NATURE PODCAST

After decades of trying, scientists coax plastic particles into a diamond-like structure

Coaxing tiny colloid particles into a diamond structure, and manipulating cell death and homeostasis in neurodegenerative disease.

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Listen to the latest science news, with Benjamin Thompson and Nick Howe.

In this episode:

00:45 Creating colloidal crystals

For decades, researchers have attempted to create crystals with a diamond-like structure using tiny colloid particles. Now, a team thinks they’ve cracked it, which could open the door for new optical technologies. Research Article: He et al.

07:50 Coronapod

Rapid antigen tests for coronavirus have been described in some circles as ‘game changers’ in the fight against COVID-19. We discuss their strengths and weaknesses, and how they could fit into an overall testing strategy. News Feature: Fast coronavirus tests: what they can and can’t do; If you are involved in a clinical trial for a coronavirus vaccine or treatment, please fill in our survey.

23:52 Research Highlights

Climate change causes greening in the Arctic, and the peptide that gives the Giant Stinging Tree its sting. Research Highlight: A frozen land goes green as Earth warms; Research Highlight: How the giant stinging tree of Australia can inflict months of agony

26:04 Controlling cellular death

In neurodegenerative disease, cell death can be prevented, however this can lead to the accumulation of incorrectly folded proteins. Now researchers have found targets that can be used to both stop cell death and protein aggregation. Research Article: Xu et al.

32:20 Briefing Chat

We discuss some of the latest stories highlighted in the Nature Briefing. This week we talk about the increasing complexity of scientific writing, and uncovering the real origins of charcoal. Nature Index: Science is getting harder to read; Nature News: Microscopy illuminates charcoal’s sketchy origins

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Transcript

Listen to the latest science news, with Benjamin Thompson and Nick Howe.

Host: Benjamin Thompson

Welcome back to the Nature Podcast. This week, a self-assembling crystal with a diamond-like structure…

Host: Nick Howe

And the proteins involved in controlling cell death. I'm Nick Howe.

Host: Benjamin Thompson

And I'm Benjamin Thompson.

[Jingle]

Interviewer: Benjamin Thompson

First up on the podcast this week, I've been finding out about tiny particles – often less than a micrometre in diameter – called colloids. These tiny particles can be made up of all sorts of things, plastics, fats, metals, you name it, and in some cases, when suspended in liquid, they can be assembled into crystals. For decades, it's been thought that if transparent colloids could be coaxed into a specific diamond-like arrangement, it would form crystals with some very useful optical properties that could be used in things like quantum computers. However, despite a lot of work from a lot of people, this colloidal diamond structure has proved elusive. David Pine from New York University in the US has been working on the problem for almost 20 years, and it looks like he's finally cracked it. This week in Nature, he and his colleagues have demonstrated a way to get colloidal particles to self-assemble into a 3D diamond-like structure. I gave him a call to find out how he did it, and started by asking what sort of structures colloids typically assemble into and why a diamond structure is so tough to make.

Interviewee: David Pine

Colloids and colloidal suspensions do assemble into some nice crystalline structures, but the crystalline structures they assemble into are more like the way you might see oranges packed in a grocery stand, or cannonballs in former times. A diamond structure is much more open. It's not nearly as compact as your oranges, and that's part of the reason why it's so hard to coax colloidal suspensions to assemble themselves into a diamond structure. The second thing is that each particle has only four neighbours, and that's not a lot in order to support them. Compare that again to oranges in a grocer’s stand, each orange there has 12 neighbours to restrict its motion. So, those two things are really the things that make it very difficult.

Interviewer: Benjamin Thompson

And why would you want to coax the colloids into this diamond-like structure then?

Interviewee: David Pine

Well, because the diamond structure is one of the best-known structures, based on calculations, for making a material with a photonic bandgap. That’s the holy grail.

Interviewer: Benjamin Thompson

What is a photonic bandgap then and what could a crystal with one be used for, because there's been a lot of interest in this area for a very long time?

Interviewee: David Pine

So, a photonic bandgap is the optical analogue of a semiconductor. So, what a semiconductor does for electrons, a material with a photonic bandgap does for light. It has a number of interesting properties. Fundamentally, there's the idea of making little micro-photonic circuits, little waveguides that can direct the propagation of light on a very small scale that can split the light, could make essentially all optical switches that would sort of operate something like a transistor does for electricity, and it can be used, in principle, to make better micro lasers. So, there's both fundamental reasons and technological reasons for making these materials.

