This week, horse racing, equine flu, a hedgehog hospital and a trip to the local zoo - we’re looking at how vets keep animals healthy and why that’s good news for humans too. Plus, how a dose of caffeine perks up a solar panel, cell transplants to boost wound and tissue repair, and a gene breakthrough for obesity...
In this episode
Sticky cells to heal wounds
with Adam Perriman, University of Bristol
Initial steps towards developing a better way to use transplanted cells to repair wounds and regenerate tissues has been developed by scientists at the University of Bristol. The breakthrough was coating the cells with a molecule called thrombin; this is normally produced in a wound to help blood to clot, which it does by converting a substance from the bloodstream, called fibrinogen, into a sticky meshwork that glues the wound together. The ultimate goal is to take a patient’s own stem cells, culture them in a dish and then endow them with this ability. This means they can then be injected into a wound where they will lay down the repair material and, in the process, enable themselves to better survive and stimulate healing. Chris Smith heard about the challenges in cell therapy, and the importance of this breakthrough, from the University of Bristol's Adam Perriman...
Adam - One of the big challenges in cell therapy, so these are therapies where we use for example patients own cells to treat, is that the environments that the cells face, when either injected or transplanted, are quite aggressive and so we were trying to come up with a way to effectively coat the cells to make them more resistant to those harsh environments.
Chris - Is this like anatomical Velcro for cells; you're decorating cells with molecules that make them stickier and make the environment more receptive to them coming in and living and surviving?
Adam - It is a bit like Velcro. We put on the first molecule, which is what we call an enzyme, and what that does is actually it can take molecules that are naturally in the body and can assemble them into what we call a hydrogel, which is a bit like the jelly that you have in your fridge when you're perhaps making jello shots.
Chris - So what molecule is it you're putting on, to do that?
Adam - So we put on molecule called thrombin. This is a molecule which gets switched on when we cut ourselves - we have a wound, and then it actually causes a second molecule fibrinogen to self assemble into this gel.
Chris - How do you get the thrombin onto the cells in the first place?
Adam - Okay, well that's a great question. We take this thrombin, it's what we call a macromolecule, it's a big protein, and we effectively decorate this molecule with detergent molecules, very specialised detergent molecules similar perhaps to a detergent that you would have in a laundry detergent. And what this does is that it allows these thrombin molecules to basically insert into the membrane of the cells, so the bit that surrounds the cells.
Chris - You end up then, with a cell that is a bit like a spiky meatball; it's got these thrombin enzymes sticking out of the surface so they retain their ability to be an enzyme, to make that fibrinogen turn into sticky fibrin, but they're sticking on the surface of the cells to do it?
Adam - That's right. Actually, what happens, you can literally take this solution of this thrombin and you can incubate the cells, so just mix it with the cells, and then it will spontaneously start to stick and assemble on the surface. And what's interesting about this is that then when we start to form this hydrogel, this special type of material, it actually glues or welds these cells together, and that's what's really different about what we are doing in this research.
Chris - Does it just come down to gluing things in place or does that fibrin meshwork, the matrix that you end up making, does that have other properties in the sense that does it encourage things like blood vessels to come in? Because one of the other things that is a challenge for cell transplantation is making sure that the cells have a ready supply of raw materials brought in by things like the bloodstream.
Adam - Yeah, okay. So fibrin as what we would call the biomaterial is quite special. One of the important components is that it allows cells to actually crawl around and move around in 3D. So cells don't like to just necessarily sit where you put them, they might want to move around and start to if you're growing tissue - a piece of skin - you might need the cell to move around and connect with another cell. They're a bit like computers, they really interpret the localised environment and so there are special types of buttons on a cell and materials like fibrin can sort of push those buttons and tell the cell that it's in a happy place, it's in a good environment to survive.
When it comes down to blood vessel formation, again, this obviously involves cells assembling into tubes and those sorts of systems. Obviously, fibrin again would provide a nice environment for the formation of blood vessels.
Chris - And have you actually tried doing this, what we would dub in vivo, if you take a real world example like a wound or a situation where you would want to graft tissue in, in the living entity, have you actually demonstrated that this has improved performance when you do it like this?
Adam - The initial focus of the paper was on developing the synthetic biology and the chemistry of the molecules, but towards the end of the research we did some experiments on a model organism. So we worked with zebrafish, partly because when they're really young they're transparent so you can image them. So in that situation we actually took fish skin cells, we painted them with our special thrombin, and injected those into a zebrafish and showed that the cells were still viable and it wasn't bad for the zebrafish. But really the next phase of the research will be looking at wound models to see whether or not we can increase wound closure in a model organism like this.
06:07 - Caffeinated solar panels
Caffeinated solar panels
with Paul Coxon, University of Cambridge
Most of us have experienced the “pick me up” that comes from a cup of coffee or tea. But this week, scientists in the US and China made the surprising announcement that adding caffeine to their solar panels made them work better! To find out why, Katie Haylor stuck the kettle on and took a look at the results with Cambridge University solar panel expert Paul Coxon...
