Naked in Norway

06 May 2012
Presented by Chris Smith.

.... with a scientific climax in bird masturbation!

In this episode

01:00 - Reassembling the Remains of Ancient Sea Creatures

Espen Knutsen is reassembling the remains of ancient pleiosaurs.

Reassembling the Remains of Ancient Sea Creatures
with Espen Knutsen, Natural History Museum in Oslo, University of Oslo

Chris -  Espen Knutsen is reassembling the remains of something you really wouldn't want to swim with...

Espen -  If you think of a turtle maybe without the shell and you add a long neck to that and sometimes a small head and sometimes a large head, depending on what sort of plesiosaur we're talking about, and you basically have the plesiosaur body plan sort of laid out.

Chris -  Were they vicious?

Espen - Some were.  Most of the ones we have here from our locality at leastplesiosaur are small-headed.  I mean, the head is probably about 30 centimetres long and the teeth are very slender up to maybe 2 centimetres long and very thin, perhaps it's half a centimetre or so in thickness, and probably ate mostly squids and small fish.  And then you have the large-headed pliosaurs which is another group of plesiosaurs that had heads up to maybe 2 ½ to 3 metres.

Chris -  Metres?

Espen -  Yeah.

Chris -  And teeth.  How big?

Espen - And teeth like cucumbers basically, yeah.

Chris -  And probably quite a bit sharper too.  So they're eating things they would've found in the sea.

Espen -  Yeah, the pliosaurs obviously would probably eat anything they would come across - the plesiosaurs or ichthyosaurus which are the other group of marine reptiles you find there, and also larger fish.

Chris -  If they're living in the ocean, it would've been pretty cold here, wouldn't it?

Espen -  Yeah, the temperature in the ocean 150 million years ago in Svalbard is estimated to have been about 10 degrees based on isotope analysis, which is obviously cold for a modern day reptile at least - if you put a snake in a 10-degree water, it's not going to do much.  So obviously, these reptiles would've had some way of keeping themselves warm, whether they were endothermic or just stayed warm due to their large sizes.  It's still unknown but maybe in the future, we'll know something more about that.

Chris -  Big fish like salmon sharks are effectively warm-blooded because the core of the animal is so far from the outer part of the animal, where the water is cold, that just metabolism alone means that they're running at near human body temperature inside and stuff closer to the surface less so.  So do you think these plesiosaurus are probably similar?

Espen -  Yeah, possibly at least the large pliosaurs.  It's a bit different with the smaller plesiosaurs because they have a fairly large surface area compared to body volume and they might even have migrated south, parts of the year.  Maybe the sea temperature was a bit warmer in the summer and obviously, that's comparable to faunas in England at the same time and they might have migrated back and forth through our locality and the English localities annually perhaps.

Chris -  When were they swimming around?

Espen -  All of our animals are from the late Jurassic which is right on the border to the Cretaceous. We're talking about 150, 140 million years ago.

Chris -  Would they have evolved originally in the ocean and stayed there or could they have come out of the land and gone back into the water?  Do we know where they came from?

Espen -  We don't know too much about the origin of plesiosaurs, other than that they originated from land living tetrapods. So they were some sort of reptile that once in time, in the early to middle Triassic, started wondering into the water and adapted to an aquatic lifestyle there and we do have middle to late Triassic sauropterygia, which is this group of fossils from other places in the world, which are sort of a precursor group to these plesiosaurians.

Chris -  It's quite interesting that the invasion of the land happens from water onto land and then the animals go back into the water obviously because there is some kind of niche there and now, here we are 100 million plus years later, finding them.  So how do you go and get these specimens?

Espen -  Well how this all started is basically, we go walk around on the Svalbard and it's quite barren up there.  It's basically an Arctic desert so there's not much vegetation so we can walk around and look at the surface for bones that are weathered out from the surface and roll down the hill, and then we follow these little bone pieces uphill and we can find the source sometimes and other times we don't.  And if we do find the source of the pieces then we can start brushing slowly and then maybe there's more coming out, and maybe there's not.  If there is, then we can start excavating whatever's in there, based on what we can see from the preliminary excavations, we decide whether or not it's worth starting to excavate because it's quite an ordeal to remove tonnes and tonnes of overburden and every year, we remove by hand 100 tonnes or so of shale.  So, we want to be a bit picky about what we're actually taking out.

Chris -  And when you spot one, how do you get it out?

Espen -  Once we've finally decided which one to take out, we remove the older burden, brush clean the surface of the bone and then we add wet toilet paper, and some wet plaster, and a piece of burlap dipped in that plaster and then we cover the whole thing with plaster and iron and so on, until we have lid and then we dig down around the lid, around the specimen, cover the sides with more plaster. Eventually, we have sort of a mushroom of plaster, shale and bone that we flip over to the other side and then cover the other side with the same wet toilet paper and plaster again and we cocoon the whole thing in that and transport it back to the museum.

Chris -  So that's the summer job and then winter time comes and you're here in the lab, now picking apart that mushroom or that cocoon, that plaster cocoon to get the find out.  So how do you then process it?  What have we got here?  This looks like a bed of plaster.  Is this one that you've basically got going here?