Interviewer: Benjamin Thompson

And you've turned to your colloids then and it looks like you've got these little spheres to orient themselves into the correct position and, even better, you've got to do it themselves. What's the overview of how you got these free-floating colloid spheres into the diamond structure?

Interviewee: David Pine

In the end, there's two really important points. One, is we've managed to put patches on the particle surfaces that attract each other, and these patches are tetrahedrally oriented. So, the fact that they have a natural affinity to attract and form these tetrahedral bonds, that's one element of it. The other thing which took us a long time to really appreciate is they’re not spheres. We use particles that are shaped like tetrahedral. They’re actually four spheres sort of welded together, so those two things turn out to be the essential elements, at least for our approach.

Interviewer: Benjamin Thompson

You've got your four-lobed particles with their patches then. Do you just mix them all together in some water, give it a bit of a shake and wait till morning? What happens and what does it look like?

Interviewee: David Pine

That's not too far from the truth. I mean, that's the beauty of this whole area of self-assembly. And yes, you make these particles, you put them in some water and you come back in the morning and you look under the microscope, and you see these beautiful patterns that are characteristic of a diamond crystal, so they do it all by themselves.

Interviewer: Benjamin Thompson

So, you've got the crystals then, right? Do they exhibit a bandgap and what happens now?

Interviewee: David Pine

Okay, so the story continues. The particles aren't made out of the right kind of material to exhibit a photonic bandgap, and I don't know how to make the metal the right material. What we use are plastics, but they don't bend the light enough. What you need is you need a material that bends light even more. So, there's another step, and we're working on this next step. So, what we're doing is we use the diamond crystals we make as templates, and we fill the open areas between the colloidal particles with high-refractive-index materials. Once that's done, we burn out the plastic colloids and what's left behind is sort of the inverse diamond crystal, and that should have a photonic bandgap, and a very good one at that.

Interviewer: Benjamin Thompson

So, what you're trying to do then is make an inverse crystal, a Swiss cheese version of what you've already made?

Interviewee: David Pine

It’s exactly that. That's a good way to describe it. It's a Swiss cheese version of the original crystal that we made.

Interviewer: Benjamin Thompson

And maybe it's a weird question to ask, but it's taken you a while to get to this stage –obviously, it's been difficult – is it going to take you as long to get to the inverse stage? What do you think?

Interviewee: David Pine

No, no, we've already done some preliminary experiments. We were just starting this when the COVID pandemic hit. I fully expect that we'll have the materials with a photonic bandgap in the next, I don't know, four to six months, something like that.

Interviewer: Benjamin Thompson

That's exciting, right?

Interviewee: David Pine

It's a very exciting. We're going to have a lot of fun, and I'm hopeful that other groups will pick up on our methods and perhaps improve them and to see what new kinds of physics, what new kinds of optics, what new kinds of devices we can realise with this.

Host: Nick Howe

That was David Pine. Look out for a link to his paper in this week's show notes.

Host: Benjamin Thompson

Next up on the show, it's time for Coronapod, where we discuss the latest coronavirus news. This week, I'm joined by Noah Baker and Richard van Noorden. Hello to you both.

Richard Van Noorden

Hello.

Noah Baker

Hi there, Ben.

Host: Benjamin Thompson

So, two things that have come up time and again on Coronapod that are fundamental to getting on top of this pandemic are testing and tracing and this week, we're going to be focusing on testing, in particular rapid antigen tests, which have been described in some circles as game changers when it comes to letting governments and health services increase their testing capacity and strategy. But before we get into whether these really are game changers, let's maybe define what these rapid antigen tests are and how they differ from what's currently being done. Who'd like to take that one?

Noah Baker

I think Richard is better to take it, to be honest, but I do think that it feels like Groundhog Day to come back to testing yet again on Coronapod. But the question of how do they compare to other tests is important because I think people use the word ‘test’ freely when they're talking about coronavirus as though there is a coronavirus test but, in fact, there are way more than one coronavirus test and they all test in different ways and for different things, and rapid antigen testing is the latest in a long list.