Paul - Solar cells take light from the sun. They're usually made of a semiconductor material which is halfway between a metal and an insulator. They're a special sandwich of different materials together and they absorb the light inside the crystal of this material, you excite the atoms inside making these charges, these positive and negative particles, this is forming your current.
Katie - Currently, if I look at some solar panels on my roof or if I travel past a solar farm, how much of the light going in is actually been converted to electricity at the end?
Paul - Well, most of the solar panels which you see out and about today will be made from silicon. About 93% of the world's solar electricity is made with silicon solar cells and so they have a limit of about 20 to 23% at the moment.
Katie - So what did this group do then, because they weren't looking at silicon were they?
Paul - No. They were working on a new classification of material called perovskites, and these have attracted a lot of attention in recent years. These are quite different to silicon solar cells in that you can make the material at very low temperature. They're just wet chemicals that you can mix together and they form a crystal structure. This crystal structure is very very good at turning light into electricity. What they did was they added some caffeine into the mix and this affected how the crystals In these layers grew.
Katie - So hang on. I mean I'm sitting here with a cup of tea, you've got a cup of coffee, what made them decide to put caffeine in a solar cell?
Paul - Well, caffeine has got special chemical groups called carboxyl groups. This is a carbon atom joined to an oxygen atom with two bonds. By adding this into the chemical mix of your perovskite solar cell, this passivated or stabilised the material in a special way which influenced how the crystals grew within the solar cell layer, and this made the layer slightly more crystalline. It gave you better crystals, and better quality crystals which are bigger crystals, and this improved how the solar cell behaved.
Katie - Why is that then? What's the caffeine actually doing to benefit this process?
Paul - It actually made it slightly harder to grow lots and lots of little crystals. So as you're coating these wet chemicals together and forming a crystalline layer, imagine you've got lots and lots of little crystals growing in all different directions, and when these little crystals come together at the boundaries, these are where defects can occur and these can impinge or slow down the charges moving through the film. By adding the caffeine, you made it slightly harder for these random crystals to grow and it made the crystals grow in a preferential direction, in one way more likely. This gave you bigger crystals so it gave you a more uniform layer. So by having bigger crystals in the layer, it changed how the electrons moved through the layer, and it led to a higher voltage of your solar cell and it gave you a higher power conversion efficiency. So they managed to increase it using caffeine to about 20%, which is a great achievement for them.
Katie - So is it fair to say that because of the effect the caffeine had on the growth of the crystals, these perovskite crystals, this could potentially increase the efficiency of solar panels made from perovskite, which are currently not mainstream, right?
Paul - No. They're still quite new so there's a lot of research in this area. So yes, by adding the caffeine in this way you can influence how these crystals grow and give higher conversion efficiencies. But also, it made these crystals more stable against heat. One of the problems which perovskite can have is that under heat the layer can degrade, but they found that the caffeine influenced how the ions, the charged particles in these layers moved, and this meant that they were more stable at higher temperatures. This means that out and about in a real-world situation they're more stable and they could last longer.
Katie - I can see why having a material that degrades with heat is a bit of a problem when it comes to trying to make a solar panel. What is the point of doing this with perovskite if most solar cells are made out of silicon? Can we put caffeine in silicon and make that more efficient?
Paul - Well, you can't put the caffeine in the silicon, but we can put the perovskite, maybe with the caffeine, on top of silicon. And this means that we can tune the top layer of your perovskite to harvest the blue light from the sun and the red light passes through and get absorbed by the silicon underneath. So imagine having the perovskite piggybacking on top of the silicon. This allows you to capture more of that solar light and turn it into electricity much more efficiently.
12:45 - A gene breakthrough for obesity
A gene breakthrough for obesity
with Luca Lotta, University of Cambridge
Scientists at Cambridge University have identified how a gene called MC4R affects the chance of someone becoming obese and carrying a higher risk of diabetes and heart disease. Chris Smith was joined in the studio by the study’s author, Luca Lotta explained what this gene was, and how it worked...
Luca - Thank you for having me here. The MC4R for the Melanocortin 4a receptor is a receptor that is expressed in our brain and helps us control our appetite. The way it works is that when you have a meal there is a hormone and a response to the food intake, this response activates MC4R, and MC4R our tells our body, “hey, you have just had a meal. It's time to feel full”.
Chris - And so you stop taking on board more fuel, more calories?
Luca - Yes, exactly. And that's why we studied this gene and genetic variation in this gene, to understand the mechanisms of appetite regulation and their link to obesity.
Chris - It was already known that this gene is linked to obesity and appetite, wasn't it? Before you started looking at it?
Luca - Yes. Colleagues at the Institute of Metabolic Science in Cambridge discovered this gene in 1998, when they described mutations that disrupted this genes, they were associated with a higher risk of obesity. Our finding here is the opposite: that there are other genetic variants in the same gene that are actually associated with lower weight to lower risk of obesity, blood pressure, diabetes, and heart disease.