Espen -  Yeah, so this is a plesiosaur lap.  We've already prepared from one side, so what we do when we come into the lab, we first let it dry for a couple of months because we can't glue it when the specimen is wet, and then have a little saw, we cut the cocoon open and start picking away with little tweezers and little brushes, so all the loose shale, and simultaneously glue and stabilise the bones.  And then once one surface is done, we can toilet paper and jacket, plaster jacket, that side and then we flip the whole thing, take the lid off the other side and do the same thing there.  Eventually, we get this nicer-looking specimen here with no shale and basically, stabilised bones and then Myalee is sitting here.  She has to prepare it, really - she scrapes away excess shale and gypsum crystals that sometimes grow on these bones, and stabilises these specimens further.

Chris -  Can you give us a guided tour of this one that we're looking at?  So, there is in front of me, the size of a large dining table with - I can see some of the obvious bones.  There are vertebrae and things, all encased in here, but can you talk us through this fossil and just explain what the various bits are?

Espen -  Yes, so this is part of a plesiosaur that we excavated 2 years ago and what we have here is we have the whole vertebral column from the head which isn't here now, but we have that in separate jackets and through to the body and the shoulder, and then we have parts of the body and just before the hip, the rest of the skeleton has weathered out and we have...

Chris -  And ribs there?

Espen -  Yeah, all these. They're body ribs and then you have the neural arches which goes on top of the vertebra there, and then all these flat bones, the four flat bones here are from the shoulder girdle which is on the plesiosaur and is basically as a flat plate on the front of the chest. That connects the front limbs.  So we have the upper arm bones here and the lower arm bones are reduced to these very short triangular-looking things and then all the fingers are coming out nicely forming a flipper.

Chris -  Is that effectively the wrist there?  Are they sort of the equivalent of carpal bones?

Espen -  Yeah, all of these little round bits are the wrist, and this one and this one, these two triangular bones which are the size of...One is the size of a coin and the other one is twice that size.  They're the lower arm bones, so the radius and ulna that we have.

Chris -  And then these little ones, are they the equivalent of phalanges in me, the finger digits?

Espen -  Yeah, that's all phalanges.  So, what we have in plesiosaurs is something called hyperphalangy which means that they increase the number of phalanges within each digit, which is something they do to form this paddle shape of the limb.

Chris -  So what's special about the dinosaurs that you're getting out or what's special about the Svalbard specimens compared with ones that we'd find elsewhere in the world?

Espen -  Faunal composition-wise, it's basically the same.  We have the large headed pliosaurs, we have the long-necked plesiosaurus and ichthyosaurs, but all of these, when you look and go into detail, and look at all the details of the limbs and the vertebral column and the shoulder and so on are slightly different from what we see from other places like the Kimmeridge and Oxford plain in England for instance, and all actually constitute new species.  We have five new species of plesiosaurs and four new species of ichthyosaurs from this place and we still keep digging out more every year.  We have 30...

Chris -  And lots of them.

Espen -  Yeah, we have 31 specimens so far and probably another 60 out in the field that we have mapped already and we find another 10 or so every year as well.

Chris -  So, what do you think will be ultimate outcome for this one because I can see the bones have all been glued together?  Will you actually be able to assemble this?

Espen -  Well this one is actually special that it's articulated.  All the bones are laying in the position that they were when the animal was alive.  The problem is that the animal has fallen onto its back when it's at the sea bottom, so the rib cage and everything has collapsed on top of the vertebral column, but all of these bones go nicely together so what we're going to do eventually when we get the room as well in the museum, this is a big animal, probably 4 or 5 metres long, we want to reassemble all the bits and lay it out nicely so people can come and view it.

11:20 - Harvesting Energy from all forms of Sunlight

Solar cells waste much of the energy from the Sun because they cannot use it efficiently, but Per-Anders Hansen from the University of Oslo may have a way to improve the situation...

Harvesting Energy from all forms of Sunlight
with Per-Anders Hansen, Department of Chemistry, University of Oslo

Per -  Sunlight consists of small energy particles called photons and these can have a lot of energy like ultraviolet light or blue light or they can have medium energy like red light or visible light, or they can have very little energy like infrared or heat radiation.  When these photons hit the solar cell, what they do is that they knock loose one electron and this electron can then travel around in our circuit and give us power.  And to do this, the photon needs a minimum amount of energy.  But if they have more than this, they still only knock loose one electron and this is why solar cells are not more efficient.  They could be like two or three times more efficient.

Chris -  So if we had a way of taking some of those photons that have verySolar panel high energy, and converting them into more photons at a lower energy, we could get more electrons out and therefore, the overall efficiency of the cells would be much higher.

Per -  Exactly.  If you take these high energy UV photons and simply cut them in two, cut the energy in two so we have two particles of half the energy, then you would get twice the amount of power out of those photons.

Chris -  Can we do that?  Can you convert light of one wavelength like UV into a longer wavelength like that, like you're saying?  Is that possible?

Per -  Yeah, it's possible and it's actually quite easy.  It's easy to turn one photon, one ultraviolet photon, into one visible or one red photon, that's actually quite easy.  That's what's going on in fluorescent tube lightings actually.  So that we sort of know how to do.  The trickier part comes when you want to cut it in two so that you get actually twice the amount of light or photons out from the ultraviolet light.  That's where the trouble is.  We can do that for very high energy photons.  That has been done very efficiently.  The trick is to do it for photons that actually exist in the sunlight.  That, no one has done yet.

Chris -  So, we know how to do this for high energy photons like ultraviolet but because there's not much ultraviolet reaching us here at the ground, you're saying that although the materials exist to do it, we haven't got really the light that can make use of that.  So we need a new material that will work with the photons we do have and cut them in this way.

