a submerged platform in a water maze using visual cues. Down's mice usually take twice as long to find the platform as healthy mice. However, after four days of oral treatment with NAP and SAL, the Down's mice learned to navigate the maze just as easily as normal mice.

NAP and SAL are fragments of proteins normally produced by glial cells - brain cells that provide nourishment to neurons. We know that glial cells malfunction in people with Down's. Mice treated with the proteins had markers of healthy glial function that were missing in the untreated Down's mice.

In a second experiment, the team investigated whether the treatment caused changes in chemicals known to be involved in "long-term potentiation" (LTP) - a type of brain activity key to memory formation. People and mice with Down's have decreased levels of many chemicals involved in this process. However, treated mice appeared to have increased levels of a receptor called NR2B that is responsible for initiating LTP (Obstetrics & Gynecology, DOI: 10.1097/AOG.0b013e3182051ca5). Craig Heller, co-director of Stanford University's Down Syndrome Research Center in California, says this study makes one thing clear: "Learning disabilities and mental retardations that were considered permanent are treatable."

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Robots

Robots in 1921, there has been an expectation that robots would some day deliver us from the drudgery of hard work. The word - from the Czech "robota", for hard labour and servitude - described intelligent machines used as slaves in his play R.U.R. (Rossum's Universal Robots).

Today, over one million household robots, and a further 1.1 million industrial robots, are operating worldwide. Robots are used to perform tasks that require great levels of precision or are simply repetitive and boring. Many also do jobs that are hazardous to people, such as exploring shipwrecks, helping out after disasters, studying other planets and defusing bombs or mines.

Robots are increasingly marching into our lives. In the future, robots will act as carers, medics, bionic enhancements, companions, entertainers, security guards, traffic police and even soldiers.

Domestic invasion

Despite the longevity of the robot concept, robotic butlers that roam our homes and relieve us from housework still seemed far from reality until very recently. Instead, the vast majority of robots worked in factories performing the industrial functions of brainless machines.

However, a combination of increased computing power and advances made in the field of artificial intelligence, or AI, have now made software smart enough to make robots considerably more useful.

A recent report published by the United Nations revealed that sales of domestic robots had tripled in a single year. What's more, they were well on their way to outstripping their industrial cousins.

While a large portion of the household robots were made up of robotic vacuum cleaners, mops, lawn mowers, pool cleaners, security bots and even robotic baby-rockers - the real boom was in entertainment robots.

Suddenly people were happy to pay for robots that had no specific functional value. Instead these bots, such as Sony's Aibo robotic dog and its robo-pups served as robo-pets and companions, rather than slaves.

This is partly because many domestic chores still pose a real challenge for robots, in terms of dexterity and intelligence, even with seemingly simple chores such as ironing.

Movers and shakers

Away from the domestic front, the modern bot can take many other forms. Some are even designed to change their form, such as shape-shifting tetrabots or self-cloning robots.

And while we often think of robots being humanoid, such as Honda's Asimo and Sony's Qrio, there is as much interest, if not more, in emulating other creatures like insects, lobsters, orang-utans, alligators, snakes and fish. A robot guard dragon has even been created.

Whether they have two legs, many legs, or no legs at all, considerable advances have been made in robot locomotion, including bipedal walking, rambling, crawling, rock-climbing, bouncing, slithering and swimming.

There are also wheeled bots that work as autonomous vehicles, such as the desert racers that compete in the DARPA Grand Challenge to be the fastest to cross a desert without any human control.

Robot wars

One area where even more advances in autonomy have been made is the development of unmanned aerial vehicles, or UAVs. These are essentially remotely-controlled spy planes that are capable of flying themselves if they lose contact with their pilot. These planes can also be used to monitor forest fires. Some robots have even learnt to fly of their own accord.

The Pentagon has started arming some UAVs, making them capable of responding with firepower against aggressive attacks - so-called unmanned combat vehicles, or UCVs. Robots that act as battlefield spies have also been designed.

