The team investigates the latest developments in global warming, stem cell research and the effect of dopamine on the brain. They also answer the age old question ‘does it take seven years for chewing gum to be digested?’
Chris Smith: Hello and welcome to the Naked Scientist’s Up All Night with me, Chris Smith. Coming up - why the global warming scenario just got a lot worse.
Helen Scales: It's long been assumed and hoped for, let’s admit it, that there’s actually one good thing about the increasing carbon dioxide in the atmosphere, and that comes down to plants. Because, if you think about it, if you increase the abundance of the raw material that plants absorb and turn into sugars, surely they’ll then grow faster and ultimately fix more carbon dioxide. But it now seems that exactly the opposite might actually be true.
Chris Smith: And we'll be finding out why in just a moment, when we'll also be meeting a scientist who’s developed a new technique to keep track of where stem cells go in the body.
Helen Blau: We were very much aided by developing non-invasive imaging technology, which means that you can see where the stem cells are in a live mouse without sacrificing that mouse. Which is also, of course, advantageous because you can watch them over time and monitor what’s happening to the stem cells.
Chris Smith: That’s Helen Blau. She’s also now discovered a stem cell that makes new muscle. So we'll be hearing how it works in just a moment. Plus we'll also be solving the mystery of what happens to those pieces of chewing gum that accidentally get swallowed. Do they really loiter in your intestines for seven years? We'll be getting to the bottom of that mystery later. That’s all coming up on the Naked Scientist’s Up All Night.
But first, let’s take a look at some of the top scientific discoveries from around the world this week with our science correspondent Helen Scales. First Helen, researchers have made an interesting discovery in relation to how treatment with bone marrow stem cells could help patients that have suffered a stroke.
Helen Scales: This is a study published in the journal PNAS by Darwin Prockop and his colleagues from the Tulane University Health Sciences Centre in New Orleans, and they’ve described how stem cells extracted from bone marrow and injected into the brain could help reduce the damage caused by a stroke. Now previous studies have suggested that what’s going on when stem cells are injected into the brain of mice is that they’re actually inducing the growth of new brain cells. But what Prockop and his team have done now is discovered that in fact it seems to be that we’re actually leading to a reduction in the number of brain cells that are dying and damaged when a stroke happens.
Chris Smith: Oh right, so rather than replacing cells, the benefit he’s arguing is because more cells are surviving when you do this, but does he know why?
Helen Scales: What seems to be happening is that the stem cells are actually triggering existing neural cells called microglia and also part of the immune system called macrophage cells to produce substances that actually protect the brain cells against the damage caused by a stroke but also by reducing the inflammation that’s associated when blood flow to the brain actually is restricted.
They’ve also been looking at this at a genetic level, and they’ve actually discovered that following a stroke nearly 600 genes seem to be switched on. And what Prockop and his teams have found is that by adding stem cells 10% fewer of those genes are actually switched on. Which really suggest that it's this anti-inflammatory and immune response that the stem cells are triggering is somehow linked to the activity of those genes.
Chris Smith: Where are they getting the stem cells from that they’re injecting?
Helen Scales: These are bone marrow stem cells extracted from the bone marrow of the mice that were being treated. And this potentially means that this will be applicable to human subjects because we know that stem cells can quite easily be extracted from bone marrow.
Certainly this could be opening up a new avenue of research and potentially for new treatments in the future for stroke patients so this is quite exciting news.
Chris Smith: Well it certainly is important because obviously the number of people suffering a stroke every year is measured in the tens of thousands. So anything we can do to make that better is definitely a step forward. Now from the health of humans to the health of the planet, because there’s a bit of a quandary over CO2 levels in plants and things this week?
Helen Scales: Yes, that’s right. Now when it comes to predicting the effects of climate change, it's long been assumed and hoped for, let’s admit it, that there is actually one good thing about the increasing carbon dioxide in the atmosphere and that comes down to plants. Because, if you think about it, if you increase the abundance of the raw material that plants absorb and turn into sugars, surely they’ll then grow faster and ultimately fix more carbon dioxide. But it now seems that exactly opposite might actually be true.