Per -  Yeah.  We know how to convert very high energy ultraviolet light that exists like in space outside our atmosphere, but the ultraviolet light that comes down to Earth that we get sunburnt off, it doesn't have enough energy to work with those kind of materials.

Chris -  How are you grappling with it?  What are you doing to try and overcome that?

Per -  Well, I use very peculiar synthesis method called atomic layer deposition.  It gives me a very high control of which atoms sit next to each other.  You usually have two components in this kind of material, something that absorbs the light you want, and something that emits the light you want.  And you need these to be sort of in every other position, so you have something that absorbs and around it has to sit these emitters and around the emitters, it has to sit absorbers.  So, if they are mixed up randomly so that you have one bunch of emitters over there and one bunch of absorbers over there, it's not going to work.  But if you kind of really control what's next to each other, you have a lot more control of what's going on and the physics that's going on in the material.

Chris -  So would that array work because the absorber soaks up the energy and passes it to the emitter next door which then spits out the photons of the wavelength you do want and they're then carried off and absorbed into the semi-conducting material to actually make the current.

Per -  Yeah, that's exactly how it will work.

Chris -  So what materials can we use?  Are you basically trying different combinations of anything to see if you can get the right sorts of absorption and emission or do you already have some candidates that you know are the right sorts of chemicals to use?

Per -  Yes, to both.  We know what we need.  We just need something that absorbs ultraviolet light and blue light, and many things do that so for example, sun cream absorbs ultraviolet light.  Sun cream consists of titanium oxide for example.  OK, titanium oxide, that could maybe be a good candidate.  Then you just need to find something that emits light very well, so then I thought of, ok, what emits red, a TV emits red.  In a TV, what is it that makes TV go red is europium.  So, combine those two and that works.  So of course, that is not my big secret.  My big secret is more fancier than that, but that is kind of the quest you're going through - just what can absorb it and what can emit what I want and then just combine it.  And then you need to combine it in these very particular ways that everything sits at the right place.

Chris -  So those atoms are deposited in just the right configuration.

Per -  Yes.

Chris -  If you can get this to work, what sort of step change in efficiency could we achieve with a photovoltaic?  What will it go from to?

Per -  Well, a normal silicon solar cell that you can buy on the market today is between 16 and 20% efficient usually, maybe a bit more sometimes. For red light or light between red and 900 nanometres or something like that, it's actually much more efficient. It's more like 60, 70, 80% efficient.  So, if you actually can take all that other energy, convert it to red light then it's actually no problem to just take the normal solar cell that you have at your cabin and you suddenly get 50% efficiency out of it.

Chris -  Which is a dramatic improvement.  I think the figure is something like the amount of sunlight that falls on the Earth in one day is equivalent to the amount of energy that the entire world consumes in a year.  So if we can get cells up to those sorts of efficiencies, we actually could do quite a lot to offset what we're concerned about, sort out climate change and all that kind of thing from the energy industry.

Per -  Yeah, we have plenty of sunlight.  If we can just convert it efficiently and of course, cheaply, then actually we don't really need anything else.

Chris -  So, how far away do you think you are from realizing the technology you're working on?  How long before we see these novel coatings going on to photovoltaics so that you can harness the extra energy we're currently just chucking away?

Per -  There is some testing going on now around the world doing this - one ultraviolet into one red or something like that. But this one to two photon cutting, that hasn't been done yet.  I hope that we can maybe see that around the world in maybe 5 years, 10 years, I hope.

Chris -  So I need to come back in 5 or 10 years and see if you were right.

Per -  Yeah, come back then and see how I'm doing.

Chris -  I'll do that.

18:35 - Falling Lemming Populations

Nils Christian Stenseth discusses the dwindling lemming population cycles...

Falling Lemming Populations
with Nils Christian Stenseth, CEES, Department of Biology, University of Oslo

Chris -  Lemmings now, and although these animals don't really throw themselves off precipices, in recent years, their population cycles have nosedived.  The reason, discovered by ecologist Nils Christian Stenseth, is one that British train companies would be proud of.  It's down to climate change causing - you've guessed it - the wrong sort of snow.

Nils -  A lemming is a small rodent and the Norwegian lemming is a very charismatic one, yellow and black.  It used to be that every 3 to 4 years, there were massive numbers of lemmings in the mountains then the next year it was gone.  That is what we referred to as the lemming cycle.  And the lemming cycle occurs for lemmings as well as for many other small rodent species, and the lemming cycle was a characteristic feature.  There are many stories written about this. A translation of the bible to the Nordic languages, the swarms of grasshoppers in the middle east, there was a footnote by the translator saying that this is like lemming cycles.  So, it's a well-known phenomenon.  Since the mid '90s, there have been no regular lemming cycles.

Chris -  Well, they just stopped, just vanished.

Nils -  They had vanished and that is well-known.

Chris -  But the lemmings are still there.

Nils -  Lemmings are still there, but the massive occurrence at the regular time periods disappeared.  So that has been an interesting thing to try to find out why.  We did work doing statistical time series analysis, where we looked at the dynamic structure of the lemming population and how that was affected byLemming climate, temperature and precipitation and the like.  What we found was that the kind of snow that was falling was a critical determinant on whether it was going to be a regular cyclic phenomenon or not.  It used to be that when snow came in this part of the world, it was cold so it came as dry and soft, so that a small space between the ground and the snow could build up.  And within that space, lemmings could survive very well and they reproduced and built up a population that was high in the spring and couldn't continue to be high if it didn't crash during the summer.

