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Breaking Science: Mice memory, X-ray tape ...

Updated Friday, 24th October 2008

Erasing memories, amazing butterflies, X-rays from sticky tape and cracking your knuckles – there's something for everyone.

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On this week's show, science fiction becomes reality as Dr Chris discovers that it's possible to wipe specific memories from the mind of a mouse. Where will this lead? He talks to Carlos Camara about X-rays powered tape, and marvels at the resilience of the butterfly: if it loses two of its four wings it can still fly.

Lastly, in 'Stuff and Non-Science', does cracking your knuckles give you arthritis?


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Chris Smith: Hello, welcome to the Naked Scientists: Up All Night which is produced in association with the Open University. I'm Chris Smith. In this week’s show, how scientists have found a way to selectively wipe out memories from the minds of mice.

Helen Scales: Crucially, it was at the point of recall that they were doing this switching on and off of the gene, and by doing that, it only affected that specific memory that they were trying to remember. They were in that box thinking, you know, I know this, I’ve been here before and I’ve been shocked before, something about this I remember, but by putting the gene on at that exact point, that’s the only memory that’s affected. It leaves all the other ones alone.

Chris Smith: That’s how memories can be selectively deleted when mice recall them, and if you think that’s memorable, what about the possibility of producing X-rays by unrolling sticky tape.

Carlos Camara: Generally, what’s going on is that a tremendous amount of charge is being separated between the two faces of the tape, between the sticky side of the tape and the roll. You get these miniature lightning strikes, and if the conditions are right, then the electrons moving in the strong electric fields can attain sufficient velocity that when they strike the tape they emit X-rays.

Chris Smith: Carlos Camara, whose team have used sticky tape to take X-ray photos of their own fingers, and you can find out how it works later in the show, when we'll also be delving into the question of whether it's true that cracking your knuckles can cause arthritis. That’s all coming up on this week’s Naked Scientists: Up All Night.

First, let’s take a look at some of this week’s other top science news stories from around the world, and to bring us right up-to-date, here’s our science news guru, Helen Scales. Now, Helen, we've all got a few memories we'd rather not remember, but now scientists are saying that they can selectively erase specific memories from a mouse’s mind?

Helen Scales: Yes, have you seen a film called the Eternal Sunshine of the Spotless Mind? I quite enjoyed it actually.

Chris Smith: I haven't actually. Who’s in it?

Helen Scales: Jim Carey and Kate Winslet, and I believe what happens is she wants to have the memories of an ex-boyfriend, I believe, taken out of her brain. But, actually, this kind of fantastical idea might not be confined to the realm of make-believe, because one day this could be a human reality. A team of scientists, led by Joe Tsien from the Brain & Behaviour Discovery Institute at the Medical College of Georgia in the States, have developed a way of rapidly and specifically erasing memories from mice.

Now the study’s in this week’s edition of the journal Neuron, and it revolves around an enzyme called calcium/calmodulin-dependent protein kinase II. A big mouthful but otherwise known as CaMKII, and this has been linked to many different aspects of learning and memory. And they used mice that have actually been genetically modified to have an over-expression of this CaMKII gene, but they also were able to turn it on and off for specific lengths of time by injecting a specific inhibitor molecule into the brains of these mice.

Chris Smith: So what exactly did they do in this study, and how did they prove that they were able to erase these memories?

Helen Scales: They took these mice, and they did various different things to them, but one of the main things was they actually gave them a shock. They put them in containers and actually put a really loud noise in them, and then later on you can look and see if that mouse has actually remembered that shock and that fear by something called the freezing response. You can put them back in the same container, and if they stop and don’t move, except for breathing, then that gives you the idea that they’ve actually remembered that shock from before.

Chris Smith: And they’re frozen because they’re anticipating it might be going to happen again?

Helen Scales: Exactly, and so what the scientists did was they actually put these, having exposed these mice previously to that fear, to that shock, they put them back into the container, up to a month later, and then they turned this gene back on again so that what they think actually is linked to the erasure of that memory, and it turned out, by doing that, the mice didn’t actually freeze so much. They didn’t freeze, they didn’t remember that fear memory from before.

Crucially, it was at the point of recall that they were doing this, switching on and off of the gene, and by doing that, it only affected that specific memory that they were trying to remember. They were in that box thinking you know, I know this, I’ve been here before and I’ve been shocked before, something about this I remember, but by putting the gene on at that exact point, that’s the only memory that’s affected. It leaves all the other ones alone.

