Features

Online stargazers have reported 90 potential new planets to Oxford University's planet seekers' website.

Planethunters.org was set up by Oxford’s Department of Physics to test NASA's Kepler project which is searching for planets in the 'Goldilocks zone', the region around a star in which planets can have liquid water and are neither too hot nor too cold for life to exist.

This week NASA confirmed the discovery of the 15th planet since the project began nearly two years ago.

The Kepler telescopes detect new planets by recording tiny changes in the brightness of stars. This dimming is caused by planets crossing in front of them. Volunteers visiting planethunters.org sort through thousands of images of stars searching for examples of these dimming events (known as 'transits') which NASA’s small team of experts may have missed.

The 90 planets, less than half of which have been picked up by NASA, are now in a queue for further observation probably using the world’s largest telescopes in Hawaii.

Arfon Smith, one of the Oxford University scientists behind planethunters.org, said: 'People have turned out to be very good at identifying potential planets and the 90 we’ve had reported so far could all be worthy of being on the Kepler list.'

'Astronomy is an incredibly competitive research area and in six months’ time someone else might claim credit for seeing one of our 90 candidates. All we are saying is that we saw them first.'

The naming of new planets is less straight forward and the International Astronomical Union [IAU] has yet to rule on how that will be done. 'Given that there are going to be millions of new planets eventually it’s highly unlikely that we will have one named after us,' Arfon said.

The findings have fuelled his passion for astronomy: 'I don’t believe in God and I’ve always wanted to know how the universe works.

'I’m interested in how good a fit are humans to living elsewhere. For example, we wouldn't necessarily need four fingers and a thumb because the pinching mechanism might be all we required.

'I think there’s a very real chance that if we met life from another planet we wouldn’t recognise it as life at all.'

Dr Arfon Smith is based at Oxford University’s Department of Physics.

The majority of hospital cases of Clostridium difficile at the John Radcliffe Hospital in Oxford are not caused by transmission of the bug within the hospital, so early results of a new project suggest.

It was one example used by Professor Peter Donnelly last night, in giving the first Oxford London Lecture at Church House in Westminster, to illustrate how the modern revolution in genetics is already beginning to affect healthcare for us all.

The research, carried out jointly by researchers at the University and the Oxford Radcliffe Hospitals through the Oxford Biomedical Research Centre, uses the latest genomic screening technologies to identify DNA variations present in the C difficile bugs causing the infection.

It works as a kind of ‘genetic fingerprinting for germs’, explained Peter Donnelly, allowing the researchers led by Professors Derrick Crook and Tim Peto to trace whether the same bug has been transmitted between patients.

C. difficile can cause infections that lead to diarrhoea and fever, often after antibiotics have been used to treat other health conditions, and can be serious or life-threatening. Significant efforts have been made by the NHS to reduce cases in hospitals and numbers have come down.

The research, taking place after these changes have been made in the NHS, are reassuring in showing most cases are from C. difficile bugs with different genetic profiles. That means these cases can’t have been down to the same bug being transmitted between patients in the hospital wards.

In his overview of recent advances in genetics for the Oxford London Lecture, Peter Donnelly looked at what we have learned since the human genome was decoded 10 years ago, and the research it had facilitated.

In particular, he outlined how technologies have allowed the identification of genetic variants –single changes in the DNA code – that are associated with increased risk of common diseases like diabetes, heart disease and many types of cancer.

Peter Donnelly has played a large role in these efforts himself as director of the Wellcome Trust Centre for Human Genetics at Oxford University.

The approach involves scanning the whole genomes of a large group of people with a condition at around 0.5m positions along the 3bn DNA letters in their genomes, and comparing these to the DNA letters found at the same positions in the genomes of a large number of healthy people. Any DNA variations that occur a lot more frequently in those with the condition can be considered to confer some kind of increased susceptibility to the condition.

The first genetic variant (associated with age-related macular degeneration) was discovered in this way in 2005. By 2007, only two years later, there had been an explosion in the genetic variants linked to different diseases, and by summer 2010 there were around 1000 variants known to be associated with 200 different diseases and conditions.

‘We know remarkably little about the biological causes of disease,’ said Peter Donnelly. ‘[Identifying these genetic variants] has given us a whole new set of clues about what is happening in the disease processes.’

The hope is that this will lead to new treatments and drugs targeted against the disease processes, and possibly new interventions to reduce someone’s risk of that disease.