Chris - Now how did you find those variants and why did your colleagues back in the 1990s, why did they miss the fact that the gene seemed to work in both directions like that?
Luca - We studied 60 different genetic variants in MC4R and we studied this in a very large study of half a million people from the general population in the UK. Some of these genetic variants are rare, in particular the variants that we identified in this study require a large sample size to be able to detect certain associations.
Chris - Indeed. Where did you get data from half a million people?
Luca - There's a very large study in the UK which is called the UK bio bank which is a study of a half a million volunteers from the general population in the UK. UK Biobank makes data widely available to researchers, in particular in this area. We applied and we got the data and we studied this particular research question.
Chris - Were you asking of those people what's your form of MC4R? What's your gene look like and are you fat or thin? Is that basically what you're asking?
Luca - Yeah, it's what we've looked. Genetic data are part of the data that are available in UK bio bank and there's over 60 different genetic variants in this gene. We studied the association of these genetic variants with fatness, of thinness, and the risk of these diseases. And we also studied this genetic variance in lab experiments in cell cultures, where we found that genetic variance that are associated with a lower risk of obesity in this gene increase the activity of these receptors. The receptors are switched on and we think that this suggests that some people may find it easier to control their appetite because of their genetic makeup, because their appetite suppressing activity of MC4R stays activated for longer.
Chris - And does this mean then that we may be able to manipulate the gene in this way in order to make a person who would otherwise want to eat more, eat less? In other words feel fuller sooner?
Luca - Yes, so what we hope is that now drug developers may use what we've learned from this genetic study and try to copy the protective effect of this naturally occurring genetic variance with the medicines that suppress appetite, by activating this receptor and, in particular, a pathway that we've studied for the first time in relation to this receptor called Beta arrestin in which we strongly linked with this protective effect.
Chris - Now when you say this new way of interacting with cells is beta arrestin and how does that work then?
Luca - The way it works is that the receptor binds to beta arrestin and stays on the cell surface for longer.
Chris - So that’s how it leaves this I feel fuller for longer sensation?
Luca - Exactly. The normal receptor that is carried by most people in the general population, once it's activated and gets recruited within the cells so it can stay on the surface after it's been activated, whereas the mutant receptor for these particularly beneficial genetic variants stays on the cell surface for longer in these experiments suggesting that these people may find it easier to control their appetite because their receptors stays switched on.
Chris - And if we look at a range of people what proportion of obesity in those people is attributable to this effect because, obviously, obesity isn't just down to this one gene is it? There's a whole range of factors that can lead to this.
Luca - Yes.
Chris - So what contribution to the overall picture of the person in front of you is this particular component.
Luca - Yes. We know from other studies that obesity is 50 percent due to the environment and 50 percent due to genetics. By genetics, I mean several different genetic variants, in different genes in the genome. The main reason, actually, why obesity is so prevalent in the population is due to the environment, the availability of calorie-rich food, trends in physical inactivity. But the reason why we study the genetic aspects of obesity is that obesity helps us gain insights into the mechanisms that lead to obesity and, therefore, ways that we can prevent or treat this condition.
18:24 - Down to Earth: sniffing out bedbugs
Down to Earth: sniffing out bedbugs
with Stuart Higgins, Imperial College London
It’s time to get “down to Earth”, with Stuart Higgins and hear about another invention originally intended for space that’s also changing life for the better back here on the ground...
Stuart - What happens when the science and technology of space comes Down to Earth?
Welcome to Down to Earth from the Naked Scientists, the miniseries that explores spin-offs from space technology that are being used on earth. I'm Dr Stuart Higgins.
This episode: how the technology developed to detect gases on the surface of a comet is now being used to hunt out bedbugs in hotels.
On November 12, 2014, scientists from the Rosetta mission pulled off one of the most audacious manoeuvres in space science history. They managed to land a probe called Philae on the surface of a comet. Philae discovered a rich aroma of organic molecules suggesting that the chemical ingredients for life were present in the early universe when the comet was formed. Philae had multiple scientific instruments on board including a gas chromatography mass spectrometer, which is actually two instruments built into one.
The gas chromatograph was used to split up a sample into its fundamental molecules. It does this by blowing the sample through a long tube. The tube is heated and the molecules are vaporised. Different molecules stick and unstick to the walls of the tube at different speeds. Slowly they separate out arriving at the end of the tube at different times.
The mass spectrometer takes these separated molecules and ionises them, bombarding them with electrons which breaks up into electrically charged parts. These charged parts are separated using an electric field and are measured by a detector. Using signals from both parts of the system and comparing the results to experiments carried out on Earth with known materials, it's possible to work out what the original sample was.
A gas chromatography mass spectrometer can smell the air and work out what chemicals it contains. Back on Earth this machine can take up the same space as two kitchen ovens but for the Philae probe engineers needed to cram the technology into the size of a small shoebox, and it's this development that one British company is using to help hunt for unwanted life closer to home.
