Host: Shamini Bundell
Welcome back to the Nature Podcast. This week, a new way of cooling electronic circuits…
Host: Nick Howe
And the benefits of including genetic data from minority groups. I’m Nick Howe.
Host: Shamini Bundell
And I’m Shamini Bundell.
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Host: Shamini Bundell
First up, in the quest to make evermore powerful electronics, researchers have come up with a cool new trick. Reporter Alex Lathbridge is here to tell us more.
Interviewer: Alex Lathbridge
From mobile phones to solar panels – we’re constantly trying to make electronic systems smaller but filled with more powerful and complex hardware. But ask anyone that’s tried to play Football Manager on a laptop older than six months and they’ll tell you that one thing standing in the way of this electronic evolution is heat.
Interviewee: Elison Matioli
So, dealing with the heat generated by electronics in any kind of application is the problem, and this comes especially by the constant pursuit of reducing and packaging more and more components in a single surface.
Interviewer: Alex Lathbridge
This is Elison Matioli from École Polytechnique Fédérale de Lausanne in Switzerland. He’s just published a paper with a potential new solution to this problem of too much heat.
Interviewee: Elison Matioli
So, the work is related to the field of thermal management, especially in electronics. It was basically how to design new technologies that can deal with high heats like this in electronics in a different way to compared to the typical ones that are done up to date.
Interviewer: Alex Lathbridge
Current technologies for dealing with heat go far beyond my loud, constantly humming laptop fan. Supercomputers use cooling systems that require massive amounts of water and electricity to keep them running. It’s not very efficient, but there are other options. Elison and his team use a technique called microchannel cooling. The technique itself is not new. It involves very small channels of fluid being used to carry the heat away from electronic components. But their chips use microchannel cooling in a new and potentially more efficient way. I gave him a call to find out more about the work.
Interviewee: Elison Matioli
What we’ve done here is design the electronics put together with this thermal management in a way that the microchannel cooling is basically designed together with the electronics in a single chip.
Interviewer: Alex Lathbridge
What do these chips that you’ve made look like? I mean, how big are they?
Interviewee: Elison Matioli
These are very small chips. They are just a few millimetres by a few millimetres square. In a tiny coin, you could fit a few of these chips with several power transistors on top of it. They are all integrated doing their conversion of power, and just underneath you have the liquid flowing. Every microchannel is aligned to a place that heats up a lot in the device, so everything was thought right at the beginning to have the maximum extraction of heat when the device is on.
Interviewer: Alex Lathbridge
Okay, so, you can’t see me because this is an audio interview, but I’m currently drawing out what I can imagine in my head to be this chip and, in my head, it’s sort of like some rivers running underneath the circuitry, and they’re perfectly aligned and so they’re drawing out heat wherever they can. Is that kind of like that?
Interviewee: Elison Matioli
That’s exactly correct, and by doing this optimised, three-dimensional structure, we extract the heat before it even starts to propagate, so this is a major difference compared to leaving the heat to propagate all the way down and you put in a heat sink underneath and then you flow in some sort of air to it.
Interviewer: Alex Lathbridge
I mean, so this kind of cooling has been done before just not as personalised, so what’s the real difference there?
Interviewee: Elison Matioli
The difference is, in a way, we could get very high performance compared to straight microchannels that people have shown before. So, our solution here has a coefficient of performance that’s 50 times better than the typical microchannel cooling has been shown before. But the whole point, in my opinion, is that we could demonstrate that together with the integration of electronics on the same chip.
Interviewer: Alex Lathbridge
Okay, I get that. 50 times is a lot. That’s a lot better. But if you were to compare it to something much bigger, say a heat sink that is used in a computer or a laptop, can you compare those yet?
Interviewee: Elison Matioli
This comparison is difficult to say because when you have a heat sink, you rely on blowing air to the heat sink to extract heat, so you’re basically heating up the entire air next to your chip.
Interviewer: Alex Lathbridge
And that limits the amount of space that’s available to put more components in.
Interviewee: Elison Matioli
Yeah, exactly. So, today, you have your electronic chip and you have a heat sink underneath. Sometimes you have a fan to blow air. You have to propagate quite a large space before extracting that heat. If you take the layer where the electrons are flowing, this layer is about maybe a few nanometres, and that’s the layer that heats up the most. So, in a typical device, you leave that heat to propagate maybe a whole millimetre before it’s extracted. So, it’s equivalent as you being maybe here in Switzerland and someone blowing air in Greece to try to cool you down.