Also aiming to remove humans from dangerous situations are space agencies, such as NASA, who have developed many space exploration robots. For example, the robonaut is a remotely-operated robot, designed to perform dangerous space walks in the place of an astronaut.

In addition, NASA has already sent robotic rovers to Mars, developed robotic dirt scoopers, "flying eyes" and probes for interplanetary exploration and even sent droids off to try to explore asteroids. Space probes such as Huygens (which landed on Titan) and Russia's Venera 9 (which landed on Venus) are sometimes considered robots too.

And it's not just other planets that robots are good for exploring. Robotic submarines, also known as remotely operated vehicles, or ROVs, have now become important way of exploring the deep ocean or ice-capped waters, while heat resistant robots are now used to patrol and monitor the activity in volcanoes. A robotic rover has even been used to explore Egyptian pyramids.

Precision surgeons

Operating on the human body requires high skill but also great control, something robots can provide. The idea of robotic surgery prompted early fears of unsupervised robots let loose to operate, but the reality is that robots now assist surgeons to perform precision procedures.

The most successful of these is arguably the da Vinci robotic surgical system, which is used for keyhole surgery, to operate on anything from gall bladder removals and brain surgery to heart bypasses.

Similarly, tiny, wireless and robotic camera-capsules have been used diagnostically, by allowing them to pass through a patient's digestive system. Others have been designed to move about by remote control in the abdominal cavity, beaming images back to the surgeon, or even taking biopsy samples. Robot hands have even been developed to scan for breast cancer.

Such life-saving robots have proved so successful that dentists are considering using robotic dental drill to make implant dental surgery cheaper, quicker and, crucially, less painful.

Actuators and sensors

But despite all the successes, there are still many challenges in robotics. These include producing better actuators (which control how robots move), sensors (which allow them to detect their environment) and ultimately making bots much smarter.

Current motors, and hydraulic or pneumatic actuators, are either too weak, or too bulky and noisy. Artificial muscle might be one solution, but so far these have failed to be strong enough to beat even a teenage girl in a robotic arm wrestling match.

Bipedal and humanoid robots have proved a particular problem. Robots on wheels, or those that move like insects, have found it much easier to balance and get around.

And while much early research in robotics focused on using sonar sensors because they were cheap and easy to use, the focus today is on the more challenging, yet richer, vision-based navigation systems.

Similarly, while there is much research on making robotic arms and hands, the difficulty lies in making electronic skin sensitive enough to detect fragile or slippery objects by touch alone. A robot that mimics human speech is also under development.

To encourage advances in these all these fields, it is now common for the robotic community to use contests. These include baseball catching contests, to improve dexterity; goldfish-catching contests, to improve underwater manoeuvrability; even robotic camel jockeying contests have been held, though they were created to replace child jockeys.

The ultimate test perhaps is robot soccer. This is driving development in just about every area of robotics from the ability to run and kick a ball to communicating and demonstrating teamwork. The grand aim is to have a team of humanoid robots that can beat the best human soccer team in the world by 2050.

Until then the question remains that if robots are ever made smart enough to do our ironing will they also be smart enough to refuse to do it for us? Would we suddenly have a robotic-rebellion on our hands?

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Amputees regain control with bionic arm wired to chest

Nikzad Studio Presents

Amputees regain control with bionic arm wired to chest

The video above captures the moment when a malaria parasite invades a human red blood cell - the first time the event has been caught in high resolution.
The Plasmodium parasite responsible for malaria is transmitted by the bite of infected mosquitoes, and is thought to kill almost 1 million people worldwide each year.

