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Meet Ossie: a friendly green popsicle who has already been fired through the LHC and frozen to absolute zero in a bid to explain cutting edge science.

In his latest adventure the star of the Oxford Sparks portal ends up getting a close encounter with a broken heart and finds out about the potentially dire consequences of one genetic mistake.

'Genetics has come such a long way, it really does impact on the way we look after patients already and will do so more and more,' said Hugh Watkins, the lead scientific advisor on this new animation.

'But it's the 'simple' end of the genetic spectrum, where a single genetic change causes an inherited condition that runs in a family, where we've made most headway so far. And the condition covered, hypertrophic cardiomyopathy, is one of the most common and important of these.'

Hugh says that, as part of explaining where the latest Oxford research has got to in investigating such conditions, he told 'some stories (one involving a forklift!) to illustrate the way it impacts on patients,' and that this tale made it into the finished animation.

He adds: 'I like the way that the animation and script make an inherently scary condition, and a serious science story, fun.'

Look hard enough, string theory says, and at a scale so small that atoms loom as large as entire continents do to us you would see that every particle in the universe is just the product of vibrating strings.

It's a powerful idea that could help to explain everything from black holes to hidden dimensions, and lead to a new understanding of gravity.

But string theory is also enigmatic and baffling, describing a realm that is, with current technology, too small for us to explore directly.

A new website, Why String Theory?, aims to tell the story of the theory's past, present, and (possible) future in a way that anyone can understand.

'We all instinctively want to explore the world around us. String theory gives us a chance to uncover the most fundamental laws of nature. So much of fundamental physics nowadays is completely inaccessible… We wanted to rectify this, conveying the excitement of contemporary research,' Edward Hughes, a Cambridge University undergraduate and member of the team behind the website, tells me.

'I'm still on the fence as to whether I think string theory is the right direction, but there are certainly elements of it that are very simple and appealing,' says team member Charlotte Mason, an Oxford University undergraduate. 'The idea that the myriad of particles in the universe could arise from different vibrational patterns of tiny strings is a very elegant explanation. Though the mathematics beyond that is often not so elegant!'

Joseph Conlon of Oxford University, another member of the team, explains that part of the theory's appeal lies in 'string miracles', these are 'calculations that look like they are going to fail and show that the theory is inconsistent, but then something comes in and suddenly saves the day. Once you see this happening several times you realise that the theory has a very deep structure and your understanding of it only scratches the surface.'

String theory is not the only approach that it is hoped might one day encompass the behaviour of everything from galaxies to sub-atomic particles, but it does appear to offer some tantalising insights. One of these concerns some of the universe's most mysterious objects: black holes.

'Objects in string theory called branes can be used to count the number of possible ways you can make a black hole,' Joseph tells me. 'For certain types of black holes this agrees with a famous calculation of Stephen Hawking of the entropy of the black hole.

'Entropy is a measure of how many ways there is of making something. Hawking used clever arguments to say what the answer must be. In string theory you can count the number of ways explicitly and find that it agrees with Hawking's answer.

'String theory can help solve problems with quantising gravity by treating particles as strings rather than points. This smears out interactions and makes infinite quantities finite.'

But, however powerful its insights, there is a problem: so far no one has been able to prove that those tiny vibrating strings the theory depends on actually exist. Joseph admits that they will be hard to find: it will, he thinks, take a major technological advance, a brilliant insight, or wonderful luck to turn up the right kind of evidence.

Yet string theory has a habit of turning up surprises, as Joseph says: 'Working on it is also good for humility, you are perennially aware that the theory is smarter than you.'

Caught between hostile land and sea, an oyster's life is a daily battle against the elements, predators, and disease.

Now a team, including Peter Holland of Oxford University’s Department of Zoology, has decoded the oyster's genome to gain a better understanding of one of life's great survivors. The work is reported in this week's Nature.

I asked Peter what their genes tell us about these marvellous molluscs, their evolution, and how they might be farmed more efficiently…

OxSciBlog: What makes the seashore so challenging for life?
Peter Holland: The seashore looks tranquil enough, but spare a thought for the animals living in the intertidal zone, between land and sea. Twice a day, every day, as tides move in and out, these animals are plunged between two different worlds. It is hard to know which is more hostile.