Chris Smith: And you can see why that would be really helpful because there are lots of human conditions like post traumatic stress disorder where people remember certain memories too well and they experience all the stress that goes with it. So if you could selectively abolish a memory, in that way, that could be therapeutically very useful?

Helen Scales: It is the exactly sort of thing they’re looking to apply this to, but Tsien and his colleagues are really eager to point out this is very early stage and you won't be seeing memory wiping pills on pharmacy shelves any time soon.

Chris Smith: Well hopefully people won't erase their memory of what you’ve just told them - fingers crossed. But look, moving on to something totally different, and that’s the story of butterflies. Beautiful as they are, scientists this week have made some interesting discoveries about the way in which they fly.

Helen Scales: Butterflies have two pairs of wings. If you cut one pair off, they can still fly – which is amazing, considering it makes up over half the total wing area. But it seems that without their back wings, butterflies aren't able to perform the high speed, mid-air acrobatics that actually put off their airborne predators.

Now two American researchers, Benjamin Jantzen from the Carnegie Mellon University in Pittsburgh, and Thomas Eisner from Cornell University, published a paper in this week’s journal PNAS and describes what happened when they pulled the back wings off butterflies and let them fly off. And what they found was that they did flutter away quite happily, but they didn’t move around quite as beautifully perhaps as they would normally. To test this, what they did was they put these butterflies and moths into the lab and filmed them with 3D cameras and then analysed very carefully their flight path to see what they did and how they flew with their back wings and without their back wings.

Chris Smith: Well evolution says that the simplest and most effective strategy is what an animal will have. So why do these butterflies have four wings rather than two if they can still fly with two?

Helen Scales: They obviously need those back wings, and that’s really for their agility, and if you think about it, one of the things that’s really notorious about butterflies is how hard they are to catch. If you’ve ever skipped through a summertime meadow, chased after a butterfly, you’ll know just how tricky they are to follow, and that’s their erratic zig-zig fluttery flight. So that’s really important for them to evade their predators. Another idea is also that actually the colourful markings on those big wings that they have could actually be one way of telling their predators watch out, I'm a fast moving butterfly, you’re never going to catch me so don’t even bother.

Chris Smith: Well here’s something you can catch, which is sexually transmitted infections, just to finish off. And this is a big problem, and one person in ten in the UK who’s female in the 16 to 19 year age group has chlamydia, and this is a major worry, and it's like that in other countries worldwide as well. But now scientists and doctors have come up with a clever strategy to contact-trace people to hopefully nip this in the bud.

Helen Scales: Yes, that’s right. Now you can send online virtual postcards to tell your former sexual partners that you’ve actually just been diagnosed with a sexually transmitted disease or an STD. Now why would you want to do this? Well the idea behind it has been put forward by Andrew Woodruff in the journal PLoS Med this week, and it's essentially the idea that contacting sexual partners, especially if you’ve had quite a lot of them, is something that people just can’t face doing, but it's really important that if someone is diagnosed with an STD that they do tell anyone else who might have caught it off them to go and get themselves checked out as well.

So there’s a new website, inSPOT, which provides an easy way of sending these STD postcards, and it's really very similar to the way you send a normal greetings card online. You can choose a picture. You can type in your recipient’s email address or addresses, depending on what you’ve been up to, and from a dropdown menu you simply choose the STD that you’ve been diagnosed with. Now the good thing about this is that when your recipient gets their card, they can click on links which provides them with lots of specific information about that STD. So they can then look at what it's about and even look to see where their local clinic is so they can easily go and get themselves checked out.

Chris Smith: Do they know how effective this is? In other words, have they sort of closed the loop and looked back to see how many people who get these postcards actually act on them?

Helen Scales: There haven't been any specific studies that actually assess how effective they are at getting people to the clinics themselves, but the site is very popular, 750 people a day log on. Since it began, in 2004, 30,000 people have sent nearly 50,000 e-cards, that’s quite a few each, and the people who receive them, between 20 and 40% of them do click on information at least. So at least there’s some level of information getting through there. But yes, we don’t know exactly how many of them are stepping through the door and getting themselves checked out.

Chris Smith: Because I guess that’s the next crucial step, isn't it, to say right, you’ve got this system, it's cheap because the internet’s cheap and we know it can scale up, you could just translate the same system to anywhere in the world and in any language effectively but does it actually motivate people to go and get the problem solved? I think that’s the big question that still needs answering then?

Helen Scales: I think it is, yes, absolutely.

Chris Smith: Do they outline how they might do that?

Helen Scales: No but I'm sure that’s the next step that they want to do because this is obviously a very encouraging thing that people are using this but we'll need to know, as you say, you need to close that link and show that people are actually doing the thing they need to do and getting themselves checked out.