Bedbugs are bloodsucking parasites that hide inside mattresses and come out at night to feed on unsuspecting humans. While not dangerous, bedbugs aren't particularly pleasant. They can be hard to get rid of and dealing with outbreaks in hotels can be expensive. One company is using the technology from the Philae probe to help develop a portable bedbug detector. Bedbugs give off a range of organic molecules so analysing air samples can reveal their presence.
The detector aims to help hotels avoid unwanted guests and outbreaks and is currently on trial across the UK. So that's how the technology developed to carry out science experiments on a comet is helping hotels in the UK stay bedbug free.
That was Down-to-Earth from the Naked Scientists. My name is Dr Stuart Higgins and join me again soon to learn more about space technology that is being used back on Earth.
23:53 - Visiting a hedgehog hospital
Visiting a hedgehog hospital
with Alex Masterman, Shepreth Wildlife Conservation Charity
We’re taking a stroll into the garden, where if you’re quiet enough, and lucky enough, you might get to see a hedgehog worming its way through the undergrowth. Once a familiar sight in British gardens, these animals are sadly disappearing. But some places are working to help out our spiny friends. Adam Murphy made the trip Shepreth Wildlife Conservation Charity to chat to Welfare Officer Alex Masterman about their hedgehog hospital...
Adam - Hedgehogs, the spiky little mammals that like to roam around our gardens snuffling out insects. They like hedges and they have little pig like snouts, hence... hedgehog. They're adorable little things that mean none of us any harm. Sadly, hedgehogs are in decline. Their habitats are getting walled off into gardens, and they often fall victim to parasites and strimmers. One place helping them out is the Shepreth Wildlife Conservation charity Hedgehog Hospital here in Cambridgeshire. I spoke with Alex Masterman, welfare officer at the charity who first of all showed me one of their adorable little patients...
Alex - So this is Rosemary.
Adam - So what's wrong with Rosemary; what happened?
Alex - I'll have a little look at her chart and I can tell you. Yeah, so Rosemary was out during the day several times so she was brought in. They thought she might be quite old and she had fleas and she was quite lethargic. And then when we checked her she had capalarya and crenosoma, so lungworm and roundworm, things like that. She was about 500g when she came in and she is now much bigger than that, she's now in the 1200g range so she is doing really well. She's actually on our ‘clean shelf’, which means that she is now completely parasite free and were actually looking for a home for her to be released into now.
Adam - And when I was finished fawning over the hedgehog - the first one I'd ever seen in the flesh I'm ashamed to say, I wanted to know how you treat something whose first instinct is to curl into a ball of spikes...
Alex - Some hedgehogs are more prone to curling up than others, especially our older ones, if you pick them up sometimes they won’t curl. Rosemary is doing quite a good job of when you pick her up she will. One of the ways we can kind of see underneath them so for like our general first-aid when they come in, we want to make sure there's no cuts or injuries underneath is if you sort of wheelbarrow them like that, their instinct it's sort of put their feet down and that will make them uncurl.
Adam - Nearly onto their heads?
Alex - Yeah. That sort of gives an opportunity to look underneath and check their bellies are nice and fluffy and things. Some of them, especially the new young ones when they come in, you’ll put them down and they’ll curl into a ball and they won’t uncurl, and then to get them to do that you can just tickle their back here and if you sort of lightly brush the spines they will slowly curl. No idea why!
In terms of the medication we give here, it all goes into the skin, none into the veins or the muscles, and for that we actually like them to be curled up into a ball. What we do is we put them on their back and there's a ring of muscle around the front and that's how they curl up. If you just take some of the spines around the edge and gently pull out, and what that does is exposes some of the skin - tense it - so then we can get the needle and put it in parallel to the body and just get it under the skin.
Adam - What kinds of things are their pokey patients treated for here?
Alex - I'd say the majority is parasite burdens. Things like lungworm and B. Erin and the stuff can make them unwell. Ringworm as well which causes them to lose a lot of their spines and fur and obviously, that's no good because they lose their main defence mechanism. We also do get injuries - a common one is strimmer victims. Early in the season, we have one at the moment that, luckily, just avoided a strimmer and has just had some of her spines taken off. All sorts we get ones coming in with missing limbs; ones that are blind. I'd say that the majority is definitely parasite burdens.
Adam - But what is the state of hedgehog kind? Why is a hospital like this necessary?
Alex - So, hedgehogs in the UK are actually on the same decline as tigers. They are really struggling and experts reckon that in the next 10/15 years we could no longer have hedgehogs in the UK, and that's largely because of population loss and fragmentation. A lot of people close off their gardens and obviously there's new roads being built and things like that, and it just means that hedgehogs can't move freely and breed. As well as that people think they are vermin and pests and they’re really not, they’re actually very useful for us in our gardens because they obviously keep down insects and things like that.
Adam - What can we do to help them? If we wanted to make it easier for hedgehogs what's the best thing to do?
Alex - One of the easiest things you can do to just create 'hedgehog highways' in your garden. So making holes in your fence just to allow hedgehogs to pass through and that just makes it a lot easier for them to move about. Also putting out food and water, so hedgehogs will eat cat and dog food, wet and dry, as long as it's not gravy or fish based because that can give them an upset stomach. But especially at this time of year when they're waking up from hibernation they can often be dehydrated and really appreciate some food and water.