Chris Smith: How can that possibly be the case?
Helen Scales: Well this study actually hit the front cover of the journal Nature this week, and it comes from a team led by John Arnone from the Desert Research Institute in Nevada and David Schimel from the National Centre for Atmospheric Research in Boulder, Colorado, and they conducted a four year experiment with tallgrass prairie ecosystems.
Now what they did was that they dug out large chunks about five cubic metres each of natural grass ecosystems, soil and everything else, and they took them from the wild prairies in Oklahoma and put them inside huge chambers that allowed them to precisely control the climate.
Chris Smith: So this was a sealed environment so they could monitor gas in, gases out, how the grass and the appropriate ecosystem that goes with it would respond?
Helen Scales: Exactly. So everything was controlled. And inside the chambers, what they did was actually closely mimic what would have happened in the wild for the first year of the experiment. So they had the same temperature, the same rainfall, everything was the same as it would have been if it had been left outside. And then, for the second year of the experiment, they actually took half the plots and then simulated a heatwave, putting up the temperature by four degrees.
And what this did, and this is now the key to this, what seems to have switched our thinking on this, is that it caused a drought - which may be we would have predicted actually. It dried out the plants to the extent that they actually weren't growing so much. But the amount of carbon dioxide that they fixed dropped by two-thirds which is a huge amount. And perhaps what’s most important is this happened not just for the year when the heatwave was there but for the following year as well.
Chris Smith: Oh that’s interesting. So, in other words, they were growing and fixing less CO2, the next year there was a knock-on effect of the drought?
Helen Scales: That’s it.
Chris Smith: Even though, presumably, the conditions were restored to normal?
Helen Scales: Yes, third year, it was all put back to normal. But it took a long time for the system to recover to what was going on pre-heatwave. And you might say well a four degree temperature increase, that’s quite a lot. You know, current models aren't really predicting that much of an increase. But actually, in terms of local peaks in temperature, we are actually seeing this kind of thing starting to happen.
So this could mean that in the near future, if we are seeing more heatwaves, it could seriously reduce the amount of carbon dioxide that land-based ecosystems are able to absorb, making the whole situation of climate change potentially even worse.
Chris Smith: But do they know why they saw the effect they did with this knock-on effect? Do they understand why that’s occurred?
Helen Scales: I think at this stage this is really just an observation. So more studies are going to be needed to understand more about exactly why it's going on. But I think the bottom line here is that climate modellers are going to have to maybe start taking into account what’s going on with these plants and that we can’t necessarily just rely on plants to mop up our excess carbon dioxide for us.
Chris Smith: It certainly sounds dodgy and I hope we get to the bottom of that one and it's not going to turn out like that because if that’s the case things could be quite serious in the future. One other thing that’s had a rough ride because of rising temperatures and possibly global warming is coral. So what’s the story with coral this week?
Helen Scales: Yes, I'm going to pick things up from slightly gloomy news to slightly happier news. With the latest update from the Census of Marine Life Project - whose researchers have just discovered hundreds of new species of coral and other reef critters living in the tropical waters of Australia.
Now this year is International Year of the Reef, and among the activities to mark the year is a series of expeditions to the famous Great Barrier Reef off the Queensland coast and also to Ningaloo on Australia’s western coast where scientists have been systematically hunting for new species that until now have kept themselves secrets to human divers.
Chris Smith: Which sorts, just corals?
Helen Scales: Most of the time we kind of concentrate on the hard corals which actually build the reef, but soft corals, which are the brightly covered creatures that live on reefs and they look a bit like bunches of flowers and trees and they actually provide an important habitant for lots of other reef inhabitants as well. But it's expeditions like these and many others that form part of the Census of Marine Life which is a phenomenal ten year programme which is aiming to map and catalogue as much of the biodiversity in mysterious wide oceans as possible.
