Plague in the population, and preventing potholes
This week on the Naked Scientists, did the Black Death cause a change in our genes? Also, we'll be finding out whether smaller wine glasses could be key to reducing alcohol consumption in the population, and how scientists are plugging the potholes in our roads with science. Plus, a crucial piece of the puzzle in understanding long Covid...
In this episode
01:01 - Did the Black Death change our genetics?
Did the Black Death change our genetics?
Christiana Scheib & Fiona Gilsenan
Archaeologists and geneticists have been looking at the ancient DNA of almost 300 people who lived in Cambridgeshire before and after the Black Death - the plague that repeatedly rampaged across mediaeval England between the 14th until the 17th Centuries. They’ve been able to put to the test a theory that’s been been around for decades that, because the plague was so vicious, carrying off as it did maybe maybe a third of the European population at the time, it had the effect of altering the genetics of the population, selecting for genetically fit survivors, and weeding out the genetically more vulnerable.
The results suggest that’s not true. The study also offers intriguing new details about the evolving social landscape at the time. Some of the victims studied in the research were buried in mass graves, one of which was found under an earlier entrance to one of Cambridge’s oldest colleges. Chris Smith ventured there - on the coldest day of the year so far - to meet researcher Christiana Scheib, and Corpus Christi college’s Fiona Gilsenan…
Fiona - We're standing at what was the original entrance to Corpus Christi College. The college was founded in 1352 in the wake of the Black Death, the Plague, and the original entrance to the college ran across this passageway here from Bene't Street, past St. Bene’t's Church and into what's now called Old Court.
Chris - Indeed, this does look a bit like the tradesman's entrance. I can see why you moved it. It's much more prestigious now. But what's special about this entrance?
Fiona - Well, some years ago, we had to do some work on the building of what is now the Taylor Library. So we excavated part of this pathway and when we did that, the archaeologists found that there were some skeletons down there that were buried in an unusual way.
Chris - Is it relevant that right next door to where we're standing there is also a church.
Fiona - It's very relevant and this in fact is the oldest church in Cambridge and there are lots of burials here, but they were standard burials. The ones that we're talking about today were found stacked and not properly buried as individuals. And so that's an indication that they were probably buried quickly. The thinking by archaeologists who've worked on them was that they were probably victims of the Plague. And I think that there's some evidence that came out to indicate that that was the case.
Chris - Standing next to me is one of those researchers who worked on this. Tell us who you are and why you've come along today.
Christiana - I'm Dr. Christiana Scheib, I'm a fellow at St. John's College and a group leader at the Department of Zoology here in Cambridge.
Chris - You had access to some of the material that came out from under our feet. What were you looking for?
Christiana - I had access to four individuals, plus a fragment of cranium, so five individuals probably. And what I was looking for was, one, the human genome - we wanted to know more about mediaeval Cambridge, but also I was looking for evidence of plague.
Chris - There's been this question about the Plague which is, people say that because it killed so many people, it had an effect on the genetics of the people that are around today. It killed off a vulnerable group, left a survivor group. Were you able to get at any of those sorts of questions with this?
Christiana - That has been a longstanding question in the area, in the field. You would expect that anytime you have a pandemic, you will have a pressure on the population that's affected to adapt. And with the Plague, we know that the mortality rate was 30 to 50/60%. It was very high. So you would expect there would be a huge impact on the genetics of the people who survived. And that was what this project was about.
Chris - Was it just here you looked at or did you have material from other burials around the town?
Christiana - So the project itself comprised more than 10 sites across Cambridge. We were going all the way back to the Neolithic, so the earliest individuals are from an early Neolithic monumental burial in Trumpington. And the most recent are from the mid 19th century, from Holy Trinity Church just a few doors down. We wanted to get an idea of the overall population structure of Cambridge through time and how this might have affected them.