Adam - And when the inpatients are ready to become outpatients, how do you put a hedgehog back into the wild?
Alex - We have people on record that are release sites. So when we have one that's ready, we always try to get them back to or as close to where they come from as possible. So when someone brings in a hedgehog we will try and talk to them about being a release site, if not, we will find someone in the same area or the same postcode. And then we do what we called a 'soft release'. The hedgehogs go into like a rabbit pen for a few days and get fed in that garden and then after no more than six days, they get let out and people often still feed them. They're really good just getting back into the wild, they don't tend to have any issues at all.
Treating equine flu
with Richard Newton, Animal Health Trust
Keeping animals together in large numbers, moving them around the world and bringing them into close contact with humans can lead to outbreaks of infectious diseases, both in them and us. Recently the horseracing industry was temporarily brought to a standstill by an outbreak of equine flu. To explain how it happened, and why we need to be vigilant, Chris Smith was joined in studio by, Richard Newton from the Animal Health Trust in Newmarket...
Richard - Yes, it is. All flu viruses that affect all animals originate from the same source which are wild foul, waterbirds. And some of those viruses will adapt to new hosts. So the horse flu virus that we've got that we encountered this year, not just in this country but across northern Europe originated as far as we know back from birds only in 1963 and it's been adapting and changing and circulating in horses ever since. All flu viruses in mammals require chains of transmission that have to be kept going and if we can break those chains of transmission then we can stop those viruses and we stop the evolution of them. But horse flu virus very much like human flu viruses loves environments where those horses are in close proximity to each other. The virus will cause them to cough. They will shed lots of virus and it will spread onto the next victim if you like.
Chris - So coughs and sneezes spread diseases for horses as well as humans.
Richard - Absolutely.
Chris - Some of those victims of the Newmarket outbreak and and elsewhere in the racing industry, they'd been vaccinated those horses though hadn't they? So this was an example of a virus that grew through and surmounted the vaccine.
Richard - It was. Most of the flu virus, equine influenza, that we see occurs in non vaccinated animals and unfortunately in many parts of the world whilst vaccines are used there's a sufficient proportion of the population that are not protected by vaccination. So this can circulate and occasionally that will spill over into the vaccinated population. And what we see is the flu viruses, the reason it's successful is that it adapts. It changes, it mutates and eventually it evades the protection that it gets from vaccination and that's when we see the outbreaks, such as we saw this year in vaccinated animals.
Chris - And if the horse coughs on the jockey as well as on the other horses in the race can the jockey catch it?
Richard - In theory there is a very small risk but we've never seen horse flu transmitted into humans and obviously horses are domesticated animals and they have a lot of human interaction. And so we believe the risk is very small. The flu virus has become very well adapted to the host that they're in. And so whilst they're superficially very similar they are well adapted and they don't tend to spread over into new species.
Chris - Nevertheless though, I suppose that situations where you have big groups of animals, that's an artificial situation isn't it? Because in nature, animals might live in a herd but they wouldn't be moved around the way we move animals and they wouldn't be kept on the scale that we keep animals in the modern era would they? So we are kind of creating an opportunity for diseases to come in and then create outbreaks.
Richard - Yes. If you think that the horse after humans is the most widely travelled animal and we do that on aeroplanes across the world in the same way. There are numerous examples where we have spread this infection across the world because we've travelled animals that are infected and then become infectious to other animals, and the latest example of that was back in 2007 when Australia had horse flu for the first time and despite intensive quarantine it still managed to get out, probably indirectly via humans carrying the virus, not being infected.
Chris - You mean on their feet or on something
Richard - On something, and then getting out into a completely susceptible population. And from there it could spread very very readily.
Chris - I suppose one of the challenges with flu, because you pointed this out, that it's originally a bird virus and birds don't have passports and they do have wings they can go wherever they want pretty much, and so they are the best way, if you're a virus of going anywhere around the world because birds don't observe international boundaries, do they, in quarantine or is it just going to fly down land somewhere and potentially shed the virus and if it could jump into the nearby flora and fauna it will.
Richard - Yeah absolutely right. And that's why many times in the news we will hear about avian flu and the concern when it gets into large intensively farmed flocks and it can wreak havoc in a very short time and avian flu in the wrong species can be fatal very quickly and you just have dead birds in a very short period of time.
Chris - So what sorts of measures are in place to safeguard against this sort of thing?
Richard - Well in race horses and other types of horses, where this time of year they're starting to move and mix, people use them for sport. We do rely and we recommend very strongly that they undertake vaccination and most times vaccination is highly effective and it will prevent the infection. Also it's a matter of being responsible when owners have sick animals with infections that are spreading rapidly that they call in veterinary surgeons who could take samples get the diagnosis and then keep those animals in isolation and they will get over it they will stop shedding virus and they will recover.
