Nature Podcast

This is a transcript of the 10th July edition of the weekly Nature Podcast. Audio files for the current show and archive episodes can be accessed from the Nature Podcast index page (http://www.nature.com/nature/podcast), which also contains details on how to subscribe to the Nature Podcast for FREE, and has troubleshooting top-tips. Send us your feedback to podcast@nature.com.

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Adam Rutherford: Coming up, why would you possibly have both eyes on one side of your head?

Matt Friedman: This is one of the reasons why flatfishes have been listed in so many evolutionary debates. They were used in some of the first attacks on Natural Selection.

Adam Rutherford: But a new fossil fills one of the fishier gaps in the theory of evolution.

Kerri Smith: A pool of cells in the brain's amygdala could be tweaked to treat people with abnormal fear responses.

Denis Pare: The hope is that by changing the excitability of intercalated cells enhancing it, we might be able to compensate for these abnormalities.

Adam Rutherford: And the sly Ebola virus.

Erica Ollmann Saphire: The virus hides itself with a thick layer of carbohydrate, so if you wanted to use a Harry Potter analogy, it would even be like a cloak of invisibility around the virus.

Adam Rutherford: This is the Nature Podcast, I am Adam Rutherford.

Kerri Smith: And I am Kerri Smith. BOO-OO-H !!! If that scared you, there is a chance that you might develop an unfortunate fear of the Nature Podcast, but if the next time you tuned in nothing fear inducing happened, you might give us another try. Two papers in the journal this week look at how the brain controls fear and helps us get over it. We know that the amygdala is a big player when it comes to fear. Andreas Lüthi and his team from the Friedrich Miescher Institute in Basel, Switzerland have located two networks in this region that make us afraid and help us unlearn our fears. Another group from Rutgers University in New Jersey led by Denis Paré, have found clusters of cells responsible for causing fearful reactions. Here's Denis Paré first of all with more on the brain's scare switch. Nature advance online publication (9 July 2008) ; Nature advance online publication (9 July 2008)

Denis Paré: We knew as you said that the amygdala is involved in the acquisition of new fear responses to stimuli, you know, as a function of experience and we also had evidence that that same structure the amygdala was involved in learning a stimuli that were previously associated to adverse outcomes no longer signalled danger and this phenomenon is called extinction and we knew that the amygdala was also involved in this form of learning.

Kerri Smith: So we previously knew then that the amygdala was responsible for all of this stuff, but you've been able to kind of go down to the next level if you like and you've been looking at a specific population of amygdala neurons, haven't you?

Denis Paré: It's correct, we knew that the amygdala was also involved in the formation of this new inhibitor memory this extinction memory, but we didn't know what kind of cells and mechanisms were involved. Here in our study, by using a peptide toxin conjugate that selectively kills a specific type of neurons, neurons that express a kind of receptors called new opioid receptors, we were able to kill selectively intercalated cells, because intercalated cells express these receptors at very, very high levels compared to other cell types and these lesions cause an extinction deficit. So when rats were trained on fear conditioning they acquired to condition fear responses as shown before then they were trained on extinction by presenting the tone in the absence of the foot shock multiple times, the day after one set of rats received intercalated lesions and the other set of rats were infused with the blank peptide that had no effect and one week later we tested recall of extinction and animals that had intercalated lesions showed an extinction deficit, they couldn't remember the extinction training.

Kerri Smith: The other thing I am wondering about and you mentioned it briefly at the end of your paper, could these cells be therapeutically useful for dulling overly fearful responses, people with posttraumatic stress disorder or phobias.

Denis Paré: Of course, this is the hope. We know that for instance PTSD subjects, human subjects with PTSD have an extinction deficit in controlled laboratory studies where Vietnam War veterans or other war veterans were trained on a fear conditioning protocol and then trained on extinction. When subjects with or without PTSD were compared, there was a clear deficit of extinction in the PTSD subjects. Now the hope is that by changing the excitability of intercalated cells, enhancing it we might be able to compensate for these abnormalities. In rats intercalated cells have very unusual properties in terms of receptor expression. So the hope we might be able by using targeted drug injections that will selectively target these receptors that are so abundantly expressed by these cells, we might be able to accelerate extinction and facilitate it.

Kerri Smith: The second paper looks in a different portion of the amygdala and finds two opposing networks that aggravates and switch fear. I called Andreas Lüthi to find out more.