Chris Smith: So what have the team discovered this week?
Helen Scales: Well so far they’ve discovered three hundred different types of soft coral, which half of which they think are new to science. They’ve also uncovered loads of other new things. Tiny crustaceans called isopods which live on the corals. I think they’ve found about a hundred new species of those. These are often nicknamed the vultures of the sea because they like to eat dead fish which is rather nice. They’ve also found lots of new species of things called bristle worm which also hide in the crevices of reefs.
This kind of information seems very basic but it's very important to know about the number and the location of species in systems like coral reefs for us to really begin to understand how they work and, more importantly, how they’re actually changing and being affected by the habits of mankind in the current world.
Chris Smith: Quite because we can’t conserve something unless we actually understand it to start with I presume?
Helen Scales: Absolutely. So a bunch of lucky researchers get to go back to these sites for the next three years to continue gathering data like this and also to monitor how the reefs are getting on.
Chris Smith: And to finish off, Helen, on a high note, because actually this is quite an amazing feat of microbial engineering isn't it? The fastest organism on the planet, it turns out, is a fungus?
Helen Scales: Absolutely, and not only that but it's fungus that loves nothing more than a steaming pile of manure. In fact, we mustn’t overlook these microscopic relatives of toadstools because they do us a big favour - because without them our world would quite quickly fill up with dung.
Chris Smith: But what do they actually do?
Helen Scales: Well they break down manure basically. They live on it, they eat it, they break it down - it would sort of hang around if they weren't there to help us. Now what Nick Money and his colleagues from Miami University in Oxford, Ohio in the States have revealed, in their paper in the open access journal PLoS One, is just how these microscopic fungi fling their spores around like miniature ballistic missiles at record-breaking speeds.
Chris Smith: Why do they need to do that?
Helen Scales: Right, well this is because they have a problem. You might imagine that life is bad enough if you’re confined to live and feed on animal droppings. But to make matters worse, the only way these fungi survive and spread is when their spores are eaten by herbivores and scattered far and wide in their droppings.
Now except for a few rarities like mountain gorillas, there aren't many herbivores that really go in for eating their own faeces, so instead the fungi have got to come up with ways of flinging their spores away from the offending paths of poo. Now it's been known for quite a while that these fungi have evolved high pressure water pistols to squirt their spores out. But it happens so fast that up to now no one’s actually studied how they work.
Now what Money and his team have done is put these fungi in front of ultra high speed cameras running at 250,000 frames a second to capture that moment when the spores are launched. And they’ve discovered that they actually shoot out at twenty-five metres a second.
Chris Smith: That’s about a hundred kilometres an hour isn't it?
Helen Scales: It's huge and actually it corresponds to a whopping 180,000 Gs of acceleration over the distance of a couple of metres. So really in terms of acceleration, this is the fastest flight that’s ever been recorded in nature.
Chris Smith: But these particles that they’re projecting are just a fraction of a millimetre. So that’s an amazing feat isn't it really?
Helen Scales: They are.
Chris Smith: So how do they actually do it? That’s the key question isn't it? How are they achieving that?
Helen Scales: Right, well it comes down to a phenomenon known as osmosis. Now what the fungi do is they pump sugars and other small molecules into their cells, and because this raises the concentration inside the cell, water naturally follows it and builds up pressure inside the cells. But what the researchers have discovered is that the pressure inside the fungal cells that fling out the spores are actually no higher than in any others parts of the fungi. So the key to the ultra high speed spore launch is the way that the cells rupture and very, very quickly release all the energy at once.
Chris Smith: So it just goes sort of spurt and the spores come out? An intriguing finding but how do we think this could be used. Because usually when people make a discovery like this, there’s some kind of application on the end of it isn't there?
Helen Scales: Absolutely. Well understanding how these fungi propel their spores around could have a lot of applications because similar fungi we know cause diseases in humans and lots of them actually kill off crops as well. So if we can perhaps interfere with the way that they spread their spores around, it might be a good way of stopping them from being quite so prolific. And also the squirting mechanism is similar to the way droplets of ink are sprayed through the nozzles of inkjet printers. So perhaps the world of technology will have something to learn from dung-loving fungi’s speedy seeds.