35:41 - Keeping zoo animals healthy
Keeping zoo animals healthy
with Yve Morrin, Shepreth Wildlife Park
How do you keep all the different kinds of animals that live in zoos happy and healthy? To find out, Adam Murphy went to the Shepreth Wildlife Park to meet Yve Morrin, a zookeeper, with a laundry list of animals, including owls, red pandas, and some naughty monkeys under her care...
Yve - They all have very different needs. Monkeys, for example, are quite challenging to work with because they are very smart, they're very curious animals, they'll challenge you. They will test your padlocks after you leave to make sure that you've locked them properly so you have to be very security conscious. Sometimes I can't go in wearing sunglasses because they'll take them and run away with them, and they seem to do it almost as a way of teasing you. They know they're being cheeky and they do it for fun.
Whereas animals like owls, thinking about their biological need. Providing the right sort of nesting boxes and knowing when they've got seasonal moults coming on or when they're about to lay eggs and so on. So it's knowing all your different animals' biological needs, veterinary needs, husbandry needs, psychological needs as well.
Adam - Now when one of them unfortunately gets sick, how can you tell and what do you do?
Yve - You start off with a distance exam. Distance exams are incredibly important for zookeepers because it's possible for animals to hide when they're feeling ill. So an animal might be limping from a distance, you see that. You come up close to it and suddenly it's not limping and you think that's a bit strange. But you have to remember that these animals still have wild instincts, and their wild instincts are to hide anything that's physically wrong with them. They hide that because, obviously, a predator is going to look for the weakest animal and it's going to single them out for attack. So they are conditioned pretty much to try and disguise illness, so it can be very difficult to spot unless they know you're not looking at them.
But then when we do a close-up exam we look for any problems with any of the orifices, for example; eyes, nose, ears, and the ones lower down. We also look for what comes out of an animal. But, you know, I've had animals in the past, monkeys in particular, if you have a good relationship with them, if they have a wound they may actually even come and show you - look, I've got this, can you treat it please.
Adam - And then how would you go about treating it for the different animals?
Yve - It can be difficult with some animals. There are lots of different methods by which you can treat animals. Obviously you can give them oral medication. Now that's one of the easiest ones if you've got an animal that's greedy. So I recently had a routine faecal done for my red pandas; they came back having an illness. Now they didn't show any signs at all that they were sick. They probably weren't sick, they were just carrying a parasite, so it was just a simple case of oral medication for them and the easiest way for me to do it was to inject the medication into grapes, and then feed them the grapes.
Now if we've got something more serious going on, we may actually have to do a physical catch-up for an animal, manipulate it, hold it, and inject it and that can be really stressful. So what I'm doing with some of my animals is I am training them to voluntarily take an injection. That is quite stressful for an animal and they have to build up a lot of trust in you to understand what you're doing but usually, you know, a banana helps.
Adam - What about if it's something more serious, would you ever intervene say surgically?
Yve - Yes we do, frequently. Now if it's a small animal we have to bring it into the vet room. A little gas mask goes over their nose, and then we can do surgery on them. With big knockdowns of a dangerous animal, such as tigers that we have here, or in the past I've seen knockdowns of chimpanzees happening. That actually has to happen for security's sake in the animal's enclosure, so the vet will usually dart the animal . Once the animal is asleep we all have to be incredibly careful that it really is asleep. There's all sorts of tests that the vet can do, and then the surgery takes place right there, on the ground in the animal's enclosure. Everyone is being very safety conscious; you've usually got a team of people' you've got someone watching the door making sure that if the animal wakes up everyone can run out quickly. Once it all is finished we leave the enclosure, the vet reverses the sedative and then hopefully everything will be fine.
Adam - Is there a tension between doing everything you can to help an animal and letting nature take its course?
Yve - Sometimes you do have to make a judgement call over what's in the animal's best interest and what's in its best welfare. And euthanasia does happen at zoos, but it's always under the vet's advisement and in cases where the animal is suffering, and has illnesses that are causing it pain that are never going to get better again, and we do make those decisions. Every single time it breaks your heart but, you can be comforted by the fact that you know that you actually did make the best decision for that animal.
Adam - Why is what you do here important? Why do we keep animals in zoos; what's the purpose of keeping them here?
Yve - Our yellow breasted Capuchins are representatives of their species. There are only about 185 individuals left in the wild along coastal Brazil and that number is declining every year. It's getting to the point where that is not a viable breeding population - 185 individuals breeding in the wild do not have the genetic diversity to actually be sustainable. So one of the things that zoos do is we do conserve genetic variability. Now, obviously, we can't just release our captive Capuchins into the wild right now because they'll just be in danger of poaching and deforestation the same way as their wild cousins are. But, in the future, we can be maintaining that genetic stock in order to release once we're able to re-wild if humanity ever wakes up and gives us a place to release them into, then we can do that.