Chris - And the benefit of that huge time window is of course that straddles the time when the Plague circulated in Europe, doesn't it? Because it had gone by the 1800s and you predated it a bit. So I guess you can then ask, is there a before and after effect in terms of any impact on genetics?
Christiana - Exactly. What we were primarily looking at initially was the potential genetic impact of the Black Death or the second pandemic. That started in 1347 and came in recurring waves up until the 18th century.
Chris - How did you actually do it?
Christiana - So we screened a lot of dead people for both human genome, what their immune systems looked like, as well as what diseases they had and whether or not they did have plague. We had two sets, people who had plague and then people who did not have plague. And really for this study, we ended up not looking so much at the people who had plague because we know that those people actually died from plague. What we're interested in are the people who were living before the general population, before the second pandemic or the Black Death, and then the people who were definitely born afterwards, so therefore they were children of survivors.
Chris - And I guess you can then ask the question, are there any genes different between those two groups? Because if there was some effect of the plague killing off vulnerable people or preserving people who were more immune, I suppose you'd expect to see them more or less represented in those populations?
Christiana - That's exactly what we were looking for. Is there a difference in the genetics of the population before the Black Death and the people who were born, presumably of survivors?
Chris - And what did you find?
Christiana - We actually found that there was no difference. I mean there were minor differences, but nothing that you would call statistically significant.
Chris - So that sort of blows out of the water this idea that plague did have a big moulding effect on the genetics of Europe?
Christiana - The social impact was huge and the impact on the individual's lives would've been huge. But from a population standpoint, probably because we had so much mobility afterwards, we don't see a strong genetic impact, at least in Cambridgeshire. And it could also be because of the way that the plague kills. It's not maybe targeting a specific gene or something like that, it's maybe a more complicated route to death, if you will. And so therefore there's a lot of things being worked on and therefore there's not one particular target. It sort of muddies the waters.
Chris - What about the social question as in, because you were looking at a range of individuals from a range of different backgrounds, did you see that any particular groups were more susceptible? Because one of the things we see with disease, we often say people who are in poor conditions or poor health, generally, they don't have good food, don't have good living conditions, are more vulnerable. People who were better fed, et cetera, less so. Was the plague taking no prisoners or did it follow that pattern?
Christiana - People have long said plague is an indiscriminate killer and that seems to be reflected in our data. It doesn't matter how rich you are or how poor you are, you are still susceptible to the Plague. Now, whether you survived, if you had good resources that might have helped you survive. And unfortunately with this kind of study, we're only looking at the dead people that we can see. So we're seeing people who we know died of plague or people who we don't know whether they were ever exposed. We can assume they were exposed, but perhaps they never were. Maybe they moved to the country and they managed to avoid it, which did happen amongst people who could afford it.
Chris - Can you answer a question that's outside the scope of your present paper, but one which has baffled people for a long time, which is why plague just disappeared?
Christiana - Yes. This is a really interesting question and lots of people are working on it. It could have to do with the vectors. So we believe that it's carried in fleas on rats and perhaps something changed in the environment or the way that the bacterium was infecting the vectors and maybe improvements in sanitation helped eventually for it to die out, but it seems unlikely that it went away simply because everybody became immune.
Chris - And are there any more plague pits that you can dip into in Cambridge? Or have you run out of resources now?
Christiana - I think there are plague pits everywhere. In fact, my other work is on the first pandemic, the earlier plague, which came to England, that I've worked on as part of the 'After the Plague' project, but it's also known as the Plague of Justinian. So during the early Anglo-Saxon period, we also had a pandemic that came to England and affected people in very much the same way.
Chris - You're working on that now?
Christiana - I am, yes.
Chris - You'll have to tell us what you find.
Christiana - I will, I'll keep you updated.
Chris - And hopefully it'll be a warmer day.
Christiana - I'll publish in the summer.