Interviewer: Alex Lathbridge
And so, my final question might be asking a lot but, based on what you’ve achieved here, where do you see the field, as a whole, going?
Interviewee: Elison Matioli
By increasing the heat flux that can be managed, we can now allow to integrate many more devices in the same chip, but also what we demonstrated is that we can start having integrated power chips, and this is a new thing. Today, power electronics are based on separate transistors. So, now, what we think is that by enabling the integration of these power chips, we could potentially have a similar impact as the silicon microchips had a few decades ago.
Host: Shamini Bundell
That was Elison Matioli talking to Alex Lathbridge. Elison’s paper is in this week’s issue of Nature, and we’ll put a link to that in the show notes.
Host: Nick Howe
Next up, it’s time for our weekly update on coronavirus with Coronapod.
Host: Benjamin Thompson
Yes, that’s right, Nick. It’s time, once more, for Coronapod, and I’m joined as ever by Noah Baker, but making his Coronapod debut is Ewen Callaway. Hello to you both.
Ewen Callaway
Hello there.
Noah Baker
Hi, Ben.
Host: Benjamin Thompson
Ewen, long-time listeners will know you and know your voice, of course, but for newer listeners, what do you do here at Nature?
Ewen Callaway
I’m a life sciences reporter covering molecular biology, genetics, evolution – all that sort of thing – and I’ve been covering coronavirus, really since the beginning, looking at the initial spread of the virus, a lot on vaccines, and most recently, what I think we’re here to talk about, is on how the virus is changing or not changing.
Host: Benjamin Thompson
Yeah, I mean, that is one of the long-standing areas of interest then, is whether the genome of the virus will mutate and what this might mean for disease severity and things like that. But maybe just as a quick refresher for people who aren’t virologists, what do we mean when we say ‘mutate’? What does it mean in this context?
Ewen Callaway
Yeah, I mean birds chirp and viruses mutate. It’s just a fact of life. They’re copying their genome to infect cells. They make the occasional errors, and most of these errors are wintered out through the process of natural selection but occasionally you have some errors that stick, but by and large these errors don’t do anything. So, it’s just a natural process of a virus going about its business of mutation.
Host: Benjamin Thompson
So, when it comes to coronavirus then, by tracking these small mutations in the virus’ genome, researchers have been able to track how the virus has spread through the human population.
Ewen Callaway
Yeah, that’s really been probably the most powerful application of mutation in this pandemic, is that even if these mutations do nothing to change the virus’ properties, they’re a really powerful tool for allowing you to track, as you say, the spread of the virus from Wuhan, through China, East Asia and the world, and you can really reconstruct viral lineages is the term by using these single-letter differences, which has just been an amazingly powerful tool for epidemiologists to study this infection in real time. So, that’s been a big boost here.
Host: Benjamin Thompson
And you yourself have been looking at one mutation in particular in the SARS-Cov-2 genome, and that’s called D614G, and you’ve written a feature about it for Nature, and this mutation has caused some concern. What is it? What does it mean – those sort of numbers and letters – and what do we know about it?
Ewen Callaway
Yeah, so just as I said that all viruses mutate, sometimes, rarely, but sometimes, these mutations change the properties of a virus, and that’s been one the real outstanding questions since the beginning of this outbreak, is will the virus change in any meaningful way? And you had a lot of people kind of stamp collecting mutations for a while, and the first stamp that really drew a lot of attention was this D614G mutation, and it’s a lot of jargon so I’ll break it down. D614G is a way of describing a change in the spike protein that coronavirus particles use to penetrate cells, and so this mutation is a change from one amino acid to another, from an aspartate acid to a glutamate amino acid. It’s caused by a single-letter mutation in the virus’ genome. So, this mutation was first kind of spotted at the beginning of the pandemic, and people noticed that it was becoming more common, especially in European countries as we were kind of locking down. Now, almost all the viruses in the world have this mutation, and there’s been a lot of intense study on what the mutation means, if anything.
Host: Benjamin Thompson
Well, Ewen, you’ve said that this mutation has become very, very prevalent then. I mean, that suggests to me that maybe there is some natural selection at play, that this has offered an advantage to the virus which is why it is all over the place now.