Chris Smith: And wouldn’t it be ironic if those e-postcards in turn developed a way to spread computer viruses – let’s hope not. Thanks Helen. That was Helen Scales with a round up of some of this week’s top science news stories. And if you’d like to follow up on any of those items, the details are on the Open University’s website at

In just a moment we'll be looking at the processes that trigger someone to develop an enlarged heart, which can be a sign of heart disease, and now scientists think they know why it happens. First though, to a novel discovery about a very common piece of stationery, and that’s sticky tape. But who would have thought that just unrolling it can produce intense bursts of X-rays. To tell us more, here’s Carlos Camara.

Carlos Camara: In our group, we’re generally interested in energy-focusing phenomena. In particular, triboluminescence, which is the emission of visible light from relative motion of surfaces; like, for example, when you chew on winter green candy in a dark room, you can see that it glows when it breaks and it rubs.

Chris Smith: I think I’ve seen something similar when you’re tearing the seal of a self-sealing envelope apart and the glue molecules seem to glow a sort of blue colour.

Carlos Camara: Yes, absolutely, and the same thing happens with sticky tape. If you take a roll of regular sticky tape into a dark room, and you let your eyes adapt for about ten minutes, and you peel the tape, you don’t even have to do it fast, just peel it slowly, you’ll see that the peeling verdicts of the tape as you’re separating it glows in this beautiful fluorescent blue.

Chris Smith: And what’s actually the physics that’s making that tape light up like that?

Carlos Camara: Well there are many mysteries that remain to be solved, especially now that we've shown that the energies are so huge at that peeling point, but generally what’s going on is that a tremendous amount of charge is being separated between the two faces of the tape, between the sticky side of the tape and the roll, so very large electric fields get formed in between the two faces at that little interface in about a region that’s not more than a tenth of a millimetre.

Chris Smith: And so, presumably, as you build up this very high potential difference, voltage, eventually you get to a point where the voltage is big enough or sufficiently large that it will discharge?

Carlos Camara: Absolutely.

Chris Smith: And overcome the resistance of the material and you get a sort of spark?

Carlos Camara: Absolutely. You get these miniature lightning strikes, to picture it in some way. You get a spark. You get a tremendous flow of current. And if the conditions are right, then the electrons moving in the strong electric field can attain sufficient velocity that when they strike the tape they emit X-rays.

Chris Smith: Well, so it's not just visible light, it's X-ray light as well that’s coming off?

Carlos Camara: That’s what we have shown, indeed. But for you to get X-rays out of sticky tape, as far as we know, you have to put it in a vacuum. So what happens in the vacuum is that by removing the gas particles from that peeling point, then you allow the electrons to move freely across the gap from one side of the tape to the other without striking any gas molecules. So they attain full speed before they hit the other side. So they hit the other side going very, very fast and emit X-rays when they get stopped.

Chris Smith: But if you didn’t do it in a vacuum, they would bash into air molecules which would slow them down and they wouldn’t be going fast enough to make x-rays?

Carlos Camara: Exactly, but certainly fast enough to make light, and that, I really strongly encourage all your listeners to try to peel sticky tape in a dark room, it's spectacular.

Chris Smith: Spectacular it might be but why is this useful? What does this mean we might be able to do or what do we understand now about this that we didn’t before?

Carlos Camara: When scientists think of triboluminescence, they now must think that the emission can be high enough to make X-rays, so this is new. The X-ray emission is remarkable because it comes out in these bursts, so a lot of X-rays come out together in roughly a billionth of a second. You can get almost a hundred thousand X-rays coming out at once. Now, there’s also the surprising fact that we got so many X-rays out of this effect that we were able to take X-ray images.

Chris Smith: When you actually do this, could you see any other application of doing this and what sort of dose of X-rays come out? What sorts of things could you see? If this were a medical setting, let’s say, to give it some perspective, what sorts of things could you image like this?

Carlos Camara: Well we were able to image the bones in our fingers, for starters, so the dosage is equivalent to a low dose dental X-ray. If you unroll tape in a vacuum, you can get sufficient X-rays to image the bones in your fingers.

Chris Smith: So does this mean then, this could be a very clever way of making X-rays without having to have massive accelerators and high voltage apparatus? You could do this with something obviously a little bit more complicated than a reel of tape but the principle would be pretty much the same?

Carlos Camara: That’s exactly the point, and it is a completely new way. Possibly it has a potential of becoming the least expensive way of generating sufficient X-rays to take an image.