09:22 - Removing largest wine glass lowers alcohol consumption
Removing largest wine glass lowers alcohol consumption
Eleni Mantzari, University of Cambridge
Now, more and more people are knocking alcohol on the head in January in a bid to give their bodies a welcome break following a period of boozy excess over Christmas. One other - and some argue better - approach is to just drink less alcohol in the first place and behavioural scientists think they may have found a way to do exactly that. Eleni Mantzari is a lecturer at City University of London…
Eleni - If you go into a pub and you ask for a glass of wine and you're asked whether you want a small one or a large one, and you might say large, it's usually a 250 millilitre portion. It's a third of a standard bottle of wine. So we wanted to see whether not offering that and capping the size that you can get to 175ml, which is what pubs call the medium size, whether that would affect how much people would drink.
Chris - How did you actually do this and do it meaningfully so that it wasn't just a lab experiment. Because we know that when we try to do lab experiments on people, we always end up wondering whether or not we've biassed people because they know they're in a study.
Eleni - This had been done in the lab before and we wanted to see what happens when you go out into the real world. So we asked 21 pubs, bars and restaurants in England to take away their largest serving size so that the largest they offered was 175ml. The pubs took part in a 12 week study. So the first four weeks they just went about their business as usual, they offered all the serving sizes of wine, we didn't make any changes and they just shared their sales reports. And then for the next four weeks we asked them to remove that large size of wine by the glass. And again, they shared their sales reports and we could see the amount of wine that they sold during those four weeks. And then the final four weeks of the study, we asked them to reintroduce the large glass of wine. And again, they shared their sales report and we could see how much wine they sold. We took into account various things because we know that the weather influences how much people drink, the time of year and other major events, so people might drink more on a bank holiday, for example. So we took these factors into consideration, into our analysis.
Chris - Do they order differently if you take that top one away?
Eleni - Yes. So what we found was that when you take the large glass away, on average each venue sold around 420 millimetres less wine per day. So that's about 7.6% less. And just to illustrate, that's one and a half large glasses of wine. So not tremendous amounts, but it was an effect that we would call significant. So it did make a difference.
Chris - When you look at the point of sale data - because you're lucky you got the till receipts, effectively, from these venues so you can tell really what the behaviour may have switched to, not an individual, but you can tell what the volumes are doing - could you see that people were compensating? If you give them less of the big ones, do they just drink more of the small ones to compensate?
Eleni - The interesting thing that we found is that when you do not offer that large glass, which is usually the 250ml, we thought that people would just switch to the immediately smaller one, which is the 175ml. But actually, what we found is, people were switching more to the 124ml, which is the smallest one you can get.
Chris - And they weren't switching to other beverages like beer that are not wine. And so you're not missing cases because someone went and had a pint of lager rather than a big glass of wine.
Eleni - Yeah, that's a really good point. So we looked at beer and cider and we didn't find that this had any effect on those drinks. What we weren't able to look at is other things such as cocktails and spirits. But we know that beer, cider and wine is what most people order and, from the drinks that most people order, we didn't really find any switching around going on.
Chris - What do you think the public health implications of this are? Is this something that policymakers should now be actively thinking about deploying? Because we know that alcohol is a top five killer, isn't it? If you look at the World Health Organization figures, alcohol causes more disease and more loss of life than many other things that we regard as major threats.
Eleni - This is just one study. For policy makers to make a decision, they would probably want to see more research on the topic. But this study does suggest that there could potentially be some regulation about the larger sizes and maybe capping it. There are many things to consider, such as the acceptability of this by the public and the hospitality industry and the alcohol industry as well.
Chris - Is it me or have glasses of wine got larger in recent years, though? I'm sure, when I was in my student days - wasn't that long ago - you didn't see people walking around with what looks like a bucket full of wine and now you can get a half a bottle of wine in some of these wine glasses that you're routinely seeing for sale.