Chris -  Why would their population have this 4-year cycle because the snow is going to come every year?  So, why does their population grow and then suddenly plummet?

Nils -  When they crash, they crash to very low densities and they crash most likely because of the predator population building up. So they crash to very low levels and it takes time for them to build up.  And to build up very high densities, they need a period that they are free from heavy predation and that's what they get during the snow, during the winter period, and it takes 3 to 4 years to build up such a population.  But in the mid '90s, all this was gone and what we found in this paper published in Nature was that the snow had changed also from being soft and dry to wet.  Hence, the lemmings could not build up.  One year ago, I predicted that there would be a lemming peak all over Norway, as a matter of fact, all over Scandinavia because the previous year had been very cold, very good snow conditions and we were then in a middle of a good winter. And true enough, there was a lemming peak last year all over Norway.

Chris -  So, are you seeing a return to nice cold winters again or is the snow still unreliable and soft and wet?

Nils -  Well, I'm not a climatologist.  I think that there were two good winters for lemmings.  Climatologists tell us that won't be as regular a phenomenon as it used to be.  So, I think the lemming cycle has not come back.  I think the lemming cycle has gone, but you will occasionally have high years with lots of lemmings, but it won't be regular.

Chris -  What's that done to the predators and from an ecological point of view, what are the onward consequences?  Is this just sort of a mathematical phenomenon that if the conditions come right again, it will re-establish or are they going to be onward impacts which are irreversible?

Nils -  I think the lemming cycle will come back if the climate changes, but it might take quite a bit of time for the whole ecosystem to recover because when the lemmings are gone, that affects the ptarmigan because when predators have no lemmings to eat then they'll go to other species including ptarmigan.  It also affects the interaction between the Arctic fox and the red fox.  The red fox being competitively superior to the Arctic fox.  Unless there are lots of lemmings, then the Arctic fox does well.  So it will change the whole ecosystem.  So maybe the Arctic fox will go extinct on the mainland and only survive on the small part of Spitsbergen in the Norwegian territories.

23:40 - Immune Attack of Cancer Cells

Cancer cells may escape attack by the body's immune system by releasing chemicals to suppress it, but we may be able to overcome this in the future.

Immune Attack of Cancer Cells
with Alexandre Corthay, Institute of Immunology, University of Oslo

Chris - And now, to cancer and how to persuade the immune system to attack it, Alexandre Corthay.

Alexandre -  We know that the immune system protects us against cancer, but there is still very little known about how this immune system protects against cancer and this is what we are trying to find out.  We are using an experimental system in the mouse.  The type of cancer we are studying is a bone marrow cancer, it's called multiple myeloma and also lymphoma.  We're interested in immune cells called T-helper cells, so we're interested in how T-helper cells fight cancer.

Chris -  Can you talk me through the experiments you've been doing in these mice to work out how the immune system usually protects them and what goes wrong when the cancer occurs?

Alexandre -  What we think is going on when people develop cancer is not that there is anything wrong with the immune system.  What we think is going on is that the cancer cells somehow manage to fool the immune system to evade the immune response presumably by producing molecules that will suppress the immune system.

Chris -  When a cell becomes cancerous, how does the immune system pick that up normally and remove that cell to stop a cancer occurring?

Alexandre -  There are two major ways.  One way is by recognising stressed cells.  So any stressed cell in your body will show it on the cell surface.  There are some stress markers and that will be recognised by the immune system and the immune system will simply kill the stressed cells.  The other way, which is even more refined, is that the immune system is able to recognise mutations in self.  Mutations that are required for normal cells to become a cancer cell.  There is a certain number of mutations in the DNA that are required and the immune system is able to recognise, not directly the mutations, but the effect on proteins.

Chris -  And any cells displaying that sort of danger signal are just going to get deleted straight away.

Alexandre -  Exactly.

Small cell lung cancerChris -  But obviously, not all the time because otherwise no-one would get cancer.

Alexandre -  So, most of time - so that's why most of us do not have any cancer.  It's also probably the reason why it takes so many years to develop cancer.  Usually, people develop cancer after the age of 50, so we are extremely well-protected against cancer.  But sometimes the cancer cells manage to evade immune response.

Chris -  And how do they do that?

Alexandre -  It is not well-known yet, but one major way to do that is to use the communication system that the immune system use.  So, immune cells communicate with each other and cancer cells are known to produce some signal molecules that the immune system use normally to suppress itself.  At the end of a normal immune response, the immune system shuts it off and this is probably what the cancer cells do - they tell the immune system to shut off.

Chris -  So by chance, the cancer evolves the ability to produce some of the chemicals that would normally damp down the immune response, thereby, effectively putting it under the immune radar.  It's just looking like healthy normal tissue to the immune system or it's basically suppressing the immune system where the cancer is, stopping it being destroyed.

Alexandre -  That's absolutely correct, but I should stress that there are some very good indications that the immune system never gives up.  So even in a cancer patient with established cancer, the immune system still fights back and there's a battle going on in the cancer patient.  This is very important because it means that it should be possible to stimulate, to help the immune system to tip the balance towards cure of the cancer patient, and this is something we really hope for the future.

Chris -  Well, people have been working on the field of immunotherapy where the idea is you would take some of the tumour out of the patient, take immune cells from the patient in the dish and use growth factors to try and drive the immune cells very hard to overcome whatever that inhibition is coming out of the tumour, and sometimes you get immune cells that will attack the tumour, but often not.  Because there have been a few case reports written up of people who have had complete remission of cancers that way, but all too often, it doesn't work.