Chris Smith: I wonder how many rolls of sticky tape they got through just doing that research. That was Carlos Camara from the University of California, at Los Angeles, where he and his team are producing X-rays with sticky tape. That work’s published in this week’s Nature.

And from the mystery of adhesives to another mystery now which is why the heart becomes enlarged under certain conditions, such as when someone develops high blood pressure, for example. Unlike the normal beneficial enlargement that takes place when someone exercises, this abnormal form of enlargement called pathological hypertrophy can have irreversible consequences for the way the heart works; for instance, it can lead to the development of a condition called dilated cardiomyopathy which in turn can cause heart failure. But now researchers think they’ve found out why it happens, which means they may also have uncovered a way to stop it. Here’s John Scott.

John Scott: Well, as I'm sure many of your audience realise that one of the major diseases that affects certainly the Western world is heart disease. What we decided to do is begin to look at the very early stages of the development of this disease, and effectively it's really quite simple. It comes down to the mechanics of the heart and how the heart is able to beat, because the heart is a muscle. And if you put stress on that muscle, for example, if you run up and down stairs all day long, you’ll develop that muscle or get stronger like your leg muscles or your arm muscles, and that’s a really good thing, and that’s why many of us, including myself, run every day. But if other aspects of stress that are less good for you happen, there’s another kind of growth that happens to the muscle, and that is a growth called pathological hypertrophy. And obviously, with the word pathology there, it's not a very good thing.

Chris Smith: And what sorts of things could unleash that stress? Could that be something like long-term high blood pressure, for example?

John Scott: Yes, hypertension is high blood pressure, just general living a very stressful life; arthrosclerosis, obviously blockage of the arteries, because it makes the heart have to work harder. And where these deleterious things really play out is in the individual cells in the heart that do the beating, and those cells are called the myocytes. And in terms of thinking about what we were studying, myocytes, when they’re under pathological stress, grow in size. But they don’t just become bigger. They also undergo a developmental change that usually means that genes are turned on

Chris Smith: So what you’re saying is that the cells in some way remodel themselves to accommodate the change that they’re being subjected to but this isn't beneficial?

John Scott: Yes, they adapt to the situation in a bad way. They undergo what has been termed a foetal gene response. So genes that are present in the foetus suddenly begin to reappear in these myocytes.

Chris Smith: And do we know why that’s bad?

John Scott: Yes, we do to some extent because it allows the cells to grow in ways at the wrong time. And we don’t really know the whole story to that but that’s the best bet. One of those genes is a protein called AKAP-Lbc, and that’s what we've been studying.

Chris Smith: How does it work and what does it do?

John Scott: Well, that’s a very good question. So this protein, it's called a scaffolding protein, and if you think of what scaffolding does on a building, it holds the outside of a building up while you are able to work on it. It provides many platforms for people to walk on. Inside myocytes, scaffolding proteins serve to provide platforms for many enzymes to be placed in one place in the cell, and so increasing the level of this protein allows more of those enzymes to be concentrated in a particular place in the cell.

Chris Smith: And is that a bad thing necessarily? I mean what are the consequences of doing that?

John Scott: Well this is the interesting thing is under normal conditions it's a good thing. But when you’ve got too much of the protein, and you’ve got too many of those enzymes in the one place, it becomes a bad thing. Because what it does is it drives the foetal gene response. It makes it more likely for this to happen.

Chris Smith: Oh so they physically are responsible for helping to switch on those genes which you have shown and which you know have a bad effect?

John Scott: Absolutely. It’d be a little bit like when you think of certain drugs that are poisons in high levels but if you get a small amount they’re good for you. This is the same thing. You’re just switching them on too much.

Chris Smith: Is this an irreversible effect? So if I had this problem and therefore I have this accumulation of these proteins that you’ve found, does that mean that if I make the problem I have go away, then I’ll get better?

John Scott: There’s ways to control it. It will never go away but you can actually, what we call, manage the situation and you can decrease your stress level, you can reverse the hypertrophy at one level, but it will never completely go away. Another important point here is that the hypertrophy, as we describe it, is just really the early warnings of heart disease. Because if you can recognise hypertrophy, you can then prevent them from moving on to the next level of the disease which is usually dilated cardiomyopathy, which is when the heart really fails and results often in death.

Chris Smith: And now that you’ve actually identified AKAP-Lbc, the protein that does this, does this mean then that this a new target where we could possibly make some drugs that might block that accumulation and therefore prevent hypertrophy from getting worse and perhaps progressing to dilated cardiomyopathy?