Ewen Callaway
I mean, that’s a really appealing theory, but viruses are funny things and there’s a lot of reasons why a mutation could come to dominate. There’s this phenomenon called a ‘founder effect’ where, especially in kind of the earlier stages of an epidemic you have a small number of people, maybe even one person, moving a virus from one region to another. So, just by chance, the viruses that seeded the outbreaks in Europe could have carried this mutation more often that it carried the unmutated version, and this could explain the apparent dominance of this mutation without having any impact whatsoever on the biology of the virus. And because Europe seeded outbreaks in a lot of the world, like North America, that chance tilt in favour of D614G carried itself and it’s continued perpetuating itself. So, what looks like a takeover because of natural selection just could be just chance and that’s a really hard thing to refute, and so people have been doing a lot of lab experiments to try and see are there any differences in this mutation compared to its ancestor.
Noah Baker
How does a lab experiment to find this out work? What does that look like because assumedly there aren’t very many labs in the world that can work with infectious SARS-CoV-2?
Ewen Callaway
There aren’t a ton of labs. It requires high containment and so, especially in the early studies of this mutation, people turned to this kind of workhorse of virology called a pseudovirus, where you take a different virus – crippled HIV is a popular one or this livestock virus called VSV – and you put the gene for a coronavirus spike protein that has this mutation into your other virus, and so you create this kind of hybrid and in doing so you can measure how well the particle infects cells. So, that’s what people have done. They’ve created these pseudovirus particles with the coronavirus spike, with the mutated version in the unmutated version and found, hands down, these guys are getting into cells much more readily. I think ten times more infectious is the top end of the measures that people are finding in lots of cells. But people point out this isn’t coronavirus. This is just a HIV particle or a VSV particle that has the spike protein, and all it says is that it could get into this cell under these conditions a little bit more easily. People say, ‘What does that tell me about the pandemic that’s spreading between people?’ Nothing, maybe.
Host: Benjamin Thompson
So, the original fear then that this mutation was making the virus potentially more easily transmissible has maybe been backed up a little bit in lab experiments, but you’re saying that you shouldn’t necessarily put two and two together to make four?
Ewen Callaway
Yeah, it’s been interesting to see this story develop because that was kind of the state of knowledge when I began, and then steadily, you’re seeing a little bit more evidence that says maybe this mutation is doing something. Recently, basically, a few hours before this story was going to press, somebody made this mutation in real SARS-CoV-2 coronavirus and, lo and behold, this mutation makes it up to ten times more infectious in either human cell lines or in airway tissue – something that’s kind of resembling human airways – and in hamsters, which are emerging as a decent model for infection and transmission. So, that’s telling you that maybe this does do something. And then I think the cherry on the top has been this really outstanding epidemiology study from the UK where they’ve sequenced the genomes of tens of thousands of viruses from people, and they’re able to look at the spread of either mutated or unmutated viruses in the UK, and they’re asking, ‘Do the mutated viruses spread any faster than the unmutated viruses?’ And they do, every so slightly. They can’t put a good number on it. It’s 20%-ish. Could be higher, could be lower, but they do seem to be spreading a little bit faster. The question remains whether it’s enough to make a huge difference in the outbreak, and the important thing to remember is this mutation happened in January or February. This is the outbreak. This is what we’re dealing with. It’s not about the future. It’s about the past. So, everything that this mutation is doing has already happened, and the reason people are studying it so much is because this is a virus that isn’t changing much at all and here’s just a window into what this virus does and how it does it. I think that’s why people are so fascinated with it.
Host: Benjamin Thompson
Yeah, that was the question I had for you, Ewen. It seems like in this instance it is, you’re right, looking back, but looking forward does seem to offer some unique challenges. How do you know what sort of mutation may occur? But there are people who are trying to figure that out, and what sort of approaches are they taking to figure that out?
Ewen Callaway
What drew the researchers to this mutation in the first place was maybe this would have some impact on how our immune system recognises the virus and deals with the virus and remember, there’s a whole suite of responses and therapies that are dependent on our immune system recognising and blocking this virus, and so they’re really interested in identifying those mutations that might hinder that ability, and that’s not a crazy idea. Influenza and HIV develop mutations all the time to thwart our immune responses. We know much less about how coronaviruses do this, and so there’s a big knowledge gap in identifying the mutations that might endow the virus with these properties to evade our immune system and whether these mutations will spread due to natural selection. That’s still a big open question, so researchers are starting to characterise these mutations that allow the virus to evade some immune responses, but these mutations tend to be very rare. They often go extinct, so it doesn’t seem like they’re giving the virus any edge. But, in the future, maybe they will, and that’s the question that people are asking right now – how do we prevent that?