Eleni - So there have been two things that have happened. The actual wine glasses have gone up, their size. So we did some research within our group at Cambridge and we measured wine glasses over time and we saw that they have increased, especially since the nineties, almost 400% in some cases. And there is research that shows that if you have larger wine glasses, you tend to pour more in them. But also the portion sizes that are being offered has increased. When I was at uni, I don't think you could ever get a 250 millilitre glass as the standard glass. The standard used to be the 125ml. It's shifted what's considered normal towards the bigger end.
16:19 - Pothole project developing smarter roads for the future
Pothole project developing smarter roads for the future
Ioannis Brilakis & Abir Al-Tabbaa, University of Cambridge
But first, the UK’s leading motoring associations - the AA and the RAC - have said the country’s potholed roads are largely to blame for a huge surge in vehicle breakdowns. Potholes are usually formed when water freezes in cracks in the road and expands. Engineers here in Cambridge are working on a research project to do something about it. One aspect of that is knowing where the potholes are in the first place and, as it turns out, that the new generations of high-tech, sensor-laden cars on our overcrowded roads are already generating reams of data about the road condition.
This, the Cambridge team intend to mine and then act on by deploying autonomous vehicles to patch up damage almost before it even gets started, using new self-healing road surface materials and embedding sensors in the roads to make the job even easier. I went along to meet the brains behind the project, pothole saviours Professors Ioannis Brilakis and Abir Al-Tabbaa…
Ioannis - The car industry has evolved dramatically over the last 40 years and is now able to give us, in real time, an amazing wealth of information. They can detect cracks, potholes, fallen street signs, damaged lane markings. It's just we have no way of taking that on board.
Chris - Are you saying modern cars, because they're endowed with all these cameras and sensors, they're just naturally passively collecting all that information anyway?
Ioannis - Yes. Some of the car companies we work with collect something like 50 gigabytes per minute. They process that onboard, come up with these detections and only share those detections in a statistical way. In other words, at least three vehicles of the same type need to go over that defect before this is reported.
Chris - Where does the data go then? It's stored on the car. Does it then get shared centrally with the manufacturer?
Ioannis - Yes, it goes straight to the manufacturer's cloud and then this is where we come in. The plan is to have a cloud system, a digital twin if you want, of the physical infrastructure that is able to take all that information, start making decisions. What does this change mean for me? Do I need to go and right now fix the problem? Or is it a problem that can wait for the next maintenance schedule and then as a result of that, send that information onto a maintenance vehicle, or to humans to make decisions.
Chris - Does this mean we can potentially get ahead of problems? You don't wake up one day and the road has a one metre across breach in it. That must start as a very small breach that then gets worse and worse and worse. So does this mean we can potentially get upstream of some of these problems and fix them before they even become a headache for motorists?
Ioannis - Imagine a world where, rather than us inspecting the roads once a year or once every two years, as soon as three vehicles drive on top of a specific defect, it's already detected and reported. That means that potholes will never form again anytime in the future. We can fix them well before they even materialise.
Chris - And who will do the fixing and how?
Ioannis - That's where our colleagues in the smart materials area come in. We have effectively autonomous vehicles that have the added function of being a repair vehicle, who can come in then and address that problem.
Chris - Do they already exist? These autonomous vehicles, though?
Ioannis - They don't. And this is another element of the project we're trying to create. We have already a team of people on the robotics front as well as the smart materials end who are trying to come up with a multipurpose vehicle that doesn't just solve one problem, but also does it using smart materials that are able to be much longer lasting and able to sense themselves and give us information that they would otherwise not have.
Chris - So there you are, Abir, you'll know where the problem is, how big it is, and how urgent it is. Now it's over to you. How are you going to fix it?
Abir - Yes. So we're going to make use of the data to understand the condition of the road, decide where to perform proactive maintenance, what damage needs to be fixed, and at the same time make the road smarter so that the road communicates with the vehicle on its state of health.
Chris - Ah, you're really delivering two solutions here then. One is using the data we've just been hearing about to optimise and get ahead of problems as they're emerging, but then also make the road itself better so that it's basically more resilient and better at telling us when it's got a problem going forward.