Alexandre -  Yeah, so this is called - what you're mentioning is called adaptive T-cell transfer.  So culturing T-lymphocytes in vitro and then giving them back to the patient and this has shown some very promising effects.  One key issue there which is also valid for the development of cancer vaccines, is to know what type of immune response to trigger.  Many different types of immune responses are used by the body against various types of infections or cancer, and it is still not very clearly known what is the right type of immune response that is the best to fight cancer, and this is what we're working on.

Chris -  What have you found so far?

Alexandre -  We have found that, in a certain mouse model, that the optimal immune response to fight cancer is an inflammatory immune response driven by the type of T-cells called TH1 cells.

Chris -  And if you could induce that in people who have a cancer where the immune system is not combating it, would that push the cancer into remission then?

Alexandre -  This is our prediction.  This would be the two arms of the immune system to stimulate - in one way, to stimulate an inflammatory environment especially in the tumour which will be very important to recruit immune cells, particularly T-cells and the other important aspect is to stimulate TH1 cells which recognise very specifically the cancer cells and which tell other cells to kill the cancer cells.

Chris -  What about risks though because one worries that if you get the immune system attacking, what is self-tissue?  It's your own body.  There's a concern that the immune response might spill over and become mistargeted away from the tumour and at healthy tissue and you then end up with an autoimmune disease.

Alexandre -  That's correct so that one should be always very careful when triggering the immune system because as you said, the immune system is very potent.  It may trigger autoimmune diseases, it will also kill you if the immune response is too strong.  However, cancer is definitely very dangerous to people.  Cancer is killing people and on the other hand, current cancer therapies are also very tough to the patients like chemotherapies, and irradiation.  So, I think there's always a balance, but I can really see a future where immunotherapy will be perfectly developed and will help the patients with minimal side effects.  But of course, when you treat a serious disease, it is very difficult not to have any damaging effect on the patient at all.

Chris -  And the results you've got in the mice with the haematological tumours, will that transfer directly to other kinds of malignancy?

Alexandre -  We cannot say that yet, but in my view yes, and from the literature, not much has been done at that level of details.  But it looks very much like this is a general way of how the immune system fights cancer.  So this TH1-driven inflammatory response.  That's my expectation that this will translate to other types of cancer and also to humans.

Chris -  Alexandre Corthay.  

31:27 - Fighting Cancer Cell Resistance to Radiotherapy

Cancer cells can develop resistance to radiotherapy, which means large doses have to be given which can damage nearby cells. Scientists Nina Edin and Erik Pettersen at the University of...

Fighting Cancer Cell Resistance to Radiotherapy
with Nina Edin, Erik Pettersen, Biophysics and Medical Physics, Department of Physics, Oslo University

Chris - One very effective cancer treatment is radiotherapy, but this can have side effects when healthy tissue is also harmed, and that's because although most cells can be killed by very small amounts of radiation, the dose has to be high enough to prevent cancer cells becoming resistant to the treatment.  Now though, Nina Edin and Erik Petterson have discovered how cancer cells become resistant and how to turn this off.

Nina -  About 80% of all cell lines that have been investigated and, we believe, most normal tissue, has a property which makes them very responsive to radiation doses at about 0.3 gray which is about a 10th of the normal dose you give in radiation therapy.  So, if you can exploit this feature then you can give much smaller doses altogether and spare the patient from the radiation to the normal tissue.

Chris -  Okay, do we understand the mechanism and are we in a position to put cells into that hypersensitive state, so that we can use very low doses of radiation to destroy them without having to do lots of other damage to healthy tissue in the body?

Nina -  The problem is that when you give a small dose then you induce a resistance to the next level dose.

Chris -  So you give the small dose, you will wipe out some cells, but there will be a small hard-core group left behind that you won't get rid of, and moreover, they will be resistant.  Then the next time you come in with another small dose, they're just not goitng to be destroyed.  So how can we get around that?

Nina -  Well, what we really have discovered is that something is secreted into the medium that can be affected by low dose irradiation, but not by high dose irradiation.

Chris -  So, you're saying that cells have an ability to detect radiation at a low level, using a receptive molecule which then leads to the secretion of a factor which then, in turn, renders the cells resistant thereafter.

Nina -  Yes, that is what I say and we have found the mechanism in the cells that keep this factor of secretion going and we've found a way to inhibiting this mechanism.

Chris -  What are the chemical nuts and bolts that are doing this?  What are the molecules that are doing it?

Nina -  The molecule that induces the resistance is TGF Beta 3 which is Transforming Growth Factor 3.  The mechanism depends on INOS - Inducible Nitric Oxide Synthase and if we inhibit the effect of this molecule, we can stop the whole process and reverse the cells to the original hypersensitive state.

Chris -  So what locks that effect in the cell?

Nina -  It has to do with how the TGF Beta 3 works because it is only active when it is not bound to a molecule called Lap.  So this Lap inhibits the effect of the molecule and it's sort of a system to control the activation of it.  So what happens is that nitric oxide synthase produces nitric oxide and these nitric oxides takes away the Lap so that this cannot re-associate with the TGF Beta 3, and that then this remains active inside the cells and start some other processes that makes it - that all go around like a self-sustaining mechanism.