Richard Van Noorden

Well, I mean, one way to think about this is to think about what happens in your body when you get infected, and thinking about that is a good way to figure out what these different tests are picking up. So, basically, before you show symptoms, the virus will be in your body if you're infected and then, very quickly, to the point where you're symptomatic, the amount of the virus that's in your body that would be caught by a swab stuck up your nose or in your mouth goes up. And then it sort of starts to tail off again, maybe a week later. The gold-standard PCR test is detecting the RNA of the virus itself, the genetic material. It will pick up that RNA if you’ve just been infected, it will pick up that RNA five weeks after you've been infected, perhaps even after you can no longer pass on the virus. There could be bits of RNA around. So, it's really accurate but not, however, very rapid. It has to be sent off to a central facility usually, analysed by technical staff. and if your country hasn't got its logistics together, it can take days or even a week to get the test back. So, separately, what we're talking about here now are these much more rapid antigen tests. Now, rather than detecting the genetic material of the virus, they're detecting proteins that are maybe on the virus’ surface, and they're not as sensitive. So, for example, a typical genetic test could detect a single molecule of RNA in a microlitre of solution. These antigen tests need thousands, maybe tens of thousands of virus particles per microlitre to produce that positive result. But they're cheap, they don't have to be processed in the lab, and they could give you results in half an hour or 20 minutes, and that's the exciting thing about them. So, if you take one of these tests just when you're infected, a week before you show symptoms, you might not get a result. As soon as the virus starts multiplying in your body, these antigen tests are going to start showing that you're infectious. If you've got a lot of virus around, they're going to pick it up. So, the hope for these rapid antigen tests is that if they can be rolled out in vast numbers and everyone can take them once or twice a week, you could more effectively stop the virus spreading than if you waited for these gold-standard genetic material tests.

Host: Benjamin Thompson

So, it seems like then it's a sort of direct competition between super accurate and slow versus cheap and pretty good. I mean, my dad was a salesman, and he always told me that you could have three things – good, fast and cheap – and you could pick two of the three, but you can never have all three at the same time, and it seems like that might be relevant here as well.

Richard Van Noorden

So, I wouldn't say it's a competition exactly. I would say that they're useful for different kinds of things. So, because they're not as sensitive, it's possible that you could be showing symptoms, you take one of these antigen tests, and you still get negative results. In fact, the advice is if you're showing symptoms and you get a negative result on this quick, fast, cheap test, definitely take a gold-standard test as well. So, it's not exactly going to solve all the problems that we have, and one of the remaining doubts is, what is the safe limit where the antigen test doesn't pick up that you have the virus but can we be sure that you're not really infectious? Like what if you have a medium-high viral load and the antigen test doesn't pick it up so you think you're okay? So, it's not quite clear that we know that. Michael Mina, this infectious disease immunologist in the US and Boston, he's been a vocal proponent of antigen tests, and he says, ‘So long as you do frequent testing and you can quickly identify people as soon as the virus ramps up to high levels, it doesn't matter so much for the purpose of controlling the pandemic if you miss one or two.’ On the other hand, in Italy, which wants to use these antigen tests at the airports, some people say, ‘I don't want us to miss one positive individual because, when you're trying to contain a small outbreak, that could lead to a very steep increase in the total number of cases.’ So, scientists are not completely sold on the idea that these quick antigen tests are going to be the answer that we need. And then the other sort of question that really hasn't been answered at all is like the psychology of this. If you ended up with something that you could take at home, which hasn't been approved yet – a lot of these antigen tests, they've still got to be checked for you by a professional – what if you get a positive result but no one can actually check that because you've done it yourself at home and you don't want to be quarantined? What if you just game the system and get someone else to take the test for you so you can be sure of a negative result? But these are still extremely exciting tests. At the end of August, the US granted emergency use approval to this antigen test from Abbott, and Abbott promises to ramp up production to 50 million a month in October. And there has been various approvals granted for other tests all around the world.

Noah Baker

As we learn more about all of these different types of tests, it's sort of crystallising in my head that a big part of this sort of journey for us as people to go on is to understand more about what they are. So, I think you mentioned psychology. I think that people, especially people that aren't scientists, will hear the word ‘test’ and they’ll think what that is doing is it's telling me if I've got coronavirus or not, and that isn't necessarily what these tests are all doing in different situations. By the sounds of things, you have to use tests in the context of like a testing strategy. And there is this danger of giving people a test that doesn't say whether or not you're positive for the virus or not. It says whether or not you have a level of antigens in your body that means you might be infectious. It feels subtly different, but it's actually very, very important. And I think to what extent do we need to focus on communicating what these tests mean to people as much as just getting them the tests in the first place, because changing their behaviour changes the outcome of any of these strategies to actually reduce transmission.

