Podcast Transcript

Brain structure makes a people-person

Do you consider yourself to be a people-person? Do you crave the company of others, are you warm and sentimental? Well, if you are, then it could come down to the structure of your brain.

Graham Murray led a team of researchers from Cambridge University and Oulu University in Finland who have discovered that the greater the concentration of tissues in certain parts of the brain, the more likely someone is to be highly sociable. Earlier studies have linked these same areas of the brain to processing simple rewards like sweet tastes and sex.

Publishing in the European Journal of Neuroscience, Murray and the team recruited 41 male volunteers who had their brains scanned by MRI scanners and were also asked to fill out a questionnaire to find out about aspects of their personality. They were asked to rate themselves on statements like ‘I make a warm personal connection with most people', or 'I like to please other people as much as I can'. The results of the questionnaire provide a measure of how sociable someone is, called the social reward dependence.

They found that people with higher social reward dependence scores tended to have a greater concentration of grey matter in both the orbitofrontal cortex (the outer strip of the brain above the eyes), and in the ventral striatum (a deep structure across the centre of the brain).

Eating energy-rich sweet foods and sex are vital for survival while social interactions are not necessarily so, but it could be that emotions like sentimentality and affection in humans evolved from structures in the brain that make animals seek out and satisfy these more basic needs.

This research could also shed light on understanding what causes various psychiatric disorders which make social interactions difficult, like autism or schizophrenia.  So far Murray and his team have found a correlation between brain structure and personality, but exactly how the two are linked is still to be uncovered.

24th May 2009

Dragons with toxic bite

They seem like the stuff of fairytales or maybe nightmares, but Komodo dragons are the closest things we have to real, man-eating dragons. At three metres long, these lizards that live on the Indonesian island of Komodo and are fearsome enough, and now scientists have discovered that they have a toxic bite. Until now it was thought that the key to their deadly bite was bacteria in their saliva which infects their prey, causing them to go into shock before the dragon returns to kill and eat their victim.

But now, Stephen Wroe from the University of New South Wales, Australia and a big international team of researchers publishing in the journal PNAS have discovered that Komodo dragons have venom glands containing a dose of anticoagulant toxin that causes their victims to bleed to death.

First the team used computer models to analyse the skull of Komodo dragons and found that they have a much weaker bite than crocodiles of a similar size suggesting that instead of biting down hard they are better suited to holding onto prey that is trying to wriggle away. The team then put a preserved head of a komodo dragon into a magnetic resonance scanner and discovered a set of complex venom glands in its jaw with ducts coming out of their teeth.

The researchers surgically removed a set of these glands from a terminally ill dragon in a zoo. Using mass spectrometry they worked out the chemical make up of the venom and discovered it is made up of a complex mix of proteins, similar the lethal cocktails used by other venomous reptiles.

These toxins induce shock in victims causing them to bleed copiously by preventing blood clotting and widening blood vessels. That finding fits with reports from humans who have been bitten by Komodo dragons and continued to bleed for a long time afterwards.

The researchers also examined the fossil teeth of an extinct relative of the Komodo dragon, called Megalania, and discovered that this two tonne, seven-metre giant probably also had venom glands, making it one of the largest venomous animals ever known. But don’t worry, these monstrous lizards haven’t been around now for 40,000 years although their smaller cousins the Komodo dragons are undoubtedly impressive predators and now we have a much better idea of how they deal their lethal blows.

24th May 2009

Down's do better in cancer stakes

Individuals with Down's syndrome have a significantly lower likelihood of developing cancer (with the exception of a form of leukaemia) compared with the general population but no one knew why.  Now a study in the journal Nature has revealed the answer.

Harvard researcher Sandra Ryeom and her colleagues have found that one of the 231 genes on chromosome 21, of which Down's patients carry an extra copy in all of their nucleated cells, controls blood vessel development.  This suggested to the team that part of the cancer-preventing effect in Down's might be because cancers find it more difficult to produce new blood vessels to support themselves.

The clue came from the observation that Down's patients also have lower risks of developing diabetic eye disease, which is caused by the growth of new blood vessels in the retina, and vascular disease in general.

As a result the Harvard team focused on a gene called Dscr1, which encodes a cellular off-switch that suppresses the effects of a blood vessel growth factor gene called VEGF (vascular endothelial growth factor).

The researchers implanted cancer cells into mice genetically engineered to have the rodent equivalent of Down's.  Compared with control animals the cancers in these mice grew significantly less well.  To prove that Dscr1 was responsible for the effect the team then removed the extra copy of this gene from their Down's mice and repeated the experiment.  As expected, the tumour-protective effect had largely disappeared.