Helping animals to help humans
with Frances Henson, University of Cambridge
There’s one creature we’ve left out so far when talking about all the different ways we can help animals, and that’s us! Humans! So how might veterinary medicine play a role in human health, and we don’t mean going to the vet instead of the doctors! Chris Smith was joined in studio by Frances Henson, who works on the concept of “One Health” at the University of Cambridge...
Frances - Well one health traditionally was looking, as we've mentioned before, at how diseases of animals transfer into man and the impact that that has on man. So examples of that are tuberculosis, which we find obviously in cattle transferred to humans in milk. But in recent years the idea of one health has become a little wider and it's now starting to include the idea of individual diseases. So I’m particularly interested in joint diseases and therefore I think many, many of these things can be linked.
Chris - One interesting point is that although dogs are animals, they share our world, so they very much are exposed to many of the same risk factors that we are. If the dog's owner smokes, for example, the dog becomes a passive smoker so is that part of what you're advocating, that actually by studying animals and humans in a shared context you can learn a lot from both.
Frances - Yeah you certainly can. As you quite rightly said, dogs do share our world and it's incredibly interesting why they both get the same diseases as us and diseases that they don't get. So dog in a smoking household, it’s very rare for dogs to get lung cancer. So trying to understand why that doesn't happen can give us huge amount of information as to why people can get it.
Chris - The other animal that doesn't get cancer is the horse, isn't it. Horses seem to get much less cancer than they should. Do we know why?
Frances - No we really don't know why. They live a long time. People have argued because they’re vegetarians and they have high degree of movement that somehow protects them. But we really don't understand that, they get very, very low incidence of solid tumors. All they seem to get some rare skin cancers.
Chris - And so are people actually actively pursuing that, to say well, what's different about the horse compared to the horse's owner, that one's more likely to succumb to cancer than the other.
Frances - Well that is a fantastic idea. Unfortunately, whilst people might want to do that, getting funding for specific veterinary research is very, very difficult. And so researchers like myself join ranks with other types of scientists and particularly with medicine, in order that we can get funds to look at basic diseases rather than relying on veterinary funding. As I say it’s a very poorly, sadly very poorly, funded field.
Chris - But is it a two way street in the sense that, ‘cause you're saying you're teaming up with medics and you use that to liberate some funding, but do you then discover things that will then go back into the veterinary clinic to help the animals too.
Francis - Yeah we certainly do, so people working on this One Health agenda really want to have treatments and therapies that can be used for all large mammalian species. So as I said before, I'm really interested in joint health and we heard earlier in the program about people developing scaffolds to put stem cells in. But if we can develop those scaffolds and perhaps growth factors to potentially help those cells grow we can put those cells back into the human defects in joints or in skin or we could put them back into animal defects and skin. So I think if we get the fundamental principles right it's equally able to apply those across all the species.
Chris - And cynically, is it that if you do an experiment on a human, a) it's an ethical nightmare and b) it's much more risky because they might sue you, whereas is an element of this that if I do an experiment on a dog, I'm doing it with the best intentions but if it goes wrong it's, and it sounds awful, but it's still a dog, it's not someone who's going to turn and sue you.
Frances - Vets do get sued. But you're quite right, the ethical permissions to do experimental work on owned animals with effective clinical disease, it's that you can do that but we do have to go through a lot of ethical frameworks and we have to get licenses from Defra [Department for Food, Agriculture and Rural Affairs] and so on. And so it's not totally straightforward but potentially it is easier. And if we're looking at something that is life threatening and terminal for these animals, many owners will want us to help them in clinical trials to see if these therapies are effective.
Chris - A friend of mine's a pathologist and she had a much loved pet dog that developed a very bizarre tumor and she, of course, knows quite a lot about those sorts of tumors. But she paid a lot of money to a very good vet to do quite radical surgery on her dog. And I think it bought him a little bit more time. But at the same time it's an important learning process because obviously for that vet seeing that tumor in that context, it's an opportunity to try to do some surgery which they might not have the option to do very often because it's so costly and many owners might decide it's kinder and cheaper to put the dog down.
Frances - Yeah that's a very good point, it's that real balance isn't it, the balance, what you put that individual animal through to try and get a few more weeks and months and some owners of course in that situation they really don't want their dog to be, as they perhaps perceive it to be, experimented upon. So certainly in our clinical practice we see that whole range of opinion from people very, very keen to go for novel therapies back to right down to people who really don't want to have any part of that.
Chris - And in your research looking at joint and tendon repairs and things, what are you actually doing and what's the problem trying to solve?
Frances - Well, from my perspective as an equine vet, so I'm a horse vet, I became very frustrated that we didn't have good treatments for arthritis and for tendon and muscle injuries. And so I really want to try and push through developing new therapies and new treatments. And so I've become involved a research project to step back and look at some of the underlying principles. To be perfectly honest we don't even know what causes arthritis in people or in humans or dogs or any of the other animals we've talked about today. And so by understanding the principles of why we get the disease we can then perhaps start to devise much better and more effective therapies.
Chris - And do the disease processes mirror one another? Does what a human ostensibly calls arthritis, is that the same thing that your average dog in their old age gets, and Dolly the sheep was allegedly suffering?