Chris -  So putting that together, you have a small amount of radiation and that triggers the activity of INOS -Inducible Nitric Oxide Synthase enzyme which makes some nitric oxide that removes the Lap molecule which activates the TGF beta molecule and that then triggers a locked-in change in the biochemistry of the cell, rendering it resistant to more radiation.  So if we block those actions then the cells would remain potentially hypersensitive to these very low doses of radiation.  So Eric, how could you use this knowledge?

Erik -  So far, we have been talking about cancer here, but this could have some influence also above or in other areas.  TGF beta then seems to be able to turn off hypersensitivity.  And for a person who have been, for example, experiencing irradiation, that could be very positive because often, that would be small doses and if you could for example increase TGF beta 3 in some way after a very small dose, that might actually influence on the response of this irradiation.  So, this could have some influence.  WRadiation therapy of the pelvis. Lasers and a mould under the legs are used to determine exact position.e don't know this yet, but this could have some influence also in other areas than just cancer research.

Chris -  So if we had a way of addressing the signal to healthy tissue, we could protect healthy tissue.  We could leave cancerous tissue vulnerable and this means that anti-cancer therapies like radiotherapy could be made much more effective at much lower doses.

Erik -  Yes.  By targeted administration for example, that could be a possibility.  The important thing is that we have sorted out the mechanism which influences radiation responses at very low radiation doses.

Chris -  And Nina, why do you think cells have this anyway?  What's it there to do, this mechanism normally?  Why has evolution selected it?

Nina -  That's a good question.  I'm not sure.  I think it does more things than we know yet, so I'm not sure that this only addresses hyper radiosensitive.  I think it's a kind of stress response, but one thing I didn't say was that we have also tried to administer the TGF beta 3 after irradiation and it has an effect also 4 hours after they've been given the radiation so it works backwards which also is interesting if you have accidents.

Chris -  And what could be the consequence of deactivating that signalling in healthy tissue if you block the ability to see TGF beta like that.  Will the cells in any way suffer?

Erik -  This is a very good question because you know, when cells respond by hyper radio sensitivity, it could be a normal response just to get rid of cells which have got some radiation damage, just to get rid of them.  If the damage is not too bad, they can be easily restored by stem cells, from stem cells.  But if the damage is going on for a long time then they have the possibility to turn off the hyper radio sensitivity, do the repair and maintain the tissue by taking care of the cells.  So, this could be a normal process which has some meaning in the restoration of tissues in general and we have some indications that this protection - we should call it protection of course - not only works against radiation but also against some toxic chemicals.  So, it's a more general stress factor than just radiation.

Chris - Erik Pettersen and Nina Edin.

38:38 - Unearthing the Cause of Mass Extinction

Dr Henrik Svensen reveals what craters in Africa can tell us and if the cause for mass extinction can be unearthed by looking at what lies beneath our feet......

Unearthing the Cause of Mass Extinction
with Henrik Svensen, Physics of Geological Processes, Department of Physics, University of Oslo

Henrik -   Let me bring you back 10 years or 15 years when my colleague discovered some amazing structures from seismic data in offshore Norway, almost like big volcano structures and you can see them on seismic reflection data extending perhaps 4 or 5 km down into the seafloor. He was really intrigued about this and wanted to understand what they were.

Chris -   How big are they then in terms of cross-section because obviously, that's very tall, but what about across?

Henrik -   Up to 10 km across.  It's a really big kind of crater structure and to make the long story short, I started doing this work in South Africa to look at fairly similar type of structures exposed on land to really get a better feeling for what this could be.  What I found was really amazing - from big structures, big craters filled with crushed rocks - but I didn't find any volcanic rocks.  So, my conclusion was that, these structures were formed by gas release, explosive gas release from the Earth's crust and that the gas release was triggered by the action of igneous rocks, melted in the Earth's crust.

Photo of caldera of Askja VolcanoChris -   Why did they form where they formed then?

Henrik -   They formed because in the subsurface, 183 million years ago, that part of South Africa was intruded by melt and the melt triggered gas formation and that led to overpressure and then blow out structures almost like volcanic structures releasing the gas to the atmosphere.

Chris -   It's like an exhaust pipe for a volcano.

Henrik -   Yes, that's a fairly good description.

Chris -   And what would be the effect of these things?  What would come up through them?  For how long? And what would be the local environment?

Henrik -   That's been our subject of research for many years and we have different approaches to this.  We do the field work, we look at the minerals inside these pipe structures, and we also do a theoretical modelling to understand what's coming out of these pipes.  And in conclusion, the gas composition that's coming out is related to what type of rocks are heated in the subsurface.  So if you heat sand with pour fluids, with water, you form watervapour.  If you heat shells which are rich in organic matter, you might form methane or CO2.  But for the case of South Africa, the main gas component we think was methane and then of course, things started to get interesting because methane is a greenhouse gas and we're trying to quantify the volumes of gas release and it's definitely within the range that it would've created global warming if it was erupted fast enough.

Chris -   Gosh!  So how long would these things have remained active do you think?

Henrik -   That's a question which is extremely difficult to answer.  We're doing the best we can with the best available methods and we can say that everything happened within half a million years.

Chris -   That's quite short, isn't it?  What sort of volume of gas are we talking about?

Henrik -   Billions of tonnes of gas.

Chris -   Gosh!  So that's going to be quite a few degrees potentially of global temperature change if all that sort of gets burped out in one convulsive release.

Henrik -   That's right and if you look at what happened on Earth at the same time as these pipe structures formed, there was indeed a global warming episode in the early Jurassic.  So we think that perhaps these two were linked together.  The main challenge today however, is to find that direct link, not only to say that this happened at the same time but actually to say that they were linked process wise and that's really difficult.