Chris Smith: Thanks Helen. That was Helen Scales with some of this week’s top science news stories. And if you’d like to follow up on any of those items, they’re all on the web at open2.net/nakedscientist. Still to come - we'll be hearing why Christmas loses its appeal as we age. Apparently it's all down to the brain’s pleasure chemical, dopamine, and we'll also be chewing over the mystery of what happens to those pieces of chewing gum that accidentally get swallowed.
But first to a discovery this week that could hold the key to treating a host of muscle disorders because scientists at Stanford University in the US have solved a longstanding mystery about muscle stem cells. Here’s Helen Blau.
Helen Blau: A fundamental question of interest is whether there are stem cells in muscle and if those stem cells that are residing in the tissue can be used and stimulated to regenerate muscle tissue. And what we've shown is that a single cell can do both and we've reached that for muscles.
Chris Smith: So how did you first of all identify those stem cells and where are they?
Helen Blau: So the stem cells are in the muscle tissue. They have their own little compartment lying along the muscle and normally they’re quite quiescent; that is inactive, unless there is injury. We have them throughout our life. But what we did was try various markers and use what’s called the fluorescence activated cell sorter which recognises, using a laser, antibodies that bind to the surface of the cells and then you can purify them which really enriched for the stem cell and we proved that it had these classic properties.
Chris Smith: So what you’re saying is you managed to find a combination of chemical markers on the cell surfaces that singled them out as having stem cell-like properties?
Helen Blau: That’s exactly right.
Chris Smith: So then how did you prove that they were genuinely producing new muscle cells because that’s the kind of hallmark of being a stem cell isn't it?
Helen Blau: Yes, it is. Well we were very much aided by developing another technology in the lab. It's a non-invasive imaging technology which means that you can see where the stem cells are in a live mouse without sacrificing that mouse. Which is also, of course, advantageous because you can watch them over time and monitor what’s happening to the stem cells.
Chris Smith: So how do you see the stem cells in situations like that?
Helen Blau: So we use a bioluminescent marker, a marker that glows. What we do is take a gene that makes that and put it into the batch of cells that we isolate. And then, when we inject that cell into the body of a mouse, then we can see whether we've gotten the cells to expand up in number because the signal gets brighter and brighter.
Chris Smith: And how do you know those stem cells are actually producing muscle cells? In other words, muscle that could work to help the mouse move, for example, and they’re not just turning into glowing cells that are just sitting there?
Helen Blau: Well we've validated that by doing the classical tissue sectioning as well. So we could show that the glowing cells also make new muscle fibres and they contributed to old muscle of the host. They had all the hallmarks that are typical of mature muscle. They could also respond to damage by greatly increasing in numbers.
Chris Smith: So given that you’ve now got this cocktail of chemical markers, it means you can go to a muscle, you can find the stem cells, sort them out and then potentially you’ve proven that they can be integrated back into muscle to do repair and turn into new muscle. How do you see this being applied because it sounds to me like there could be umpteen different physiological problems in conditions in humans that you could use this technology for?
Helen Blau: Yes, you’re right. So, of course, the next thing we’re doing, we’re working on this as we speak, that is to isolate the human muscle stem cell, and we know that there are many human conditions. We have muscle wasting. You have loss of muscle, sarcopaenia, atrophy. This happens, for instance, if you’re prone for long periods after a hip replacement. You lose your muscle strength and often you never walk again. One of our goals is to see if we can stimulate the stem cells in a person because we know that the stem cells are there in older people, and if one could find a way to stimulate them, they may be able to be mobile much sooner.
So they’re the challenges that so far no one’s been able to grow these stem cells. So now we've identified them, next challenge, grow them in culture and find out what stimulates them to do that. Because we know injury signals in the body stimulate that but we have no idea what those injury signals are yet.