Frances - Absolutely. It certainly looks like that on x-rays, it looks the same on MRI scans, it looks the same. And if you look at those joints under pathological sections the histology looks exactly the same so I think they are very similar.
Chris - And are we learning, Frances, from sort of outbreaks that you get in animals that can inform how a) to manage the human equivalent and b) how diseases evolve and change because of what happens in groups of animals.
Frances - Yes I think we can. I think I'm more interested and have more experience in single individual diseases but certainly how things behave, when we talked earlier in the program about stem cells and using bone marrow-derived stem cells in horses to repair tendon disease really informed the human practice. And so that's a really good example of how horse therapies have now become quite mainstream in human medicine.
Chris - So where is this whole field going? You're saying it's not very well funded, which is a worry given how many animals there are on Earth and, you know, that they outnumber us humans by many fold, don't they, partly because we're keeping a lot of them to eat but at the same time there's a lot of them and we move them around as Richard was saying. So there are lots of risks, why are we not putting more resource into studying this?
Frances - Well I think there are many many competitions on research funding. Lots of people have very important projects they want to get funding and whilst we may perceive that some of our areas are very important other funding bodies may not particularly think that they are more or less important. I think we get headlines when we get big outbreaks of disease and I think that can draw further funding but certainly for individual diseases that usually remains the remit of the individual disease society such as the arthritis societies.
49:34 - QotW: How do I see faint stars?
QotW: How do I see faint stars?
This week, Ben McAllister has been looking into this cosmological conundrum from Shawn...
Shawn - Why is it that when you look directly at small faint stars they disappear, but when you look at a point near them you can see them again?
Ben - Mmm, good question Shawn. That one left me feeling a bit dim. It turns out the answer is all to do with a technique known as “averted vision”. And no, we aren’t talking about what you’re supposed to do if the Queen comes in the room. We’re talking about a thing astronomers have been using for centuries to see distant objects.
A few people on the Naked Scientists forum like Colin2B, and Evan AU, and Flummoxed, all phone in with helpful answers which, like a guiding star, pointed me in the right direction. And thanks to Alistair Frith for his very helpful answer by email which shed some light on the subject.
Matt - So this is a really good question.
Ben - I thought so too. Thanks Matt.
Matt - But the answer actually isn't anything to do with astronomy.
Ben - Oh!
Matt - It's all to do with how your eyes work. There are two kinds of cells in your eyes which do the job of detecting light - they're called rods and cones. Cones give us our colour vision but they need very very bright lights to work and they don't do very well at all in dim light or at night. The rods on the other hand are much more sensitive and can see very well in dim light, so it's rods that give us our night vision.
Ben - So it's all about those pesky rods and cones. The fact that cones don't work well in low light is exactly why, if you're looking around in the dark, it's very hard to see colour, and the world appears in greyscale. The colours of light that a given object gives off don't actually change based on the time of day, it's just that the rod cells in your eyes, which worked well in darkness, can't really tell the difference between a red and a green.
Matt - Now the issue that Shawn's noticed comes from the fact that these rods and cones aren't just distributed randomly across your retina. Right in the middle of your retina - the sweet spot of your retina if you like - is a patch called the fovea which contains loads and loads and loads of cones all closely packed together, and this is what gives you your sharp colour vision. When you're looking straight at something in really nice lighting conditions, the reason you can see it so sharply it's all these cones packed together in your fovea.
Ben - So Matt, our astronomer come, I guess, I expert is saying that the middle part of your eye is really good at seeing bright, colourful things and not so great at seeing dim, dark things. You can do a little experiment here to see how this works for yourself. If you aren't actually colourblind you can go ahead and google 'colourblindness test' and pull up one that looks appealing.
If you look at it dead on, you should be able to see the different colours pretty clearly because of all those wonderful cones in the middle part of your eye. But, if you look at point on your screen off to the side so that use see the test with your peripheral vision, even in good light you'll probably find it much harder. If you are colourblind well I'm sorry, you're just going to have to take my word for it.
Anyway, back to Shawn's question; how does this relate to our ability to see dim objects like stars?
Matt - The problem is that all these densely packed cones right in the middle of your retina are the ones that really struggle to see things in dim light. So when you look at something very small and very dim, like a star, all the light's going to be falling straight on the part of your eye that really struggles to see faint things. So what you have to do, you have to move your eyes a bit to the sides and then the light will be falling onto a region with more rods which do a much better job of seeing in the dark, and so you can see the star better.
Ben - So it's the exact opposite of our color blindness test. The side parts of your eyes might be much worse at seeing colours, but they're much better at seeing faint things. So there you have it Shawn, is all about understanding the human body's odd little quirks and using them to our advantage.
Thanks to Dr Matt Bothwell for illuminating the question for us as we were a little bit in the dark. Okay... I'll stop now.
Join us next week when we tackle this breathtaking question from Greg in Canberra, Australia:
Greg - When I exhale my breath contains carbon atoms, how long ago were they in my food or drink?
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