An animal such as an oyster must cope with searing heat and desiccation when the tide goes out, and then coolness, high salinity and crushing currents when the tide washes back over it. Its gills are adapted to extract oxygen under water, but cannot absorb oxygen from dry air. The sea is also a breeding ground for innumerable parasites and pathogens. This is an environment where environmental stress is fact of daily life.

OSB: What do the oyster's genes tell us about how it evolved to cope?
PH: All animals have genes for coping with environmental stress, but the oyster genome has many more than other species studied so far.

Take the hsp70 genes, involved in protecting cellular proteins from heat. The oyster has over 80 of these genes, and this heat protection system is indeed switched on when the animal is exposed to high temperatures. The oyster also has extra genes involved in protection against oxidative stress and for defence against pathogens.

Even in these days when genome sequencing is becoming almost routine, it is rare that we can 'see' the biology of the animal in the genome so clearly. The genome shows us how the oyster genome has been adapted over millions of years to allow life in this hostile environment.

Not all of the oyster genome is so easy to understand, however. We found changes to the genes that control embryo and larval development, such as homeobox genes, and can only guess the underlying reasons. There are also unexpected genes used in formation of the oyster shell, suggesting that formation of mollusc shells is more variable and more complex than previously thought.

OSB: How does the oyster's 'genetic survival kit' compare with the genes of other intertidal species?
PH: We don't yet know how recently the oyster's genetic adaptations arose. Are they shared with all bivalves (the molluscs with two shells)? Or are they older, shared with all molluscs? Or more recent, and specific to oysters? More genome sequencing is needed to find out how many different routes there are to intertidal adaptation.

OSB: How might these insights help to boost oyster farming?
PH: Oyster farming is quite inefficient, with many animals dying before they become fully developed. Most often, the causes are unknown.

Now that the full set of oyster genes is known, it will be possible to see which genes respond to which stresses, or indeed which pathogens, and then see if there is variation between individuals. This might allow oyster farming to choose strains if oysters that are better suited to local conditions.

This would be a boost for the economics of oyster farming and hope it succeeds, but personally, I won't be partaking. I may have been part of the consortium that studied the genome, but I'm allergic to oysters. 

There is, it seems, more than one way to create an exploding star.

That's what scientists studying the origins of type 1a supernovae - important because they help to measure the accelerating expansion of the Universe and dark energy - have found.

A team, including Mark Sullivan of Oxford University’s Department of Physics, has reported in Science observations that suggest weaker stellar explosions from giant stars contribute to some of these bright supernovae. I asked Mark about the ‘second star’ mystery and dark energy…

OxSciBlog: Why study this particular supernova?
Mark Sullivan: This supernova ('PTF11kx') was found by the Palomar Transient Factory (PTF) in a galaxy 600 million light years away, quite close by cosmological standards, although still far too distant to directly view the star that exploded. The supernova was quickly identified as a 'type 1a Supernova', the same type that can be used as standard candles to measure astronomical distances, and that were used in the 1990s to detect the effects of dark energy.

PTF has found more than 1000 Type 1a Supernovae, and, at first, we thought this supernova was just like any other of its type. However, our data soon showed this was not the case - we saw dramatic evidence that the supernova was surrounded by significant amounts of gas arranged in shells, containing hydrogen, calcium, sodium and other elements. These shells were moving at different speeds, with the outermost shells travelling the slowest.

Such evidence is extremely unusual in these types of supernovae, and it prompted us to study this explosion in considerable detail to try and understand where this material had come from.

OSB: How do we think it formed?
MS: We think that this supernova, like all type 1a supernovae, formed from the explosion of a very compact white dwarf star in a binary system.

The white dwarf steals material from its companion until it cannot grow any bigger, at which point it explodes as a supernova some 10 billion times brighter than our sun. For many decades the nature of the 'second star' has been debated - is it another white dwarf star, or is it a much bigger star such as a red giant? This supernova helps answer this question. Our hypothesis was that the gas surrounding the supernova had been cast off in previous 'nova' eruptions, decades before the supernova explosion itself occurred.