Jake Baum at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, and colleagues used transmission electron microscopy, immuno-fluorescence and 3D super-resolution microscopy to record thousands of high-definition images of separate invasion events, a process that takes less than 30 seconds.
To boost their chances of catching Plasmodium parasites in the act of attacking a red blood cell the team controlled the process using two drugs. The first - heparin - prevents parasites entering a new red blood cell, while the second - E64 - prevents their exit. Carefully timing the treatments meant "we knew we were going to get huge number of invasion events", says Baum.
The parasites produce a protein called the tight junction marker and use it to attach to and drill into red blood cells, says Baum. "At the beginning of invasion it's a dot, as the parasite enters the cell it becomes a beautiful circle, and then the marker is behind the parasite."
The images that the researchers generated show that invasion is not a well-ordered process, as we had thought, says Baum. "Initial attachment using the tight junction marker is the main switch, and then the parasite does everything at once." Simultaneously, it releases a vacuole to live in and switches on a motor complex allowing it to move within the cell.
Kiaran Kirk at the Australian National University in Canberra says the "clever cell preparation and stunning microscopy" is a "tour de force".
The movie could have implications for the treatment of malaria too. Leann Tilley of La Trobe University in Melbourne, Australia, says the results confirm that interfering with the master switch would stop the parasites from entering red blood cells and "thereby stop disease".
Journal reference: Cell Host & Microbe, DOI: 10.1016/j.chom.2010.12.003
10.38 am, 21 January 2011: This article has been updated since it was first posted

Malaria parasite invades a human red blood cell - the fir

Nikzad Studio Presents

The video above captures the moment when a malaria parasite invades a human red blood cell - the first time the event has been caught in high resolution.
The Plasmodium parasite responsible for malaria is transmitted by the bite of infected mosquitoes, and is thought to kill almost 1 million people worldwide each year.
Jake Baum at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, and colleagues used transmission electron microscopy, immuno-fluorescence and 3D super-resolution microscopy to record thousands of high-definition images of separate invasion events, a process that takes less than 30 seconds.
To boost their chances of catching Plasmodium parasites in the act of attacking a red blood cell the team controlled the process using two drugs. The first - heparin - prevents parasites entering a new red blood cell, while the second - E64 - prevents their exit. Carefully timing the treatments meant "we knew we were going to get huge number of invasion events", says Baum.
The parasites produce a protein called the tight junction marker and use it to attach to and drill into red blood cells, says Baum. "At the beginning of invasion it's a dot, as the parasite enters the cell it becomes a beautiful circle, and then the marker is behind the parasite."
The images that the researchers generated show that invasion is not a well-ordered process, as we had thought, says Baum. "Initial attachment using the tight junction marker is the main switch, and then the parasite does everything at once." Simultaneously, it releases a vacuole to live in and switches on a motor complex allowing it to move within the cell.
Kiaran Kirk at the Australian National University in Canberra says the "clever cell preparation and stunning microscopy" is a "tour de force".
The movie could have implications for the treatment of malaria too. Leann Tilley of La Trobe University in Melbourne, Australia, says the results confirm that interfering with the master switch would stop the parasites from entering red blood cells and "thereby stop disease".
Journal reference: Cell Host & Microbe, DOI: 10.1016/j.chom.2010.12.003
10.38 am, 21 January 2011: This article has been updated since it was first posted

Sun New Video

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Stretchy DNA shows off its elastic qualities

YOGA fans take note. DNA can stretch to nearly twice its length without breaking. The discovery could help to develop anti-cancer drugs. It also points to a more prosaic role for the blueprint of life, as a reference material for calibrating machines that measure the tiniest of forces.

Despite its immense importance, there is still a lot we don't understand about DNA. One outstanding puzzle concerns its stretchiness. Like many polymers, the twisty molecule stretches easily under an initial, small force but gets progressively more difficult to stretch as the force increases. At 65 piconewtons, however, DNA suddenly loosens up, becoming easy to stretch again, until it reaches around 170 per cent of its original length.