Andreas Lüthi: So what we found was that there is actually a population of neurons within the amygdala that is necessary for this active fear extinction and these neurons sort of sit side by side by other neurons and are important for this fear learning.

Kerri Smith: Why wouldn't one circuit then, one pool of neurons just being, say more or less active along this kind of spectrum of how afraid you're of something, why do you think that there are these two different entirely separate populations of neurons?

Andreas Lüthi: So they prompt another series of experiments where we put stimulation electrodes in other parts of the brain, in particular into the medial prefrontal cortex which I have mentioned before but also in the hippocampus. The hippocampus has previously been shown to be important to encode contextual information and we've shown that these two populations of neurons what we called as fear neurons and the extinction neurons are differentially connected with the medial prefrontal cortex on the hippocampus, so this sort of form parts of large networks that do not receive same inputs and do not send the same outputs to other brain regions. An important open question that we have to address in the future is, how do these two populations of neurons interact locally within the amygdala.

Kerri Smith: Now one thing I was wondering about is that are there different overlapping circuits that regulate fear of different stimuli, so if I was afraid of dogs for example already and then for some other reasons separately I became afraid of pigeons or something, will that be the same circuit or a different pool of neurons that were doing dogs versus pigeons.

Andreas Lüthi: This is a very interesting question and I am afraid that I cannot really give you a solid answer to that. Of course, it's an interesting question whether there are also different kinds of circuits dealing with different kind of incoming sensory information, but these have not been addressed so far.

Kerri Smith: Do you think it is possible that we could one day, be able to tweak these networks at all, for example to treat conditions where people are overly fearful like posttraumatic stress disorder or something like that.

Andreas Lüthi: It is believed that extinction like processes are important for many different forms of therapy in psychiatric patients such as people with posttraumatic stress disorder for example. However, these therapies are occurring in certain context in a clinical context of course, and when the patient leaves this context the original problem can reappear, so it is likely that these mechanisms we have discovered contribute to these obstacles of clinical therapy. Now in order to really manipulate these processes, of course, you would have to know much more about the types of neurons involved about their properties, but of course it's providing an important entry point in identifying these neurons and further investigating their properties to see whether it will be actually possible to prevent for example the inappropriate reappearance of pathological fear.

Kerri Smith: Andreas Lüthi there and before him Denis Paré.

Adam Rutherford: In just a moment we will have you hooked on a story about some fishy friends and the fossils they have left behind, but for now we're sticking with the neuroscience theme. Over a decade ago, a new type of brain cell got researchers very excited.

Kerri Smith: These mirror neurons became pivotal to explanations of how some animals can learn to imitate others actions and even of what makes humans capable of empathy, but it is still not clear how they do what they do. In an essay this week, Antonio Damasio and Kaspar Meyer of the University of Southern California argue that a 20-year-old theory of Damsio's could help explain. Nature essay's Editor Nicola Jones has joined us in the studio to reflect on them. Welcome Nicola. Nature 454, 167–168 (10 July 2008)

Nicola Jones: Hi.

Kerri Smith: Now refresh our memories first of all what exactly are these mirror neurons.

Nicola Jones: Well, so mirror neurons were discovered about 10 years ago and what they are, are brain cells which fire not only when you are doing something like waving your hand but also when you see the same thing being done by someone else. As they discovered this first in monkeys and then subsequent studies have shown that the same thing happens in humans brains.

Kerri Smith: That sounds like a very clever thing for them to be able to do. How exactly do they work, what do we know about them?

Nicola Jones: Well, no one really knows for sure, but the prevailing theory is that mirror neurons somehow create a re-representation of this action in your own brain and that then helps you to understand what's happening. So that you know when you wave your hand you might be saying, Hello or Goodbye and when you also see someone else waving their hand, because the same neurons are activated in your brain somehow that makes you also remember, Ah, yes that's associated with hello, goodbye, those kinds of things. So you get a larger sense of meaning from having seeing somebody else do something.

Kerri Smith: So, not just the waving the hand action but also the connotations that go with that.

Nicola Jones: Yeah, possibly. So people have since their discovery people postulate that mirror neurons help us do everything from understanding that other people have a mind of their own that they have their own intentions and it gives us a sense of empathy, so that if we see someone else smile, we understand that that's related with happiness.