Noah Baker
One of the conditions that the virus would maybe not need but that could result in a mutation like this happening is when it really is under a lot of selection pressure, and pressure, in this circumstance, could mean effective treatment, it could mean things that are managing to actually succeed. Do we run the risk of the better we do at fighting the virus, the higher the likelihood of a mutation coming out that could thwart us?
Ewen Callaway
Maybe, and I’ll explain that maybe. The way our immune system works and the way most vaccines that train our immune system work is they don’t just try and illicit one type of antibody that could be thwarted by a single mutation, they try and get kind of a diversity of responses, so the thinking is that would be harder to evade through a single mutation or even a chain of mutations. But there is a class of drugs, these antibody drugs, that are made of a single antibody and they target kind of one bit of the virus, and researchers are showing that you can have a single mutation that renders these antibody drugs useless, at least in the models they’re using, and so one way to prevent it might be to give people a number of antibody drugs, should they be proven and shown effective, so the viruses develop more than one mutation. And it’s not like these combinations of mutations never develop – HIV tells us that they do – but I think maybe we can decrease the likelihood of having a virus that can evade these antibody therapies if we use them wisely. That’s what people hope, and there’s some lab experiments backing that up.
Noah Baker
I’m interested as well what this could or could not mean for a vaccine, right? So, vaccines are working with the virus in one configuration. Is it possible that all the work that’s being done on vaccines could end up being moot if there are mutations that accrue in the time the vaccines are being developed, in the same way as maybe the flu vaccine needs to be updated every year to take account of new strains?
Ewen Callaway
That’s a definite worry. Let’s start with this D614G mutation. Almost all the vaccines were designed using the unmutated spike protein. That’s most of what the vaccines are, is they show our immune systems spike protein and say, Hey, B cells, come and get it.’ But experiments are showing that if an animal is immunised with an unmutated virus, they’re just as able and perhaps even better at fending off the mutated virus for reasons we’re still going into. So, it doesn’t seem like this D614G mutation is going to make any difference with vaccines, and it might actually have been a boost. With other mutations, there is that worry. You don’t want an influenza-like situation where you do need to give a new formulation every year because of how the virus is changing. With this virus, it’s changing a lot more slowly than influenza, so that’s one reason that might not be a factor, and we still don’t know the extent to which our immune response is shaping the change in this virus. With influenza, it’s doing a lot of this shifting because of our immune responses against it. With this virus, it’s not clear. So, I think there’s a quiet confidence, I suspect, among vaccine developers and researchers that if we can develop effective vaccines, they should be effective for at least a period. That’s my hunch. But data talks, so we just need to figure that out.
Noah Baker
And that is something which is kind of, I suppose, the positive thing about this particular coronavirus is that it does seem to mutate very, very slowly, especially when compared to other RNA viruses, and my understanding is that’s because it has a proofreading enzyme.
Ewen Callaway
That’s absolutely correct. It’s changing a lot less slowly than these other RNA viruses probably because of this proofreading enzyme. It has a stonkingly huge genome, and I think people suspect that without this proofreading enzyme it would just go extinct pretty quickly. So, yeah, it’s much less error-prone than other RNA viruses we know and worry about, so that is reassuring.
Noah Baker
At least that keeps it as a relatively stationary target compared to other viruses like it.
Ewen Callaway
But viruses change. It’s just something that happens, and it’s just something scientists need to be aware of and not spark worry among the public. And that’s the thing, is people hear about mutation and they think it’s definitely bad, it’s going to make some killer super virus, and that’s not the case at all. It’s just viruses being viruses.
Host: Benjamin Thompson
Well, let’s leave it there then for another edition of Coronapod, and all that’s left for me to say is, Ewen and Noah, thank you so much for joining me.
Ewen Callaway
You’re very welcome.
Noah Baker
Thanks, Ben.
Host: Shamini Bundell
More from the Coronapod team next week. Coming up, we’ll be hearing how minority groups can be left out of the analysis in large genetic studies. Right now, though, it’s time for the Research Highlights with Dan Fox.