Peter Donnelly noted the technological challenge in managing the huge amounts of data generated by this research – for example, 50 Tb of data will be created by a new project the Wellcome Trust Centre for Human Genetics is beginning, along with US collaborators, that will sequence the whole genomes of 2700 people with and without type 2 diabetes. But he said ‘the bigger challenge will be to translate [these new discoveries] into medical care’.

The real hope, he explained, is to be able to transform information about an individual’s genetic profile into a tailored treatment for them – personalising their medical care.

Our genetic profiles can influence how we react to drugs, including the side-effects we might experience, he said. Knowing these connections would mean clinicians could get the right dose or avoid drugs that would give that particular patient nasty side-effects.

‘Cancer is fundamentally a disease of the genome,’ explained Peter Donnelly. Underlying the development of any cancer are disruptions in the DNA in individual cells, allowing them to escape normal controls and grow without restriction to form tumours.

Just in the last year or two, it has been possible to catalogue the genetic changes found in cells taken from patients’ tumours. These early pictures of the large number of genetic changes that can build up in cancerous cells are also showing something else. Breast cancers in different people, for example, can look entirely different at the level of the genome – even though the cancers are of the same part of the body.

It may be possible soon to be able to classify patients’ tumours by their genetic profiles, suggested Peter Donnelly, enabling clinicians to make better decisions about the treatments that will work best for them.

And finally, Peter Donnelly illustrated what knowing more about our genetic profiles might mean for us as individuals. You can now send off samples of your DNA to various companies who will send back information, based on current understanding, on your relative personal risk of different diseases according to your genes.

Peter has done this himself and shared some of the results, as well as what is needed to interpret what the findings mean.

His results showed he was around 6 times more likely to suffer psoriasis during his lifetime than the general population. That’s a large increase in risk, but he pointed out that only around 2% of the population get psoriasis. If he is then at a 12-13% risk of the condition, there’s still a 90% chance of not getting it.

His risk of type 2 diabetes is a little bit greater – 1.2 times more – than the population as a whole. But he explained that this effect was more serious, as he was then at a 31% lifetime risk of diabetes because so many more people in the population develop diabetes. This finding, however, does allow him to take steps to reduce this genetic risk by making healthy lifestyle choices, something he said he is trying his best to do.

‘We live in exciting times,’ he concluded. ‘There’s a good chance that we’ll look back at the first part of the 21st century as the time when we started to understand ourselves by learning the language of genes.’

Centrioles are barrel-shaped connection hubs that, like key Meccano parts, hold together the microtubule connection rods that form the structural framework of the cells in our bodies.

As cells grow and divide, they replicate their DNA before splitting into two daughter cells. Cells also duplicate centrioles every cell division, but much less is understood about the centriole formation. And as you might expect, errors in the formation of a critical component like a centriole are implicated in a number of conditions.

Dr Ioannis (John) Vakonakis, a Wellcome Trust Research Fellow in Oxford University's Department of Biochemistry , has worked with Swiss scientists on the structure of centrioles. They have just published a study in the journal Cell that offers conclusive evidence for what makes up a cartwheel structure with nine spokes seen at the centre of centrioles. We asked him about his work:

OxSciBlog: What are centrioles and what is their role in the cell?
John Vakonakis: Centrioles are large structures that exist in most eukaryotic cells. Their primary, ancient function is to organize and serve as basis for flagella and cilia, filaments that project from the cell that are used for cell motility and sensing. However, in animal cells centrioles are also used to organize the microtubule network, a kind of ‘motorway’ system in the cell used for transporting proteins and important during cell division.

OSB: Why is it important to know how they are organised?
JV: As centrioles are important for so many different processes their number inside the cell is carefully controlled. Effects that abnormally increase or decrease centriole numbers can lead directly to medical conditions, including male sterility and cancer. We need to understand how centrioles are formed and organised in order to understand how abnormalities occur.

OSB: You describe centrioles as being based on a structure like a cartwheel with nine spokes. This seems a strange symmetry for evolution to arrive at – is there a reason, is it crucial to the centriole's function?
JV: The short answer is: We don't know! Although our data show a clear preference for 9-fold symmetry, they do not tell us why evolution ended up with this symmetry as opposed to, for example, 8-fold or 10-fold. Nor is this the only odd symmetry to be seen in this system. Microtubules, organized by centrioles in animal cells, are 13-fold symmetric! Clearly, we need more work before we can fully understand this system.