John Scott: So that is exactly the long-term scenario for this project, and I think it's very important for people listening to the programme to understand that we’re definitely beginning to move towards that direction. But, in reality, drugs that will target this are going to take a long time to be developed. I think that the next step in this project will be looking to see what happens in genetically modified mice, where we can see if we can prevent the onset of hypertrophy by modifying the protein AKAP-Lbc so that it doesn’t bind all the enzymes as I described.

Chris Smith: If you look at drugs that we know save lives in people who have heart disease, is it worth exploring any of those to see what their impact is on this protein you’ve now discovered, because could it be that some of them are having their life-prolonging and disease-preventing effect by inhibiting this?

John Scott: Very good question. One of the ways that you treat heart disease at the moment is to use beta anergic blockers which are drugs that effect receptors on the surface of heart cells. The signals that come from these receptors will, ultimately, in some cases, and I stress in some cases, pass through AKAP-Lbc. So there may also be an advantage of exploring some of those drugs in the context of what happens to AKAP-Lbc.

Chris Smith: John Scott, he’s at the University of Washington in Seattle where he and his team have discovered the chemical cause of an enlarged heart. He’s published that work this week in the journal Molecular Cell.

This is the Naked Scientists: Up All Night with me, Chris Smith, and time now for this week’s Stuff and Non-Science where we massacre myths and bash bad science, and flexing, in readiness, her elbows, wrists and fingers, hopefully without cracking them, here’s Diana O’Carroll.

Diana O’Carroll: This week’s Stuff and Non-Science is all about cracking your knuckles and was contributed by Turnip Sock. Yes, it's that irritating noise that some say gives you arthritis. With the truth about joint cracking, here’s Graham Tytherleigh-Strong.

Graham Tytherleigh-Strong: Rightio, so the question is cracking your knuckles will give you arthritis. I think the short answer to that is no, there’s no evidence to prove that that is the case.

What the knuckle is, is actually the metacarpal phalangeal joint so it's the joint that joins your finger to your hand. It's actually a synovial joint that’s filled with synovial fluid which is a lubricant. The synovial fluid itself contains a number of dissolved gases like oxygen, nitrogen and carbon dioxide dissolved within it. When you crack your joint, what you effectively do is you just pull the joint and stretch it out. That causes the space inside the joint to expand and so creates a negative pressure so that the gases then come out of solution. As they come out of solution, you get a number of bubbles and it's really that rapid production of bubbles that causes the cracking sound. But it doesn’t actually damage the articular cartilage at all.

There have been no real studies that have looked into developing arthritis, but there have been a number of relatively large studies that have looked at what happens to the joints themselves, and there’s been one study that showed that if you cracked your joints for a long time, you could end up with joint swelling and a decrease in grip strength. There have been other studies that have shown that you can actually damage the ligaments around the joint, so the joint becomes more loose, and also the tendons can dislocate around the joint. But there’s certainly been no study to show that you get an increased instance of arthritis if you crack your knuckles.

Diana O’Carroll: Graham Tytherleigh-Strong there, telling us that cracking your joints won't do much harm at all. He’s from the Nuffield Hospital in Cambridge.

If you have any more non-science that needs stuffing, then send it to me,

Chris Smith: So you can crack away with impunity, although you might end up with lax joints as a result. Thanks Diana. That’s Diana O’Carroll with this week’s Stuff and Non-Science.

That’s it for this time. We’re back next week with another round up of the latest findings from the world of science. The Naked Scientists: Up All Night is produced in association with the Open University, and you can follow up on any of the items included in the programme via the OU’s website. That’s at You can, of course, also follow the links there from the BBC Radio 5 Live Up All Night web pages.

Production this week was by Diana O’Carroll from the, and I'm Chris Smith. Until next time, goodbye!

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How does a butterfly flutter by? David Robinson explains the science of flight.


Here's the research used by the team to make the programme.

In the news

‘Inducible and Selective Erasure of Memories in the Mouse Brain via Chemical-Genetic Manipulation.’
in Neuron 60

‘Hindwings are unnecessary for flight but essential for execution of normal evasive flight in Lepidoptera’
by Benjamin Jantzen and Thomas Eisner

'inSPOT: The First Online STD Partner Notification System Using Electronic Postcards'
by Deb Levine et al
in PLoS Medicine 5:10


'Correlation between nanosecond X-ray flashes and stick-slip friction in peeling tape' by Carlos Camara et al in Nature

"AKAP-Lbc Mobilizes a Cardiac Hypertrophy Signaling Pathway."
by Graeme Carnegie et al in Molecular Cell 32





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