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Dan Fox
Rock falls and rock avalanches are dangerous phenomena in their own right, but they can also sometimes unleash an additional peril – powerful blasts of air that can flatten trees more than a kilometre away. Now, scientists have discovered what makes these air blasts more likely. Using data from both ground and aerial drone surveys, they mapped the destruction caused by an air blast that followed a rock fall in the Indian Himalayas in 2015. They estimated the blast’s maximum wind speed to be 385 kilometres per hour and determined that air blasts are more likely to follow rock avalanches on steep mountain sites. They also found that the most destructive blasts occur in narrow valleys, which channel the air flow to devastating effect. Read that research in full at The Geological Society of America Bulletin.
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Dan Fox
Scientists have estimated that glacial lakes have increased in volume by nearly 50% over the past three decades due to melting glaciers. A team of researchers analysed more than 250,000 images taken by satellites using a model to calculate the volume of water in all the world’s glacial lakes, excluding those in Antarctica. Between 1990 and 2018, the number of lakes next to glaciers rose from around 9,500 to nearly 14,500. Their total surface area increased by 51% and their volume by 48% – the equivalent of 20 million Olympic swimming pools worth of extra water storage. Bigger lakes pose greater hazards to the communities that live near them, such as an increased risk of catastrophic flooding. Check out the full volume of that research at Nature Climate Change.
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Interviewer: Nick Howe
Next up on the show, genetic studies can give all sorts of useful information about people. However, in this next story, I’ve been finding out why certain groups of people often get missed out in this kind of research and what can be done about it. In the past couple of decades, there have been great strides in genetic research uncovering links between genes and disease, but often this research focuses on people who make up the majority population in rich countries. To call a spade a spade – white people. In fact, according to a 2018 study, 78% of study participants in research looking for genes linked to disease were of European heritage. This sort of underrepresentation can have real health impacts on people too, as population geneticist Simon Gravel explains.
Interviewee: Simon Gravel
The typical example is in genetic diagnostics. So, imagine a patient comes to clinic, they have a rare genetic disease, and the doctor wants to figure out which gene might be responsible for this disease or which mutation might be responsible. If the patient is from European ancestry, the doctor can scan their genome and compare it against a very large database of individuals of European ancestry and try to figure out which mutations are particular to this individual and might pre-dispose them to this disease. If the person comes from a different ancestry, there are often no databases available to do this, and therefore the doctor is left with a very large number of possible mutations that might cause the disease and therefore might not be able to give a diagnosis.
Interviewer: Nick Howe
Now, it’s well known amongst geneticists that this is a problem, so in recent years there have been efforts to tackle it. For example, the UK Biobank – a large repository of genetic data for UK individuals – has gone to great pains to make sure that the data are largely representative of the UK population. But there’s another problem. Even when such data are available, it may go unused. Simon encountered this problem recently when he was part of a group trying to recruit participants for a big genetic study.
Interviewee: Simon Gravel
Well, a bunch of us were saying, ‘Well, we have to be very careful about recruiting and being representative,’ and some other researchers were agreeing that this is a problem but were saying, ‘Well, if we do recruit in a representative way, we won’t know how to analyse that data.’
Interviewer: Nick Howe
Realising that even among his own collaborators there was a reluctance to use minority data, Simon was curious how widespread an issue this was, so he and his team looked at studies that have used data from the UK Biobank to see how often minority data was left unused. In this case, ‘minority’ referred to everyone who wasn’t from white European heritage. They started off by looking at a sample of 21 studies from a specific genetic research catalogue. Here’s Simon student, Chief Ben-Eghan, to explain what they found.
Interviewee: Chief Ben-Eghan
And so, we found that out of the 21 studies that we sampled, it’s only one study that used minority data. This was surprising, and so we tried to replicate this in another set of 20 studies that used data from the UK Biobank, from online repositories, and so we found something similar to what we did in the first scan. So, we found 1 out of the 20 studies that used data from minority populations.
Interviewer: Nick Howe
39 of the 41 studies had excluded minority data, and the team also found similar exclusion from a repository based in the US. They wanted to know why, so they scanned through the papers’ methodologies to see if there were explanations for not including the data. There were some. The most common reason was due to fear of confounding data. In other words, that some traits just happen to be more common in the minority group, and then the researchers will mistakenly think that there’s a genetic component. Another common fear was that there were just too few people in the minority group to have enough statistical power to come to any conclusions. According to Simon and Chief, these are legitimate reasons to discard data in an analysis. However, they think there are often ways to deal with these problems. Here’s Simon again.