The cause of this sudden transition has long been a mystery. "You'd think it would be easy to answer 'what happens to DNA when you stretch it?'," says Mark Williams, a biophysicist at Northeastern University in Boston, Massachusetts, who was not involved with the work. "But this is something that people have debated for years. You can't just take a picture of the structure."

One option is that the added length comes from untwisting DNA's double helix, leaving a straight structure that looks more like a ladder than a spiral staircase. However, no such structure has ever been observed.

A competing explanation says that when enough force is applied, some of the bonds between the paired strands come apart, causing the strands to lose their double-helical structure and stretch out easily (see diagram). In 2009, an experiment using dye that only binds to sections of DNA in which the two strands are bonded together favoured this option.

In the experiment, separated regions seemed only to arise near nicks in the strand, suggesting the bonds between the strands may not break under force alone but require an initial tear. Now Thomas Perkins of the US National Institute of Standards and Technology and Hern Paik of the University of Colorado, both in Boulder, show this isn't so.

After checking that a length of DNA had no nicks or tears, they attached one end to a stable surface and the other to a tiny bead that could be pushed with laser light. Activating the laser caused the bead to move, gradually stepping up the force on the DNA, which overstretched at 65 piconewtons.

The pair repeated the experiment with strands that had one and two nicks, and found that the DNA still overstretched at 65 piconewtons. They conclude that nicks are not required for overstretching, and that the phenomenon must therefore be due to force-induced breaking of bonds between the two strands, leading to elongation of the helix (Journal of the American Chemical Society, DOI: 10.1021/ja108952v).

If further tests confirm this, DNA could find a new use. Its sudden switch to stretchiness means that highly sensitive instruments, such as atomic force microscopes, could be calibrated by tugging on DNA and recording exactly when it overstretches.

Understanding how far DNA can stretch before breaking could also help with the design of anti-cancer drugs that aim to disrupt or break apart maliciously replicating DNA, Williams suggests.

HIV-like infection banished from mice

For the first time, an HIV-like infection has been cleared from an animal without the use of antiviral drugs. The infection was eliminated from mice using a human protein that peps up immune cells.

Marc Pellegrini from the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, and colleagues infected mice with lymphocytic choriomeningitis virus (LCMV), which causes a chronic infection that spreads throughout the body. "The virus overwhelms mice, mimicking the massive viral loads associated with HIV infection in humans," says Pellegrini.

Eight days after infection, some of the mice were injected with human interleukin-7 (IL-7) – a chemical messenger that plays a role in the development of immune cells – once a day for three weeks. The others received a placebo instead.

"Usually mice never clear this virus," says Pellegrini. But 30 days later, those given treatment had cleared most of the infection and removed all of it by 60 days.

Overactive response

The explanation seems to lie in a protein called SOCS3, which blocks the function of T-cells – a type of immune cell and therefore part of the body's system for fighting infection. At the beginning of an acute infection, SOCS3 becomes highly activated, suppressing the body's immune response. That sounds just the opposite of what you'd want. But it's a good thing because it stops T-cells being overzealous, which can cause damage to body tissue, says Pellegrini.

It becomes a problem when the body is trying to fight an overwhelming infection like HIV, he says: then the immune system puts on the brakes too early and the infection persists.

Blood tests taken throughout the experiment showed that IL-7 seemed to switch off the production of SOCS3, thereby ramping up the T-cell response.

Start and stop

This explanation was confirmed when the team knocked out the SOCS3 gene in a separate group of mice and infected them with LCMV. Immune cell numbers in these mice skyrocketed – T-cells increased sixfold compared with normal mice.

But knocking out SOCS3 showed the dangers of taking the immune brakes off. "Initially the mice mounted a robust immune response, but then it got out of hand," says Pellegrini. The mice developed mass inflammation and increased incidences of autoimmune diseases.

However, because IL-7 only affects T-cells, and not other types of immune cell, the researchers suggest that drugs could be developed that turn off SOCS3 for very short periods to reinvigorate T-cells without causing damage to the body.