Novae are much more frequent, weak explosions that do not destroy the star (unlike the supernova). Material blown off the red giant in a stellar wind lands on the white dwarf, and, as the material builds up, periodically explodes as a nova eruption. Such systems are well known - for example, a star in our own galaxy, RS Oph, has these explosions every 20 years or so.

This naturally explained the presence of the gas surrounding PTF11kx, and even the shells of material - the different shells correspond to different historical nova eruptions, with the outermost, oldest shells having been slowing down for longer than the innermost, younger shells. Two months after explosion of PTF11kx we saw the most compelling evidence of all - the supernova ejecta itself slamming into material left over from one of these previous nova eruptions.

Theoretical studies indicate that white dwarfs lose more mass in these nova eruptions than they gain from the red giant, and hence many astronomers concluded that novae could not produce type 1a supernovae. This new study is the first observational evidence that they can.

OSB: What does it tell us about how supernovae in general form?
MS: Previous results from PTF on the closest type 1a supernova for 25 years, have shown that that event could not have been a nova before it went supernova - the red giant star would survive the explosion, and this was not seen. So it is very unlikely that novae could explain all type 1a supernovae. So this new observation is compelling evidence that nature has more than one way to make a type 1a supernova explosion!

Predicting the exact number of supernovae that may arise from novae is difficult, as many of the signatures of the novae will depend on the angle at which the supernova explosion is seen from the Earth. If we had seen this explosion from a different perspective, it might well have been missed, or looked very different. But we estimate that novae give rise to more than 0.1 percent of all type 1a supernovae, but less than 20 percent.

OSB: How might these findings affect the search for dark energy?
MS: This result does not diminish the current evidence that we have for dark energy and the accelerating universe. But it does point to how we might make better measurements in the future. If there really are two (or more!) ways to make a type 1a supernova, then techniques that can identify these in astronomical data will be extremely valuable.

For example, some recent studies have shown that type 1a supernovae are not perfect standard candles, but instead their brightness depends on the type of galaxy in which they explode. At the moment, there is no good theory as to why this might occur - but the idea that these supernovae may come from different progenitor systems, and hence potentially have slightly different brightnesses, could help understand this mystery.

The Palomar Transient Factory is an international collaboration of scientists and engineers from the California Institute of Technology, DOE’s National Energy Research Scientific Computing Center at Lawrence Berkeley National Laboratory, NASA’s Infrared Processing and Analysis Center, the University of California at Berkeley, Las Cumbres Observatory Global Telescope Network, the University of Oxford, Columbia University, the Weizmann Institute of Science in Israel, and Pennsylvania State University.

Cancer is often described as a genetic disease, after all the transition a cell goes through in becoming cancerous tends to be driven by changes to the cell's DNA.

But genes, though hugely important, might not be the whole story. Researchers at Oxford University are interested in understanding how changes in cells' metabolism – the chemical processes through which cells get the energy they need – could also prime them to become cancerous.

They have just started collaborating with a lab at Keio University in Japan to bring large-scale techniques to the study of metabolic processes going on in cancer cells, much as gene technologies have given such insight into DNA changes involved in cancers.

'Altered cellular metabolism is a hallmark of cancer,' says Dr Patrick Pollard, who is leading this effort in the Nuffield Department of Clinical Medicine at Oxford.

This is not a new finding - it is something that has been known for a long time. The biochemist and Nobel laureate Otto Warburg pointed it out in the early 1900s. He observed that most cancer cells get the energy they need predominantly through a high rate of glycolysis (the metabolic process that breaks down glucose to release energy). It helps the cancer cells deal with the low oxygen levels that tend to be present in a tumour.

But whether dysfunctional metabolism causes cancer, as Warburg believed, or is something that happens afterwards is a different question.

In the meantime, gene studies rapidly progressed and gave us a picture of how genetic changes lead to cancer.