Kerri Smith: Well, so they are carrying quite a lot of weight around in these theories of empathy and of imitation. What does Damasio suggest in this essay that he is publishing this week about them, what's different there?

Nicola Jones: Well, as you say it's a reflection, so he is reflecting on mirror neurons and just noticing that in a way their name is almost too good, so because they're called mirror neurons everyone started to tend to think of them as little tiny mirrors in your brain that magically reflect what other people are doing and that, this somehow does have the effect of making you understand things. So he is just pointing out that we need to remember that mirror neurons are embedded in a network within our brain and that they're not acting alone; that they are somehow interacting with the rest of the parts of our brain in order to create that sense of meaning.

Kerri Smith: And that seems to be from what he writes, something that may be the mirage of most guilty of this, we overlooked that a bit, we've got a bit too excited about them.

Nicola Jones: Yeah, I think he thinks that, you know, both amongst the scientists and the public there is not so much of a huge misunderstanding but a tendency to forget that mirror neurons need to be associated with other things and he has a theory from 20 years ago about how the brain works generally, which he thinks might help to explain how mirror neurons are embedded in a network.

Kerri Smith: Talk us through that theory then.

Nicola Jones: So it's called the convergence-divergence theory and basically what it means is, let's say, you see something like with a monkey, if monkey sees a peanut being broken or breaks the peanut himself then he will have the sight of the peanut breaking and the sound of the peanut breaking and the knowledge of the fact that he is about to eat the peanut, all of these things will happen at the same time and all of these various bits of information from his motor cortex, his visual cortex, and his auditory cortex will all be triggered at the same time. So, Damasio's theory was simply that there is a centre in the higher order part of the brain that collects the fact that all of those triggers happened at once and it creates a kind of memory trace saying when this happens all these other things happened too. So what that means is that the next time a monkey hears a peanut being broken but without being able to see it and without having done it himself then that auditory signal lights up in his brain and that goes back to the centre of convergence which created the memory trace of the all of the things that happened before and it reactivates all those other things, so the signals originally converged into one place in the brain and made a memory trace and then later they diverge outwards again and activate everything, so again the monkey has an impression of all the things that go along with the breaking peanut.

Kerri Smith: It might be a naïve question, but isn't it assumed that these cells, these mirror neurons are part of a bigger system in any case, do we need this theory to, sort of, tell us that?

Nicola Jones: Well, I mean I think you're right it's obvious that all cells are part of a network and everything in our body is connected to everything else, but the thing with brains is I think it's very important to understand how signals are travelling in one direction and another. So, for example, Damasio points out that in the past it was actually not known that although signals clearly go from your eye, for example, into your brain to the visual cortex and then to the higher order part of your brain that interprets what you're seeing, it was also discovered a little bit later that signals travel outwards back towards the eye as well and that wasn't so obvious to neuroscientists. So understanding how those signals travel in different directions can be complicated even though it sounds a bit obvious.

Kerri Smith: So, I suppose mirror neurons are, I guess more of a confirmation of this older theory given that they correspond to sort of, the bits of the brain that would be doing the convergence as it were.

Nicola Jones: Yeah, so what he is saying is that mirror neurons aren't really special in themselves. It is not like they have some quality that makes them unique. What's special about them is where they are, rather then what they are. So the mirror neuron data has helped to support his 20-year-old theory and also his 20-year-old theory may help to explain how mirror neurons are acting, but that doesn't mean that either of them have proved the other, so they're both very nice and they both shed a light upon each other and Damasio's point really is that we should think about the networks, about that mirror neurons set in more thoroughly, but at this point it's still old theory.

Kerri Smith: That essay along with all the other papers on this week's show is available from http://www.nature.com/nature.

Adam Rutherford: And for the chance to win an ipod Classic, take 10 minutes to fill out our survey about the show. Follow the links from http://www.nature.com/nature.

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Adam Rutherford: And now Geoff Brumfiel on the massive earthquake that hit China earlier this year, killing nearly 90,000 people and rendering 5 million homeless.

Geoff Brumfiel: Two months ago a powerful earthquake rocked China's Sichuan province. Incredibly within just 4 days of the 7.9 magnitude quake, Nature received a paper predicting where the biggest aftershocks will be likely to occur. That paper was published this week. I called author Tom Parsons of the United States Geological Survey in Menlo Park, California to learn how those predictions were made and how they might aid the rebuilding effort. Nature advance online publication (6 July 2008)

Tom Parsons: Well, it's an area where a very large earthquake that struck just along the eastern edge of the basin in the Longmen Shan mountain range was a devastating event that destroyed many, many buildings in Sichuan basin which is immediately adjacent to this range front.