Chris Smith: Stanford’s Helen Blau explaining how she and her colleagues have tracked down the adult stem cells that can make new muscle and they’ve published that work this week in the journal Nature.
Now apart from the risk of losing muscle strength as we get older, it looks like each of us is also destined to lose our sense of excitement. It turns out that how the brain responds to the chemical dopamine changes as we get older. To tell us more, here is Karen Faith Berman.
Karen Faith Berman: Dopamine is really the neurochemical of the brain that is the hallmark of pleasure and it also helps us process painful incidents. There is a group of neurons deep in the brain called the mid brain and this is where dopamine is actually made in the brain where it's synthesised. And from this signals emerge that course to various parts of the brain, particularly the prefrontal cortex which is kind of like the CEO of the brain which helps us keep on task and process rewards, appreciate them.
So the first question we wanted to answer in human beings is what is the relationship between the amount of dopamine that’s made deep in the brain and how the brain processes rewards. So we used PET to use the dopamine, positron emission tomography, a very powerful technique. And then we put people in a PET scanner, we can measure how much dopamine is in the brain and we can map it to specific areas. And we use something called functional magnetic resonance imaging (or FMRI) which allows us to see what parts of the brain are working hard. And during that part of the testing we had people looking at a slot machine and anticipating getting a reward - in this case money - and we measured brain activity during that anticipation.
Chris Smith: And when you compare the brain signals in people who are old and young for this pleasure chemical, dopamine, what is the difference?
Karen Faith Berman: First of all, there was no difference in the amount of dopamine that was actually synthesised deep in the brain between older folks and young folks. So that was a bit of a surprise. So that is equal. But what differed is sort of the bang for the buck that you get for that dopamine synthesis when you’re aging. So for a given amount of dopamine that’s made deep in the brain, older folks had less activity in their prefrontal cortex during a rewarding experience.
Chris Smith: So does this mean then that although they get the same amount of dopamine being made deep in the brain, they’re not actually responding to it as vigorously as a young person, therefore they may not be experiencing as much pleasure. So, in other words, you’re less likely to get as switched on or as keyed up about something exciting as a young person would?
Karen Faith Berman: That’s exactly right, or at least their pleasure is quite different, and I think experientially that’s what many older folks will tell us.
Chris Smith: And so does this mean or is this the basis, do you think, of the fact that maybe we learn less quickly when we’re old? Because when we’re young, you tend to pick up things very, very fast, but as you get older, you might have to repeat them more times, and is that because you’ve got less signal, less reward signal to reinforce the good learning you’ve just done than a young person and that’s why you slow down?
Karen Faith Berman: That is actually a terrific question and I think you’re exactly right. In fact, this very same brain circuit that we've been talking about is key for learning, absolutely key. Because learning in of itself is often a rewarding experience and we all know even in children that the more you can make learning fun, the better they do.
Chris Smith: But the big question then is why? Why should I want or why should I have evolved to learn less well as I got older? Is that because I am genetically programmed to become fixed in my ways, which to me doesn’t sound like a good thing, especially with the internet and all this technology around me, I need to be able to handle that and I need to be able to learn how to use it.
Karen Faith Berman: Well I can’t tell you why we've evolved that way. I think it's an excellent question. But I would like to say that I think that something we've learned from this study, advice that I’d like to offer, if I can, to people as they age, is the more you can engage this circuit, the more you can engage in novel activities, the more fun you can have, the more new experiences you can seek out, the better this circuit is going to function.
Chris Smith: So it's a case of use it or lose it when it comes to the brain’s pleasure chemical. That was NIH researcher, Karen Faith Berman. Her study was published this week in the journal PNAS.
You’re listening to the Naked Scientist’s Up All Night with me, Chris Smith, and it's time now for this week’s stuff and non-science where we blitz myths and bash bad science. And looking at a claim that she’s found hard to swallow this week, here’s Diana O’Carroll.