Abir - Exactly. The plan is that we can introduce additives in the materials, they can tell us where there's strain, where there's stress, where there's water ingress, but at the same time we can embed some sensors so they can, again, report back to their state and condition and provide, add materials that will enhance the resilience so they last longer. Potentially they could self-heal as well so we don't even have to worry about inspecting the pavements.
Chris - Well, let's think about those two things in turn. The sensors first, what are they, how will they work and what sort of information will they deliver that we can't just learn from the cameras on people's cars already?
Abir - They will provide inside information because our pavements are layered and there's depth. The vehicles very much provide data on the surface of the road, but many of the problems start from underneath. So we can actually, by embedding those sensors, detect potential problems even earlier.
Chris - And, in terms of the materials, what are the new materials that we could use that will make potholes a bit less common?
Abir - So we can provide more resilient materials. They are stronger, they last longer, they bond more with a substrate, but also provide materials that are self-healing. So if a small crack occurs,, they heal the damage themselves. So you don't even have to go and repair them.
Chris - How do they do that?
Abir - A simple solution is capsules which contain a healing agent in them. You embed those in the pavement. A crack will just propagate through these capsules and rupture them and the healing product comes out and seals the crack.
Chris - It sounds amazing, but this sounds also expensive. Is this going to be new roads going forward, and we put this into a road as we build a road, or is it retrofittable? Because it sounds to me like you're going to have to dig roads up one way or the other to get these new materials in, but also to get the sensors in?
Abir - It will be both of them. So you can apply self-healing repair materials. You can also apply self-healing as a coating. For example, some cars have self-healing paint on them. So you don't have to dig the pavement and embed those materials in it. They could be applied to the surface.
Chris - What sort of a difference do you think this will make, ultimately, if we are able to implement this? How is this going to turn things around?
Ioannis - I think we need to look at this as a long-term and a short-term solution. On the long-term front, yes, it will take us a long time to replace all of our pavements, but the same thing happened with traffic lights when we went from incandescent light bulbs to LEDs. This didn't happen overnight. We gradually replaced them. Also, in terms of the roads themselves, we don't have to dig up the whole road. Sometimes it's just a top layer that could be resurfaced and resurfacing is something that happens fairly frequently on many of our roads. So it'll be something that will take many years, perhaps even a couple of decades, but it is possible to update the whole network. Roads in this country carry 70% to 80% of all goods and people, this is not going to change in the future. This has been stable for quite some time, and at the same time, it's a very underfunded mode of transport. It receives only 15% of the public spending, so unsurprisingly, without enough money, and if we hold that traffic, we have problems and we have to change that.
24:27 - Overactive arm of the immune system linked with long Covid
Overactive arm of the immune system linked with long Covid
Onur Boyman, University of Zurich
To SARS-CoV-2, the viral cause of Covid-19 now, and we’re going to take a closer look at the stubborn persistence of COVID-19 symptoms. It’s frequently called long COVID, and new analysis of blood samples from patients suggests that we might be closer to understanding what leads some people to develop it while others recover from the virus more quickly. Here’s Professor Onur Boyman from the department of immunology at the University of Zurich…
Onur - Long Covid is actually a combination of different symptoms. While we understand these symptoms, we don't understand actually how they are caused or what keeps them active. We said, let's measure a lot of proteins in the blood of patients that have long covid and then let's inquire what is different between those that have long Covid compared to those that don't.
Chris - Is the sort of rationale behind this then that if you look at enough people enough times and you look at enough different chemicals, you can spot patterns that keep coming up in people who do have the problem and are not there in the people who don't have the problem. And that argues that those changes must in some way be linked to the problem?
Onur - That is correct and that's exactly what we did. And then we asked, what is the most different protein, or protein group between long Covid patients and those that don't have long Covid.
Chris - And what is it? What is the biggest difference?