Geoff Brumfiel: So, rewind us of the big picture here, I mean, what plates are moving against which in this particular region.

Tom Parsons: Well, what's happening is the Indian Subcontinent is pawing northward into Asia, it is pushing up the Tibetan plateau rather spectacularly and this earthquake happened at the very eastern edge of the plateau. It's one of the most pronounced range fronts found anywhere on Earth in terms of the difference when you go from the Sichuan basin up into these mountains.

Geoff Brumfiel: And what kind of data did you pick up from this event, or did the US Geological Survey pick up from this event.

Tom Parsons: My co-author Chen Ji at University of California-Santa Barbara has mastered the art of very rapidly figuring out where the slip was in the main shock event using recordings of the earthquake from around the world, he was able to get us a model within one day of where the slip occurred and by providing that so quickly, what we could do then was simulate this earthquake in a numerical model and then looked at all the faults set around that area and looked at the arrangement of the faults right after the earthquake and realized there are a number of large faults that underlie the Sichuan basin and surroundings that might have had stress increases or decreases as a result of the main shock and given how many people live in that basin we were concerned that the large aftershocks might be happening following this event that's commonly what occurs around the world, so by doing this very quickly the idea is that we hope this will help as reconstruction efforts going to try and pin point where the efforts might be best directed.

Geoff Brumfiel: And you've had some success with this model in the past, haven't you?

Tom Parsons: The Sumatra earthquake of 2004 there was a paper in Nature where they suggested that there were some stress increases and then a few months later there was an 8.7 earthquake that happened in one of the places that they calculated a stress increase. We did this also in Turkey after the Izmit earthquake of 1999 and three months later there was magnitude 7 earthquake that hit Duzce just a little bit East of the Izmit, also in an area where stress increases were calculated. So these things can be effective. Often times though we come along after the fact and so it is a little unclear whether or not you know it's a fair test. So the idea here is to try to get ahead of the game a little bit and do a perspective test and try to outline where we think these increases happen and then we can watch and see if we are right or not.

Geoff Brumfiel: So any specific predictions based on the data from the China quake?

Tom Parsons: It's tricky to say in a particular timeframe what happens with aftershocks is that they follow what we call Omori's law and that is that the rate of the aftershocks decays as a function of the inverse of time. So the first day, you have a certain number of aftershocks, by day 2 it's half as many, by day 3 it's the third and so forth. So we know certainly that the highest likelihood of an aftershock happening is immediately after the main shock and it decays shortly after that. And globally what we see with these 7 and greater earthquakes is that on average the increased hazard can last 7 to 10 years, so the best we can do is we can show that the likelihood will follow this Omori law kind of time decay, but precisely when and where you know, in a matter of months or years we can't say.

Geoff Brumfiel: I suppose the question for lot of our listeners is that how can this really help the people in Sichuan, I mean, it's an interesting exercise certainly for you and it does provide some information, but you mean we can't stop an earthquake, right, you can't just evacuate people for something that may or may not happen.

Tom Parsons: No we think the best response for all the earthquakes is actually better construction, to be prepared for what might be coming along and there is time to actually make some useful reconstruction, in other words, kind of try to prepare for the scale of an earthquake that might occur down the road here a little bit and as you say you can't evacuate towns for 7 or 10 years but you can certainly try to provide buildings after the challenge of surviving some of these larger earthquakes.

Kerri Smith: Tom Parsons talking to Geoff. The vagaries of Geology aren't the only causes of natural disasters. Biology has a fair few up its sleeve too and a team from the Scripps Research Institute in California is hoping to stop the Ebola virus and its tracks. Here's Charlotte Stoddart.