However, as the researchers point out, there are 230 other genes on chromosome 21 and one or more of these may also be contributing to this effect.  But regardless of this, the present results confirm that Dscr1 has a powerful anti-cancer action achieved through suppressing the growth of new blood vessels that are needed to sustain solid tumours.

According to the researchers "it is, perhaps, inspiring that the Down's syndrome population provides us with new insights into mechanisms that regulate cancer growth and, by so doing, identifies potential targets for tumour prevention and therapy."

24th May 2009

Data storage that will last a billion years

Scientists have used nanotechnology to solve a serious problem of the digital age - data degradation.

Although we think of digital storage as a way to preserve photos and other data in pristine condition, the lifetime of modern storage media is as little as 20-30 years.  This is in stark contrast to the enduring properties of the stone tablets on which some of the world's oldest writing remains readable 4000 years after it was first carved and the fact that the Domesday Book, at the age of 920, is still going strong.

The modern equivalent, however, which was commissioned in 1986 by the BBC, had to be migrated to alternative media twenty years later because the original laser discs on which the material was stored had failed.

But what sets ancient media storage systems apart from the more modern counterparts is the data density.  Stone tablets contain about 2 "bits" of information per square inch compared with contemporary digital devices which store about 100 Gigabits per square inch - 50 billion times more.  At these scales, however, the storage medium is not reliable and the integrity of the data is cannot be preserved in the long term.

But to solve the problem, University of California Berkeley researcher Alex Zettl and his colleagues say they've developed a system that should last at least a billion years, within reason. Their approach is to use short nanotubes - tiny molecular straws of carbon - inside of which they place an iron-based nanoparticle "shuttle" that can move up and down the inside of the nanotube.  When a small electric current is passed through the nanotube it causes the iron shuttle to slide from one end of the tube to the other.

This, say the team, can be used like a binary digital storage system with one end of the tube representing a nought (0) and the other end a one (1). The position of the particle can be read-back from the nanotubes by measuring their resistance, which changes according to the position of the iron shuttle.

The small scale of the devices also means that storage densities in excess of 1 Terabit per square inch should be possible, more than 10 times the present achieveable.  Better still, simple calculations based on the stability of the system and the likelihood of the iron shuttle randomly moving the 200nm length of the tube to turn a 0 into a 1 or vice versa mean that the data should remain reliably preserved for at least a billion years, or 10¹⁷ seconds!

24th May 2009

Biological Link between Cancer and Depression

Chris Smith: Now also in the news this week, researchers at the University of Chicago have identified a potential biological mechanism that can link cancer with depression, and we are joined by Dr Leah Pyter to tell us a bit about it. Hello Leah? 

Leah Pyter: Hello!

Chris Smith - Welcome to The Naked Scientists! So do tell us, what is the evidence then that people who get cancer get depression, because obviously that’s a pretty traumatic diagnosis to receive. Are you saying then that people get depressed before they get their diagnosis of having cancer?

Leah Pyter: Well basically what we know is that patients with cancer have a higher likelihood of also developing depression at some point in their disease progression, so whether that occurred before and is predisposing them to cancer, or it’s due to the tumours themselves, or other aspects of having the disease, we don’t know. We were only studying right now whether the cancer itself can cause depression.

Chris Smith: How could a tumour trigger depression, because a tumour can occur anywhere in the body, therefore at the remote sites in the brain, so how could it trigger changes in brain activity?  

Leah Pyter: Sure, well what we hypothesized was that the tumours themselves can produce cytokines which has been shown before.

Chris Smith: These are inflammatory chemicals that drive the immune system?

Leah Pyter: Right, exactly! And there is also a pile of research on how cytokines can access the brain specifically regions of the brain that are associated with depression and anxiety and emotional behaviours, and they can access the brain both tumourally through the blood, or neurally through the vegas nerves.

Chris Smith: So what did you actually do to get to the bottom of how cancer might be able do that?  

Leah Pyter: First of all, we are using an animal species, rats, in order to isolate just the physiological impact of having a tumour from the psychological impact of having the disease. We induce tumours in rats and had controls, and then looked their depressive and anxiety-like behaviour along with some physiological measures of these cytokines and the stress access.

Chris Smith: So you’d give rats the cancer. Can you show that when they get the cancer they do develop a sort of depressive or anxious-like syndrome consistent with having – or contemporaneously with having the tumour?

Leah Pyter: Exactly, yes! That’s what we did – basically we used standard behavioural tests in these rats that have been used to develop pharmaceuticals, like antidepressants and you have control animals and we measured these types of behaviours and made sure that they only developed following the presence of a tumour.

Chris Smith: And once you’d confirmed that the rats do seem to get depressed when they get a cancer, how did you then find out what was going on to make them feel like that?         