Onur - We found that an arm of the immune system is actually overactive in patients that have active long Covid. It's actually a very interesting part of the immune system. It's called the complement system, which usually should be activated when we have an acute virus infection and should then go back to its normal state. In long Covid, this return to the normal state is not happening. And what this then causes is a state where the body and many of the body's cells, not only immune cells but normal cells, are in an alarmed state.
Chris - Were you able to look upstream of the Covid infections in these people in order to reassure yourself that it wasn't like that already and that it's that that makes people more susceptible to getting long Covid versus long covid, is this happening?
Onur - That's very true. So then the question of course is how can we test whether this is a cause or a consequence of their symptoms? So what we then did is compared Covid patients which either did not have any long Covid at all, or got long Covid but then recovered, versus those in whom long covid persisted. And what we could see is the complement system recovered in those which recovered from their symptoms and always at the same time.
Chris - If it's staying high, the level of this is staying active all the time, something must be driving it. It's like a switch has been thrown. So what do you think's doing that? How is that being achieved?
Onur - Yes. So, initially we think it gets activated by the virus, but then why doesn't it switch off there? We think there are loops and signals that keep it active in patients that suffer from long Covid.
Chris - It's almost like someone's turned the thermostat up and the temperature set point is now higher, so the room ends up hotter. Is there a way of turning that thermostat back down? Can we detune the immune response back down again to where it should be in these people?
Onur - That's, of course, a very important question. Some individuals seem to be able to turn it down. So if we take someone who had Covid and then long Covid and spontaneously recovers, this complement activation, it's normalised, and the symptoms go away. Why that is the case? We don't know. On the other hand, if somebody does not recover and keeps on having this complement activation turned on all the time, then another possibility would be to use specific drugs that actually act on tuning down the complement system.
Chris - Given that you've got what appears to be a sort of molecular fingerprint for someone with long Covid, could this be the basis of a test then? Because that's been the other thing that's proved a bit elusive is helping people to get a diagnosis to account for their symptoms, give them the reassurance that this is what's going on, and then obviously manage their symptoms for them. So can we use this as a test?
Onur - This is a possibility. We've identified a central piece in the puzzle to understanding long Covid, a mechanism that unifies the different findings that had been collected previously. This can of course help diagnose long Covid better and hopefully in a second step it might actually also provide new targets for treatment.
30:17 - Why does Face ID work after cataract surgery?
Why does Face ID work after cataract surgery?
Will Tingle asked Nikita Thomas from Anglia Ruskin University...
Nikita - Biometrics are essentially measurements of biological features, and facial recognition technology uses biometrics to measure certain facial landmarks that generate a unique identifier, or sometimes it's called a face print, of your own face. The landmarks measured with this type of technology include features related to your nose, your ears, your chin, and so on. But the landmarks related to the eyes are the distance between the eyes and the depth of the eye sockets. These are measured by the software detecting where your upper and lower eyelids are and where the corners of your eyes are. Intraocular lens implants replace the lens in your eye, and that is actually located inside of the eye, so it's behind the pupil and behind the iris, which is the coloured part of the eye. As the facial recognition technology only looks at the eyelids and the corners of the eye, which are structures outside of the eye itself, it's unlikely that the intraocular lens implants that are inside of the eye would affect the detection of these outside structures. However, it is the case that during the surgery your eyelids are held open with an instrument called a lid speculum. It is possible that the surgery itself and the holding of these eyelids may have slightly altered the positions or the elasticity of your eyelids post-surgery so that the facial recognition software may not detect your eyelids in the exact same precise location as they were pre-surgery.
Will - So is there anything that can be done to fix this issue?
Nikita - In this situation, it would probably be best to attempt to redo the facial ID profile for both your phone and the banking app. But if the problem persists even after doing this, then it points to more of a problem with the facial recognition software itself. This is especially true if the facial recognition software is working on your phone, but not on the app as technically they should both be reading the same unique profile.
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