Charlotte Stoddart: The Ebola virus is a sly intruder. To sneak past our body's immune system, it hides its tell-tale surface proteins under a carbohydrate cloak. This cloak and the rapid replication of the virus once inside cells makes it a difficult infection to fight, but by unravelling the structure of an Ebola virus surface protein and its sugary shroud - together known as a glycoprotein - the Scripps team have revealed several potential drug targets. Here's team member Erica Ollmann Saphire. Nature 454, 177–182 (10 July 2008)

Erica Ollmann Saphire: The challenge is the speed with which the virus can replicate itself. You know it incubates for just about a week, before you start to get symptoms and then patient's typically just live another few days after that and normally it can take several weeks for immune system to develop. Now, when one makes a vaccine in primates, you can find that you can stimulate a very effective immune response in about a month. The challenge is that a natural infection of virus out-competes those responses that you can't make. Now you can also make antibodies against the virus but these can be rare. There are a number of survivors that have elicited few or no, titres, and antibodies are really not high enough concentration of anything that can effectively neutralize the virus. So it's really a sneaky little devil.

Charlotte Stoddart: But in this new paper you have extracted one of these rare antibodies and you've worked out the structure of the antibody when it's bound to one of the viral glycoproteins. What did you see?

Erica Ollmann Saphire: Well, we saw that the antibody was quite unusual, so most viral surface proteins come in two sections or subunits. So, one section is responsible for attaching to a possible host and the other section is responsible for driving the virus membrane into the host membrane in mediating fusion. So you've an attachment section and you have a fusion section. For most other viruses that we know, the antibodies would be directed against just one of those two sections. So only against the attachment subunit, or only against the fusion subunit. This one actually bridges the two together and so it's very intriguing to speculate how it might work and might actually hold the two subunits together to prevent them from separating and mediating their activities. But we don't know as still experiments are in process now.

Charlotte Stoddart: Now you mentioned earlier Erica how difficult it is for our bodies to fight off infection from the Ebola virus and also how it's difficult to develop vaccines, so I am wondering does your work on the structure help to explain why this is?

Erica Ollmann Saphire: Well, it does absolutely and that was the main impetus for resolving the structure, so the virus coats itself with a thick layer of carbohydrate and that acts alike a cloak, so if you wanted to use a Harry Potter analogy it would even be like a cloak of invisibility around the virus, but let's say Harry wasn't very careful when he put it on and he had a foot sticking out on one end and on the top his head sticking out in the other end but then you could see that those two sides were actually Harry underneath and they were invisible. So if we could target an antibody against the exposed foot and an antibody against the top of his head then we would have some good anchors to be able to identify and attack the virus in your knees and the structure shows us what those sites are and gives us ideas about how to design immunogens and strategies to release antibodies against those very rare site.

Charlotte Stoddart: This could help researchers to develop effective treatments then.

Erica Ollmann Saphire: Yes absolutely and in fact when one try to make antibodies against the virus one was essentially hunting blindly that we didn't know what side on the virus might be an effective target where the virus were killing fields, but now that we see how the protein is folded up and importantly we see which parts of the virus are not masked by carbohydrates so we now know where we should target those antibodies. One of the truly amazing things about the structure that we've done is that it's the before, it's what the protein looks like on the surface of the virus. Ten years ago, two groups solved the after structure which is what the protein looks like, after it has mediated fusion of the virus membrane and the host membrane. So now that we have a before and now that we have an after we can make the movie modelling what happens in-between and you can see the actual beautiful and incredible symmetric gymnastics that this molecule goes through to try to change its shape and metamorphasize from a very hidden mask to pre-fusion viral surface structure to the structure after its mediated infection. You can see those movies on the Nature website.

Adam Rutherford: Erica Ollmann Saphire there. Finally this week, a distinctly fishy tale of asymmetry in nature. Symmetries are crucial indicators of fitness and indeed there are incredibly few asymmetric creatures. One startling exception are the flat fishes such as plaice, halibuts, and sole; adults have both eyes on one side and a distorted mouth on the other. The ugliness of these bottom dwelling predators is only balanced by their deliciousness. The evolutionary origins of this asymmetry are not well understood but Matt Friedman from the University of Chicago has found a new fossil flatfish that shows transitional traits that can help explain this weird lopsided head. I've got Matt on the phone. Matt, before we go to the new specimens tells us how the asymmetry develops as the fish matures. Nature 454, 209–212 (10 July 2008)

Matt Friedman: Well, flatfishes undergo one of the most bizarre metamorphosis among vertebrates and among any animal group as a whole, what happens is that every flatfish is born symmetrical; they are symmetrical larvae and at about say 10 mm total length. These individuals start to undergo a really profound metamorphosis in which one eye moves, migrates over the top of their head and then comes to rest in a final position on the opposite side of the skull. After this all the, sort of, the component bones of the skull sort of form this new model head and you arrive at the adult condition.