Sharon Lewin at the Burnet Institute in Melbourne says the finding that IL-7 can clear the virus without the help of antiviral drugs is very interesting. Viruses like HIV use the host's cells to replicate, which makes it difficult to design antivirals that stop the virus without harming healthy cells.

"[Stopping a virus] without antivirals is something we haven't seen before," she says.

Solar System Packs its planets like Sardines

If you thrill at the discovery of new exoplanets, hold tight. A sextuplet alien solar system has been glimpsed in exquisite detail, revealing six planets of varying mass, five of which are packed closer to one another than in any planetary system seen before.

"We think this is the biggest thing in exoplanets since the discovery of 51 Pegasi b, the first exoplanet, back in 1995," Jack Lissauer of NASA's Ames Research Center in Moffett Field, California, told reporters earlier this week.

The six newly found planets orbit a star dubbed Kepler-11, which sits some 2000 light years from Earth. They were glimpsed by NASA's Kepler telescope, which has been staring at the same patch of sky since its launch in March 2009.

The Kepler telescope captured periodic dips in Kepler-11's brightness, created when planets pass between the star and Earth. These "transits" allow astronomers to measure a planet's size.

But Kepler-11's inner five planets – which all orbit closer to their host than Mercury does the sun – are close enough to one another to exert gravitational tugs that continually alter the length of time it takes for each planet to orbit the star. These timing variations allowed Lissauer and a team of colleagues to estimate the planets' masses, which range from 2 to 14 times the mass of the Earth (shown in the bottom row of this image).

Planetary puzzle

The researchers then used this information to estimate the density of the innermost planets and found that all are less dense than the Earth. Some may have massive hydrogen atmospheres, they say, while others may contain significant amounts of water.

Future observations should pin down the planets' densities, which could help astronomers discern whether they formed close to or far from their present locations. Either scenario could present a challenge for planet formation models, says Phil Armitage of the University of Colorado, Boulder.

These models suggest the region close to Kepler-11 might have been hot enough to keep ice vaporised and blow away nearby gas, preventing the growing planets from capturing as much gas and ice as they seem to have.

Conversely, if the planets formed farther out, models suggest they would have exerted strong tugs on their neighbours as they migrated inwards, sending the six planets into orbits on differing planes. Yet Kepler-11's planets all seem to orbit in a single plane. "That certainly makes for a puzzle about how the system was set up," Armitage says.

Testing laboratory

Solving that puzzle could refine our understanding of how planets form. "It's a pretty big deal," says Kristen Menou of Columbia University in New York. "I think this will be one of the best laboratories for testing planetary formation theories."

The discovery of the Kepler-11 planets comes against a backdrop of recent exoplanet excitement.

Researchers just announced a fresh haul of data on exoplanets, including 54 planet candidates in the habitable zones of their stars, also captured by the Kepler telescope. And last September, the first alien planet capable of hosting life on its surface was glimpsed.

Although its existence has yet to be confirmed by further data, scientists have been using climate models to figure out whether its climate is life friendly. An even bigger prize would be the discovery of an Earth twin – a planet the size and temperature of our own.

Abnormalities discovered in stem cells from adults

ERRORS have occurred in a type of stem cell that could be used instead of embryonic stem cells - and in tissues made from them.

Joseph Ecker of the Salk Institute in La Jolla, California, and colleagues found genes inappropriately switched on and off in parts of the chromosomes of induced pluripotent stem cells. iPSCs are adult cells reprogrammed to become every type of tissue.

Most mistakes were made either where chromosome arms cross or in their tips, in both iPSCs and tissues made from them. Ecker found no errors in embryonic stem cells, but they raise ethical issues since embryos are destroyed to make ESCs (Nature, DOI: 10.1038/nature09798).

"It's premature to abandon ESCs until we understand what's going on with iPSCs," says Robert Lanza, chief scientist at Advanced Cell Technology in Massachusetts.