Chris -   So what are the outstanding questions?  Where are you thinking this needs to go next to try and resolve this?

Henrik -   I think we need to understand extinction mechanisms and what can actually lead to the demise of life on Earth, and at the moment, there is really a big confusion about process.

43:02 - Tooling around with Chimpanzees

A number of animals use primitive tools, but how does this behaviour begin? And what can it tell us about how we got started doing the same thing millions of years ago? Adriana Hernandez-...

Tooling around with Chimpanzees
with Adriana Hernandez-Aguilar, CEES, Department of Biology, University of Oslo

Adriana - These chimpanzees that I study live in the Savannah which is very different from the typical forest habitat that you see in documentaries.  They have a very harsh, 6-month long, dry season. We're trying to figure out how they can make a living there.  I spent 2 years in Tanzania studying these chimpanzees and during this time, I discovered a new kind of tool use.  

We know that chimpanzees use tools in many different contexts, but this specific kind of tool use had not been reported before.  They were using tools to dig up roots like potatoes and this behaviour is very interesting because it was one of the behaviours that people used to believe was uniquely human.  There has been a lot of debate about what made us human - if it was the eating meat, the hunting, or digging for tubers, like the hunter gatherers in Africa or other parts of the world still do today.

Chris -  So why had this been missed before?  Why had no one seen the chimpanzees doing this?

Adriana -  Because tool use in chimpanzees is not present in all the populations.  Different chimpanzee populations have different types of tools.  So we have never studied this population before.  Before my study, this place called Ugalla had only been in short term surveys and I was the first one that was there long term, so for 2 years.  And because the chimpanzees are not used to humans, that means we cannot follow them and we cannot observe their behaviour all the time. I was also trained as an archaeologist, so the discovery was based on indirect evidence.  We found the holes that they have dug up with knuckle prints from their hands, with faeces, with hairs, with finger marks, and of course, we had heard chimpanzees vocalising from those sites, and when we arrived there, the chimpanzees were gone, but the material evidence was left there.

Chris -  And the tools they use, tell us about those.

Baby and mother chimpanzee at Baltimore ZooAdriana -  The tools are very incipient.  That means they are not very developed.  For example, hunter-gatherers using tools also for getting tubers, the tools are very long, are heavy, are sticks, usually hardened by fire in the deep.  These tools the chimpanzees are using are expedient in the sense that they are very new.  We don't think they had been using them for very long.  They are very varied.  Some of them were pieces of a log that had fallen down.  Others were pieces of bark that they just scraped the soil off, we think and then when it got easier, they dug by hand.  So, we are thinking that this is a behaviour that has not been around for very long.  So it has been discovered not very long ago.  They haven't had time to have very complex tools to do such behaviour.  But the fact that they are using these tools and getting these resources makes it very interesting.

Chris -  What do we know about how the chimps pass on the knowledge?  Did they do it by passive observation - I watch you use that pencil to write on that bit of paper and I therefore work out how to do the same or is there active teaching going on?  Does a mother take a child and actively encourage it to do the same behaviour or don't we know?

Adriana -  We know that from populations where the subjects are used to humans so you can observe them.  A lot of the tool use is by observations of the mother usually using the tools.  Since chimpanzees live in a fission / fusion society, that means they never - the group never - travels together all the time, but they divide into small parties and then these parties change in composition by minutes or hours, or days.  So you are never with the same chimpanzees, but the only constant is the mother.  Dependent offspring always travel with the mother, so they have a lot of opportunity to learn by watching how the mothers uses the tools.  We also know that mothers facilitate tool using.  For example, when they crack nuts with a stone, anvils and hammers, they leave the tools for the infants to use.  They also have been observed to place the nut in a specific way to make the hammering more successful and there has been some reports of active teaching but it has not been very common.  People need to see more of this evidence to actually say that, yes, they do have active teaching.

Chris -  If you can work out how the chimps evolve this fairly new behaviour from scratch, does that tell us anything about how we, or at least our early ancestors, evolved to use tools?

Adriana -  We actually think that tool use probably evolved many times in our evolutionary history, but by learning the constraints of tool use, by learning the adaptations that tool use allowed primates to have, we can learn a lot about tool use in humans and how we evolved.  

Actually, I was just part of a paper which compares the oldest human technology Chimpanzee2.6 million years old from Gona, Ethiopia with mostly chimpanzee tools.  And all of the behaviours that you can infer from the archaeological record are present in chimpanzees except for two of them which is the distance that the tools were carried, hominids carried tools for longer distances.  The other behaviour that chimpanzees do not have is that hominids competed with big carnivores of that time - toothed cats, leopards, lions - and chimpanzees do not compete with these predators in Africa.  So those are the only two differences that we could see and I am actually working on a paper right now about transport and it seems to be that if we go deep into what we know about chimpanzee transport, it's not so different from what we know about hominid transport.  So, it may be that we will just be left with one of the differences, which is hominids competed with carnivores, but I want to make sure that we understand that this competition is not direct, but they were having access to the same food types.  They were eating meat from large animals, but we don't think the competition was direct. There is a big debate if these hominids obtained the meat by hunting or scavenging and we don't know that yet.  The very first hominids probably did not do much hunting.

50:07 - Sperm Evolution in Songbirds

Terje Laskemoen explains the speedy sperm found in the songbird and the reasons for its evolution...