Adam Rutherford: Can you describe these two new fossils which are called Heteronectes and Amphistium and how they relate to modern flatfish such as plaice?

Matt Friedman: Well, the remarkable thing about these two fossils is that they show a very clear asymmetry in the skull. The skull is profoundly asymmetrical and we can see that one of the eyes has moved, but in contrast to all living flatfishes, where both eyes are located on one side of the head in adults, these fishes maintain their eyes on opposite sides of the skull, even though one of the eyes has moved. It simply hasn't crossed over the top of the head to come to rest on the opposite side of the face.

Adam Rutherford: Okay so when do these fossils date from.

Matt Friedman: These fossils are both Eocene in age, which is about 50 million years ago, so to put that in context to about 15 million years after the dinosaurs went extinct.

Adam Rutherford: And so you just said that the fossils they are asymmetric but they don't quite have eyes on one side like the modern flatfish do, how can you tell that they're not simply immature forms and the migration of the eyes is just incomplete when the fossils were formed.

Matt Friedman: Right that's an excellent question; it's one that certainly I had to address before I was convinced that these fossils were showing what I thought they were. It turns out that we know quite a bit about the patterns of ossification, the patterns in which bones form during the development of young flatfishes and most of bones of the skull actually don't finish mineralizing, they don't become a hard bone from their cartilage precursor or other precursor until after the migration is completed. What I think the most compelling piece of evidence suggesting that these are all adults that show the final condition is that we have a range of sizes of these individuals and regardless of the size of the fossil, they all showed the same degree of asymmetry. We don't see increasing degrees of asymmetry as we look at larger fossils.

Adam Rutherford: So you're confident that they are an important transitional step between symmetrical fish and the asymmetrical modern flatfish.

Matt Friedman: Yes, I think that is pretty clear, that's borne out which is satisfying to me at least by features other than asymmetry. There are other characters that link these fossils to flatfishes independent of that asymmetry, well they also show series of characters that are more primitive than any living flatfish that indicate they fall outside the living radiation of flatfishes that are characterized by that complete asymmetry that we are so familiar with.

Adam Rutherford: Okay now we know that transitional fossils or transitional forms are important in establishing phylogenies. I am struggling to see how the small steps towards an asymmetric head could be selectively advantages.

Matt Friedman: Well precisely, and this is one of the reasons why flatfishes have been listed in so many evolutionary debates. In fact they were used in some of the first attacks on Natural Selection, sort of, gradual evolution as the mechanism of organic change. In the late 1800s this gentleman named St. George Mivart published a, sort of scathing critic on natural selection and sort of Darwinian Theory and he enlisted flatfishes as one of those prime examples and he said, well we can't imagine what these transitional forms must have been like. There is no selective advantage to have this incomplete asymmetry which is precisely what you brought up. But actually as it turns out now that we have these intermediates, we have to somehow account for what they were doing and if you look carefully at the ecology of living flatfishes, how they behave on the sea floor, it begins to make a little bit of sense. Most primitive living flatfishes are ambush predators. They lie and wait on the sea floor for fishes from above them which they then pursue and eat and it's quite clear why having both eyes on one side of the head would be advantageous there, but what I think a lot of people don't realize is that the flatfishes very rarely lay completely flat on the substrate on the sea floor. They actually prop themselves up a little bit with their fins and so even having a slightly asymmetrical skull would probably give you better view of things going on above you then having no asymmetry whatsoever. So even that small amount of change I think might have given these animals a slight advantage.

Adam Rutherford: Okay thanks Matt, one final question, how would you feel about serving a Heteronectes with breadcrumbs and a slice a lemon.

Matt Friedman: Oooh! I don't know, it depends on which side the eyed side or the migrated side.

Adam Rutherford: Matt Friedman, evolutionary biologists and Gastronome and sorry about that last question, I just thought I would throw it in for the halibuts.

Kerri Smith: Honestly, Adam, this isn't the time or plaice. That's all from us for another week.

Adam Rutherford: Join us next week when we would be looking at 30 years of in vitro fertilization. Till then, so long and thanks for all the flatfish. I'm Adam Rutherford.

Kerri Smith: And I'm Kerri Smith.

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