OSB: What did you show in your Cell paper?
JV: We showed that SAS-6, a protein essential for centriole duplication (a process that occurs along with DNA replication as cells grow and divide), is sufficient to create 9-fold symmetric assemblies in vitro. These assemblies are strikingly similar to the ‘cartwheels’ observed early on in the centriole formation process.

OSB: What are the implications for understanding how the centriole carries out its role?
JV: Understanding how the centriole is organized allows us to probe its properties and its role in ways simply not possible earlier. For example, we can now ask questions about how regulatory mechanisms affect the assembly process we saw with SAS-6. We can form hypotheses about how centriole formation is controlled, and then test these hypotheses in novel experiments. We could even devise means to interfere on-demand with the SAS-6 assembly process, thereby being able to ‘switch’ centriole formation on or off!

OSB: Are there any implications for human health?
JV: Modulating centriole formation is of medical interest in a number of disease conditions, including cancer. The self-assembly process we have identified in SAS-6 is a novel target for controlling cell division and growth. Thus, we believe it may be used for medical intervention through therapeutics, although clearly there is a lot of work before we can reach that stage.

An asteroid 'the size of the Titanic' caused the luminous scar on Jupiter's surface spotted back in July 2009.

In 1994 astronomers observed the planet being struck by the Shoemaker-Levy 9 comet, and most people assumed that only comets, with their erratic orbits, were likely to get close enough to Jupiter to be dragged to their doom.

Now a team, including Leigh Fletcher of Oxford University's Department of Physics, has analysed the debris and gases given off by the 2009 impact and concluded that it was caused by an object more like a rocky asteroid than an icy comet.

The researchers report their findings in the astronomy journal Icarus.

'Comparisons between the 2009 images and the Shoemaker-Levy 9 results are beginning to show intriguing differences between the kinds of objects that hit Jupiter,' Leigh told us.

'The dark debris, the heated atmosphere and upwelling of ammonia were similar for this impact and Shoemaker-Levy, but the debris plume in this case didn't reach such high altitudes, didn't heat the high stratosphere, and contained signatures for hydrocarbons, silicates and silicas that weren't seen before.'

The presence of hydrocarbons and the absence of carbon monoxide, he explained, are strong evidence for a dry object striking the planet's atmosphere instead of the expected giant hailstone.

The new finding hints that, rather ominously, Jupiter has not hoovered up all the asteroids near its orbit so that there may be other big rocks out there just waiting for their turn to make an impact.

Did you know that the humble robin uses quantum physics?

Researchers have been investigating the mechanism which enables birds to detect the Earth's magnetic field to help them navigate over vast distances. This ability, known as magnetoreception, has been linked to chemical reactions inside birds' eyes.

Now a team from Oxford University and Singapore believe that this 'compass' is making use of something called quantum coherence.

In a forthcoming article in Physical Review Letters the team report how they analysed data from an experiment by Oxford and Frankfurt scientists on robins.

The experiment showed that the magnetic compass used by robins could be disrupted by extremely small levels of magnetic 'noise'. When this noise, a tiny oscillating magnetic field, was introduced it completely disabled the Robins' compass sense which then returned to normal once the noise was removed - good news for robins which have to navigate on the long migration route to Scandinavia and Africa and back every year.

In their analysis the Oxford/Singapore team show that only a system with components operating at a quantum level would be this sensitive to such a small amount of noise.

'Quantum information technology is a field of physics aimed at harnessing some of the deepest phenomena in physics to create wholly new forms of technology, such as computers and communication systems,' said Erik Gauger of Oxford University's Department of Materials, an author of the paper.

'Progress in this area is proving to be very difficult because the phenomena that must be harnessed are extremely delicate. It would normally be thought almost inconceivable that a living organism could have evolved similar capabilities.'

Co-author Simon Benjamin from Singapore explained: 'Coherent quantum states decay very rapidly, so that the challenge is to hold on to them for as long as possible. The molecular structures in the bird's compass can evidently keep these states alive for at least 100 microseconds, probably much longer.'

'While this sounds like a short time, the best comparable artificial molecules can only manage 80 microseconds at room temperature. And that's in ideal laboratory conditions.'

Erik and Simon now hope that further research into how birds harness these quantum states could enable researchers to mimic them and help in the development of practical quantum technologies.

Erik Gauger is based at Oxford University's Department of Materials.