Sperm Evolution in Songbirds
with Terje Laskemoen, Natural History Museum, University of Oslo

Chris -   Now, we discuss sperm cells that biologist Terje Laskemoen describes as hugely paradoxical.

Terje -   They have such a simple task to reach the egg first to achieve the fertilisation but then it's the most variable cell, with respect to size, in the whole animal kingdom.

Chris -   What are the variations then?

Terje -   You have sperm from for instance nematodes, small worms you don't want inside you which are maybe a couple of micrometres big, to  Drosophila sperm reaching almost 6 centimetres.

Chris -   Six centimetres!? but they're flies.  They're tiny flies.

Terje -   Yeah, that correct.  The sperm length is actually 10 times length of the individual.

Chris -   Why? And how do they use something like that?

Terje -   Well, it's not fully understood actually why they're that big, but of course, there will be a trade off then. So instead of producing millions or maybe billions of sperm, they have a few but really large ones.  And for some bizarre reason, that works in these species, but that's of course an exception.

Chris -   And what about in the birds?

Terje -   The birds, they have quite special sperm compared to human sperm.  People are used to the tadpole thing - rounded head, swimming, beating with their flagella, looking like a tadpole.  In birds, the sperm are quite different.  They are actually helical-shaped (the head and the midpiece).  Their way of moving in the medium is actually to spin around their own axis while also beating their flagella.  I like to use the phrase tadpole sperm in human, Ferrari sperm in birds.

Chris -   Are they really faster then?

Terje -   They're much faster, definitely.  Up to ten times faster, yes.

Chris -   And the obvious question then with that dramatic difference is, why?

Terje -   I'm working on songbirds only.  I had to specify that because sperm from other groups of birds are not necessarily that helical-shaped.

Chris - That's intriguing.  Let me ask a question then, are the birds that you'reGreat tit studying, are they - promiscuous?

Terje -   Yup, definitely!

Chris -   So there's a sort of selection - there's a selection going on here because there's a chance that the female bird is putting it about a bit and the males are also putting about a bit.  There's a strong competition going on here.

Terje -   Yeah, definitely and that's why this system is so fascinating because you have bird species which are socially monogamous and also genetically monogamous.  In those species, we see that sperm is really variable, both within the males and also between the males.  Whereas in other bird species, they are socially monogamous, we have a mother and the father siring the offspring, but genetically highly promiscuous.  So, males fly around, females accept males coming.

Chris -   What fraction if you've got that setup where you've got pairs of birds?  What fraction of the offspring of that pair of birds is actually sired by the male in that pairing?

Terje -   Yeah, that's really, really variable.  So, the extremes are in Australia where up to 80% of the offspring are sired by another male than the social male feeding them.

Chris -   Okay, so there is massive pressure here to make sure your sperm, are the ones that actually are passed on to that generation and that's why they're going for the intense speed?

Terje -   Yes, there is a relationship between speeds and the level of promiscuity.  The more sperm competition, the faster the sperm swim.

Chris -   So intuitively then if the sperm are in that level of competition and speed is of the essence then there's much more pressure to keep the size tightly focused compared with those animals and the birds that you said tend to be more monogamous.  There's less pressure so the sperm can get away with a wide of variation in size and speed.

Terje -   Yeah, exactly.  That's what it points out to right now.  Whereas there is a strong relationship between speed and this level of promiscuity, the variation in sperm size is extremely tightly linked.  So, say in a monogamous species, genetically monogamous, you have a high variation in sperm size and the more sperm competition, the lower the variation it gets until these extremes in the far end with the really high levels of promiscuity, with the sperm almost looking identical between males.  So, we have actually published a paper stating that you can show me your sperm, I can predict your level of promiscuity.

Chris -   Does the same apply to humans?  No.

Terje -   Well, humans are, I would say moderately promiscuous.  We have a species we can compare us to.  So say, chimpanzees...

Sperm and EggChris -   They're very promiscuous, are they?

Terje -   They are more promiscuous and they have faster sperm than us.

Chris -   So it fits the model.

Terje -   Yeah, it fits the model and actually, there was a paper published some 5 years ago on this, looking at chimpanzees, humans and gorillas, and it's in the predicted direction.  So the gorillas have the slowest sperm, humans are in the middle, chimpanzees are the fastest.

Chris -   So it's not just size that's important.  Speed is of the essence.

Terje -   And then no one has looked at this variation in sperm size in great apes yet, but there was a recent paper on insects, reporting what we have found.  Some people now checked this out in social insects so, bees, bumble bees and ants, and they found the same pattern.  So the more sperm competition or higher level promiscuity, the lower variation in sperm cells.

Chris -   A slightly delicate question to finish.  Do the birds oblige when you ask them for sperm samples?  How do you get the samples?

Terje -   Well, we give them a gentle massage and that's an interesting question because some people, when they ask me what I do, if I want to go the long way, I will start out telling them I'm a biologist, I'm working with birds and so on, and finally get to that I'm working on sperm evolution.  But on the other hand, I could just tell them that I'm actually masturbating birds for my job.  

But I want to finish off in a more serious manner.  The birds, they have these sperm storage organs, just closely to their cloacae that actually makes their cloacae looks like a tube in the breeding season when they have the peak of sperm production.  Those are actually what we're actually massaging to force the ejaculate it out.  This is done in 5 seconds when you're experienced.  You can take the blood sample as we do, take the sperm sample, match the wing the size, band the bird and release it within a couple of minutes.

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