Leah Pyter: Well, we had two candidates, one were the cytokines that we have some information about associating with depression, and the other was via the hormone access that regulates stress responses; and so we were able to measure cytokines in the tumours themselves, in the blood as well as the brain in animals with and without tumours, and we also measured one of the stress hormones in response to a stressor and found that cytokines were increased in the brain if you had a tumour and your hormone response to a stressor was dampened if you had a tumour, relative to controls.

Chris Smith: So the cancer is definitely inducing biochemical changes in the brain that might trigger depressive symptoms. We can treat depression though. Why is it important to have identified this problem, and how can it help us to make people who have cancer have a better outcome?

Leah Pyter: Right. So I think one of the things we were keying in on is that a lot of chemotherapies are cytokine-based and so if you’re having a patient that is displaying depression along with the cancer you might try to switch the chemotherapies but it’s also important because cancer patients that are depressed are less likely to stick to their medical programme and are more likely to succumb to the disease. So not only treating the cancer but also the depression is important for their wellbeing.         

Chris Smith: Thank you very much. Leah, thank you for joining us! That was Dr Leah Pyter who is at the University of Chicago, she and her colleagues have published a paper in this week’s edition of the Journal, PNAS, in which they explained how things like cancers can change the behaviour and particularly to cause behaviours like depression, which as she just explained, can have a major impact on how well someone does in terms of their therapy and their long term prognosis

May 2009

This Week in Science History - Proof of General Relativity

This Week in Science History saw in 1919, the solar eclipse that proved Albert Einstein’s theory of general relativity to be correct.

Einstein had published his theory in 1916, but because of the First World War, no attempts were made to test the theory until the English physicist Arthur Eddington and his colleagues travelled to observe the total solar eclipse of May 29th from Principe, off West Africa, and from northern Brazil.

Before Einstein, Newton’s theory of gravitation, put forward in his Principia Mathematica, published in the mid 17th century, had been the way to describe how gravity works. However, it could not account for what caused gravity and the source of the force. Newton himself was uncomfortable with how to explain how gravity seemed to ‘act at a distance’ through a vacuum.

Einstein’s theory of general relativity gives rise to a geometric theory of gravitation. This basically says that gravity doesn’t make things move – it is a consequence of the shape of ‘spacetime’. The best way to imagine this is the common analogy of a rubber sheet. If you (and some friends) stretch it out so it’s flat, then roll a ball from one side to the other, the ball will go straight across. But if you then put a big heavy ball in the middle of the sheet, it will cause a big dent in it – this is kind of like what happens to spacetime around a huge object like our sun – it changes shape. If you then roll the same ball as before across the rubber sheet, it won’t just roll straight across – because the big ball in the middle has created a dip, the path of the small ball will change – it may bend, or roll right round the dip and come back towards you, or it might stay rolling around the big heavy ball. This is what gravity does – the dip in the sheet caused by the big ball is affecting the path of other objects put on the sheet. Just like gravity in the real world will affect the movement of objects and light coming close to a massive object like a star.

The idea that light travelling towards us from distant stars would be bent by the gravitational pull of large objects like the Sun was suggested before the 1915 paper and could be predicted by combining Newton’s theory of gravity with Einstein’s earlier theory on special relativity. Using the now famous equation E=mc2 to calculate a mass for the light energy coming from a distant star, Newtonian gravitation predicts that the light will be bent by the sun’s gravity, causing the perceived position of that star in the sky to shift. However, in his 1916 paper, Einstein predicted a displacement of *twice* that predicted by Newtonian gravitation, and the only way to prove who was right would be through observation.

The only time that stars could be observed when their position in the sky was close to the sun was during an eclipse, or the sun’s brightness would prevent photographs of the stars from being taken. This led to the expeditions made by Eddington and his colleagues in 1919.

On the day of the eclipse, it was cloudy in Principe. Eddington and his assistant worried that they would not get the photographs they needed. Fortunately for the future of physics, the clouds broke for long enough.

Back in England, they compared the photographs of the Hyades star field taken during the eclipse to photographic plates of the same star field when the sun was out of the way. The difference in position of the stars was just as Einstein had predicted – twice that of Newton’s theory.

Throughout the 20th century, further evidence to support Einstein’s general relativity theory has built up. The theory predicted the existence of black holes, gravitational redshift and gravitational time dilation, and the results of tests have all fitted with the theory’s predictions.General relativity is still the way we describe gravity in modern physics, although there are problems when it comes to quantum physics – the physics of the particles that make up atoms, in that the predictions of relativity do not hold on this tiny scale. Reconciling these two areas would lead to a so called ‘theory of everything’.

May 2009