Interviewee: Simon Gravel
One thing we can do that has no risks of contaminating their results would be to say, ‘Okay, I’ve also analysed the minority population separately.’ Now, it’s quite possible that by doing this, the research will not have enough participants from the minority population to find new discoveries. However, by doing this analysis and by sharing the results, the researchers make it possible for the entire research community to use these results and try to interpret it. And there’s an approach called meta-analysis where you can pull data across multiple studies and try to increase statistical power, and this is particularly important for minority populations because if you have small numbers in each study, you might not have enough power to discover interesting biology for each of these groups, but if you put them altogether, now you might start being able to learn some things.
Interviewer: Nick Howe
Making use of this data may be challenging, but Simon and Chief believe that it’s worth the effort. Not analysing it means that underrepresentation persists even when people from ethnic minorities are actively recruited into studies. These data do get used in some research but more often than not it can be easier to leave them out. Simon and Chief suggest that there are several ways to tackle this. For example, if researchers clearly state the reason for the exclusion of the data, these can be assessed in peer review to see if they’re valid. They feel that this could be enforced by the journals by making it part of the paper submission guidelines. For Simon, as well, it also comes down to just plain old fairness.
Interviewee: Simon Gravel
It just feels wrong, right? If we ask participants to participate in these studies, if we go and ask people to give their time and to have their blood drawn and so on and then we don’t use their data in the actual analysis, I think it’s unfair to them. So, there’s a moral problem, I think, if we don’t use the data, which is why I’m really keen on trying to solve this problem.
Interviewee: Simon Gravel
That was Simon Gravel. You also heard from Chief Ben-Eghan. Both are from McGill University in Canada. They’ve also written a Comment on this topic in Nature this week. There’ll be a link to that in the show notes.
Host: Shamini Bundell
Finally on the show, it’s time for the weekly Briefing chat. So, Nick, what’s caught your eye in this week’s Briefing?
Host: Nick Howe
So, I saw a story this week that was showing a way to potentially prevent the spread of dengue fever.
Host: Shamini Bundell
Ah, okay, that sounds like good news. We’ve recently had some success battling polio, and dengue might be next.
Host: Nick Howe
Yeah, well, that’s the hope. I must emphasise this is a press release so all the data needs to be vetted by scientists first, but from what has been shown, it looks like it’s a pretty substantial way to supress the spread of it. And basically, what it involves is it’s infecting mosquitoes that carry dengue – these Aedes aegypti mosquitoes – with a bacterium called Wolbachia, and that bacterium prevents the virus from reproducing in the mosquitoes so they can no longer spread it.
Host: Shamini Bundell
So, this isn’t trying to kill or hurt the actual mosquitoes. It’s not infecting them so that they become ill and then they can’t spread it. It’s if they’re infected then they can’t bite someone and pass on the virus.
Host: Nick Howe
Essentially, yeah. So, this is about a study that was performed in Yogyakarta in Indonesia, and basically showing how effective this technique can be. They split up the city into 24 different districts. 12 were controls and 12 were where Wolbachia-infected mosquitoes were, and in the places where there were Wolbachia-infected mosquitoes, there was a 77% decrease in the number of cases of dengue.
Host: Shamini Bundell
77%, so that’s pretty effective, according to this initial data.
Host: Nick Howe
Yeah, and the researchers actually think it may be somewhat of an underestimate as well because, obviously, people don’t stay in their study districts, like you can’t just restrict people in a petri dish, so they move about between them and may have got dengue from there. So, they think it could be potentially a way to eradicate the disease.
Host: Shamini Bundell
So, introducing a bunch of infected mosquitoes is great. Is the bacteria like contagious? Can they pass it on to others?
Host: Nick Howe
Yeah, so the bacteria is actually intracellular, so it exists within the cells and it gets passed on from the mother mosquitoes to their kids, so the population will eventually have more and more mosquitoes that have this Wolbachia in it.
Host: Shamini Bundell
Ah, hopefully the Wolbachia-carrying ones will outcompete the natural ones.
Host: Nick Howe
Yeah, and some of the people behind this, this World Mosquito Program, are planning on releasing millions and millions of mosquitoes bred in labs with the Wolbachia, so I think the idea is, in numbers, they will outcompete the rest of the mosquitos.