Diana O’Carroll: Hello and welcome to Stuff and Non-Science where it's all getting rather sticky with chewing gum. The myth goes that if you swallow chewing gum, it’ll stay in your intestines for seven years. Is that true? I spoke to Dr Barry Bogan of Loughborough Centre for Human Development and Ageing. This is what he had to say.
Dr Barry Bogan: Chewing gum will not stay in your intestinal track for seven years because the gum part of chewing gum, the gum base, while not digestible, will be passed along and eliminated just as most things that we eat, such as swallowing whole corn on the cob kernels will come out the other end much as they went in. So chewing gum will do the same thing. It is not sticking to the surface of your stomach or intestines the way it's sticky to the concrete pavement.
The myth in part comes from some medical cases where a one and a half year old, two and three and four year old children did swallow chewing gum and also swallowed other objects like coins and seeds, it was either pistachio or sunflower seeds, with the shells and those other objects stuck to the gum and that formed a mass which blocked their intestines and then that had to be removed by medics. But in anyone over about seven years of age the intestinal track is large enough and active enough to pass almost all of that stuff out.
Diana O’Carroll: So there we are. It’ll take a long time to digest if it gets stuck to other non-foodie objects you might happen to eat. But in most cases, it’ll just pass right through you in a matter of days. Next week, our non-science will be all about space capsules.
Chris Smith: And if you’ve got a myth that you’d like Diana to investigate on your behalf, then drop her a line to firstname.lastname@example.org.
That’s it for this week. We’re back next Monday with another round up of the world’s hottest science, including a new way to tackle blindness.
The Naked Scientist Up All Night is produced in association with the Open University and that means you can follow up any of the items that are included on the programme via the OU website. That’s at open2.net/nakedscientist. Alternatively, you can follow the links from the Five Live Up All Night website which will also take you there.
The production this week was by Diana O’Carroll from the nakedscientist.com and I'm Chris Smith. Thanks for listening and until next time, goodbye.
Emma East asks the question: Can stem cells help stroke victims?
Delve deeper into the stories featured in the programme with these references:
In the news
'Stem/progenitor cells from bone marrow decrease neuronal death in global ischemia by modulation of inflammatory/immune responses'
by Hirokazu Ohtaki, Joni H Ylostalo, Jessica E Foraker, Andrew P Robinson, Roxanne L Reger, Seiji Shioda and Darwin J Prockop
in PNAS 2008 105:14638-14643; published ahead of print on September 15, 2008
Curious? Uncover the secrets of bone marrow stem cells and stem cell therapu.
'Prolonged suppression of ecosystem carbon dioxide uptake after an anomalously warm year'
by John A Arnone, Paul S J Verburg, Dale W Johnson, Jessica D Larsen, Richard L Jasoni, Annmarie J Lucchesi, Candace M Batts, Christopher von Nagy, William G Coulombe, David E Schorran, Paul E Buck, Bobby H Braswell, James S Coleman, Rebecca A Sherry, Linda L Wallace, Yiqi Luo & David S Schimel
in Nature 455, 383-386 (18 September 2008)
The Fastest Flights in Nature: High-Speed Spore Discharge Mechanisms among Fungi
by Levi Yafetto, Loran Carroll, Yunluan Cui, Diana J. Davis, Mark W F Fischer, Andrew C Henterly, Jordan D Kessler, Hayley A Kilroy, Jacob B Shidler, Jessica L Stolze-Rybczynski, Zachary Sugawara, Nicholas P Money
In the interviews
‘Self-renewal and expansion of single transplanted muscle stem cells’
by Alessandra Sacco, Regis Doyonnas, Peggy Kraft, Stefan Vitorovic & Helen M. Blau
in Nature (advance online publication 17 September 2008)
'Age-related changes in midbrain dopaminergic regulation of the human reward system'
by Jean-Claude Dreher, Andreas Meyer-Lindenberg, Philip Kohn and Karen Faith Berman
in PNAS (published ahead of print September 15, 2008)