It goes something like this: DNA mutations spring up all the time in the body's cells, but most are quickly repaired. Alternatively the cell might shut down or be killed off before any damage is caused. However, the repair machinery is not perfect. If changes occur that bypass parts of the repair machinery or sabotage it, the cell can escape the body's normal controls on growth and further DNA changes can begin to accumulate as the cell switches to become cancerous.

So what has metabolism got to do with this? We get the energy we need from food of course, and we talk about our metabolism in the way our bodies make use of that food as a fuel for everything we do during the day. Our cells are the same. They have whole series of chemical reactions going on simultaneously to keep them working, wherever and whatever they are doing in the body – from heart cells to neurons in the brain and liver or pancreatic cells. Cellular metabolism is a constant process with thousands of metabolic reactions happening at the same time, all of which need to be regulated to keep our cells ticking over healthily.

It's what happens when the regulation of cellular metabolic processes goes wrong that could be of interest. And it's only a lot more recently that techniques to probe the entirety of metabolic processes in the cell have advanced. The result is something of a return to vogue for studies to understand how altered cellular metabolism and cancer are linked.

Studies of the genetic basis of cancer and dysfunctional metabolism in cancer cells are complementary, Patrick believes. 'Genomic data is very important, but certain changes in cells can’t always be accounted for by genetics.'

He is now collaborating with Professor Tomoyoshi Soga's large lab at Keio University in Japan, which has been at the forefront of developing the technology for metabolomics research over the past couple of decades (metabolomics being the ugly-sounding term used describe research that studies all metabolic processes at once, like genomics is the study of the entire genome).

The Japanese lab's ability to screen samples for thousands of compounds and metabolites at once, coupled with the access to tumour material and cell and animal models of disease in Oxford, should give great power to probe the metabolic changes that occur in cancer.

There is reason to believe that dysfunctional cell metabolism is important in cancer. Some genes with metabolic functions are associated with some cancers, and changes in the function of a metabolic enzyme have been implicated in the development of gliomas.

These results have led to the idea that some metabolic compounds, or metabolites, when they accumulate in cells, can cause changes to metabolic processes and set cells off on a path towards cancer.

Patrick Pollard and colleagues have now published a perspective article in the journal Frontiers in Molecular and Cellular Oncology that proposes fumarate as such an 'oncometabolite'. Fumarate is a standard compound involved in cellular metabolism.

In that article, the researchers summarise evidence (often from their own lab) that shows how accumulation of fumarate when an enzyme goes wrong affects various biological pathways in the cell. It shifts the balance of metabolic processes and disrupts the cell in ways that could favour development of cancer.

This work on metabolic pathways involving fumarate has already led to a cheap and reliable diagnostic test for a rare form of cancer caused by accumulation of fumarate within cells. Their test for hereditary leiomyomatosis and renal cell cancer (HLRCC) involves screening tumour samples for a particular molecular fingerprint unique to this type of cancer. The Oxford researchers are now hoping to develop their test for clinical use, largely to help with genetic counselling for families as the condition can be inherited.

While HLRCC is a rare type of cancer, Patrick Pollard says: 'Metabolic changes are observed in most cancers, so there could be wider implications. Lots of findings about pathways that are important in cancer come from studying rare cancers.'

This is where the collaboration with Keio University comes in. The Keio group is able to label glucose or glutamine, basic biological sources of fuel for cells, and track the pathways cells use to burn up the fuel. It allows the scientists to work out the metabolic pathways that are being used preferentially by different cell types including cancer-derived cell lines.

Patrick gives an example of how the research might progress: they could profile the metabolites in a cohort of tumour samples and matched normal tissue. This would produce a dataset of the concentrations of hundreds of different metabolites in each group. Statistical approaches could suggest which metabolic pathways were abnormal. These would then be the subject of experiments targeting the pathways to confirm the relationship between changed metabolism and uncontrolled growth of the cancer cells.

Patrick and colleagues write in their latest article that the shift in focus of cancer research to include cancer cell metabolism 'has highlighted how woefully ignorant we are about the complexities and interrelationships of cellular metabolic pathways'.

Hopefully, research efforts like this large-scale approach to understanding cell metabolism can give insight into how cells respond to shifted metabolic processes and how this is associated with the development of some cancers.