Host: Shamini Bundell
So, somewhat controversially, the researchers trying to fight mosquito-spread disease are releasing millions of mosquitoes into the air.
Host: Nick Howe
Well, yeah, I mean mosquitoes themselves don’t cause that much harm to people, it’s just the diseases they carry, and the good thing about Wolbachia as well is it actually prevents other viruses that mosquitoes often transmit from reproducing, so potentially these are a whole bunch of mosquitoes that are really basically harmless. But the next challenge is to scale things up, and that would need approval from the World Health Organization and then a lot of money as well to start growing millions and millions and millions of mosquitoes.
Host: Shamini Bundell
Well, after the apparent success of this sort of trial, hopefully that scale-up can happen. And talking of scaling things up – see, I’ve got a Nick-esque segue there – my story this week that I’ve looked at is about very large or at least very heavy objects, which are black holes, and can you tell me any fun facts to get us started about black holes?
Host: Nick Howe
Yeah, so they’re big, massive objects – I mean massive in the sense of they have a lot of mass – that basically suck in anything that gets too close to them and they’re black and yeah, scientists are super interested in them because they’re quite mysterious.
Host: Shamini Bundell
Yeah, exactly, and they are black and mysterious and hard to study. You might remember we had recently a picture of a black hole, or at least the light bending around a black hole, and before that, in 2016, we had gravitational waves being detected from a black hole by LIGO, which is a pair of detectors in the United States. And this is another story out of LIGO and also VIRGO in Italy – another gravitational wave detector – which is, again, another one of these rare observations we have of black holes, and researchers have, once again, seen gravitational waves that suggest a collision and possibly merger of two black holes.
Host: Nick Howe
So, what is different with this merging than from the 2016 one that we saw?
Host: Shamini Bundell
Well, this one seems to be raising a lot of questions and confusion because of the mass of the black holes. Now, as you’ve said, they’re incredibly massive, weighing many times more than our Sun, although not necessarily very big. They’re often smaller than planet Earth. But these two black holes that they’ve detected, or that they sort of worked out from the gravitational wave signal, are this really weird mass where apparently they shouldn’t really be black holes within this mass range, which is between 65 and 120 solar masses.
Host: Nick Howe
Okay, so why do scientists think that there shouldn’t be black holes around that size?
Host: Shamini Bundell
So, it’s all to do with how black holes form. So, there are huge black holes in the centre of the galaxy, supermassive black holes, and there are lots of, we think, smaller black holes that come from stars that go supernova and the remnants collapse into a black hole. But the reason there’s a sort of limit on that size is that the bigger the star gets, if it gets too big, it shouldn’t collapse into a black hole because of something called pair instability. They become so hot in the middle that you get fusion of oxygen nuclei and basically, stars of that size just rip apart and completely disintegrate and don’t turn into black holes. So, there should be a size limit and yet we’ve got two here, two black holes that are above that size limit, and then when they merge, they themselves form an even bigger black hole estimated to be around 150 times the size of the Sun, which is definitely in a range where no one’s ever conclusively seen a black hole that heavy before.
Host: Nick Howe
So, do scientists have any theories as to how these black holes have formed?
Host: Shamini Bundell
I mean there are always theories, but it’s definitely confusing them. So, the theories are to do with maybe since the beginning of the Universe itself, if you had smaller black holes from the start, they could start to merge with each other and then that could merge with another one and it could kind of get big that way, or they could be near the centre of the galaxy where there’s enough gravity to kind of keep them all close to each other so then they’re able to merge, but it’s definitely a mystery. One of the astrophysicists involved described both of the black holes as ‘uncomfortably massive’, so it seems like these results raise far more questions than they answer.
Host: Nick Howe
Well, hopefully we’ll get some answers soon. But thanks for talking to me, Shamini, and listeners, if you’d like more stories like these then make sure you check out the Nature Briefing – Nature’s daily pick of science news and stories. We’ll put a link of where to sign up, along with links to the stories we’ve covered, in this week’s show notes.
Host: Shamini Bundell
That’s all for this week. But that doesn’t mean we’re still not around though, and if you wanted to get in touch with us, you can. We’re on Twitter – @NaturePodcast – or you can send us an email – we’re podcast@nature.com. I’m Shamini Bundell.
Host: Nick Howe
And I’m Nick Howe. Thanks for listening.