Richard Van Noorden

I completely agree, and what's really difficult is to deal with the uncertainty. And we saw that a lot with the other kind of tests that I’ve not mentioned at all. They're the antibody tests that are taken afterwards and say, does your body have the signatures that you've had the disease. Those were way less accurate and sensitive, and it's extremely confusing. People were getting these antibody tests and thinking does that mean I know that I've had it or I know that I haven't had it. And in the end, I'm not sure that those antibody tests were very helpful at all. They're extremely helpful for statistically sampling the population but not very helpful at all on the individual level. I think that's why regulatory agencies, at the beginning, were so keen to sort of really stick to the gold-standard PCR. And I think people have kind of gradually adapted their approach and realise this is such a huge issue that we just need all these other kinds of tests. We just need to communicate very, very clearly what they are measuring and what their sensitivities are. And, extra confusing is, during your course of this disease, the virus will wax and wane in your body. If you're testing a person when they're very infectious, the antigen test, pretty great. If you're testing a person that is slightly later stage, the antigen test, yeah, not so good at picking up whether you have the virus or not. And the argument is, maybe it doesn't matter at that stage because you're less infectious. So, the sensitivity, that actually changes, and you don't get that in many reports. People just want one number or two numbers to summarise the test’s performance.

Noah Baker

And I suppose the only way around that kind of variability, it comes back to numbers again. It comes back to if you test regularly enough. So, if you test everyone three times a week, in some world where that's possible to do that, then you can control for these things, right? You don't even have to rely on individuals being able to correctly report time since their first symptoms and correctly understand and interpret what to do with that information afterwards. And you can ultimately get to a scenario that the UK Prime Minister Boris Johnson was talking about in the future where, before anyone goes into a building, they could have a test, and that could give them a result immediately, and then you can decide whether or not they can go into that building based on whether or not they are infectious. This sort of Moonshot idea of essentially testing everyone continuously all the time, wherever they go anywhere. And then it's easy to know what to do as a user. You have the test at the door and if you get the mark on the thing, you don't go and if you don't have the mark on the thing then you do go in. And these antigen tests, in theory, we would assume that Boris Johnson is talking about when he says that, but as of yet, even these exciting tests aren't at the level where they could do that yet.

Richard Van Noorden

Right, yeah, they're not at that volume, and really, your experience of what these tests will do for you depends so heavily on engineering and logistics, and if your country has not got the logistics set up, not got efficient pipelines, it doesn't really matter how good the test is, you're not going to see the benefits. So, a lot of the problems that we're hearing about testing, I think, in the United Kingdom, in the United States, compared to, say, South Korea, or New Zealand, just comes down to organisation logistics. And that really, I don't think, has that much to do with the scientists looking to create these tests and validate them and think of new ways of detecting the virus.

Host: Benjamin Thompson

Yeah, I mean, I've got a stat here that said that at the end of August, India did over a million tests in a day, which proves that mass testing is possible.

Richard Van Noorden

Right, yeah, so, in the India case, they reached a million tests in a day in late August because they were using the antigen test because they didn't have enough of these genetic material PCR tests. It’s still actually not very clear in India exactly whether it's true that their use of the rapid antigen tests actually limited the spread of COVID because, yes, the number of cases decreased and death counts plateaued in Delhi, but, of course, there was also lockdown restrictions. And when the government lifted lockdown restrictions, there was a surge in infections again, which was picked up by the antigen tests. So, we saw all this happening, but whether the idea that rapid antigen tests could actually help to control the epidemic in themselves, we'll have to see. One amazing illustration of that is in the University of Illinois in the US, where they have this mass rapid testing programme that was actually created by chemists at the university, and they developed a saliva test. So, these are things where you are spitting in a tube. They did about 10,000, sometimes 15,000 tests a day, and they have portable testing sets all over the campus, and results come back in less than a day and so on. And this was all going great, and then the university reported a spike in campus infections. Why is that? Because some of the students tested positive and then went to parties. The question of whether the test could actually stop the virus spreading on the campus, it was really nothing to do with the test at all. It was to do with the behaviour of the people who tested positive and decided to carry on partying. Now, the university has since made changes and they've seen their numbers fall, so it isn't just the test itself. It's the behaviour of what you do when you're positive. It's the logistics of how the country sets the thing up. It's the psychology of this as much as it is the capabilities of the test themselves that really matter.

Host: Benjamin Thompson

Well, you mentioned a saliva-based test there then, Richard, and there are a few of those coming online now, but that kind of isn't the end of it.

Richard Van Noorden

Yeah, I mean, there are so many other tests that scientists are coming up with. We did a big article about that called the explosion of new coronavirus tests back in July, and all of these are sort of coming out of labs all over the world, but the tests aren't the be all and end all in themselves, and there's also a lot of hype. What tends to happen is that you get a press release about the test, which sometimes has to be walked back a few hours later, and the newspaper will just report that as the latest game changer. But it actually takes quite a long time, and it should take quite a long time for the test to be validated.

Noah Baker

That was one thing that I was going to ask, actually. Earlier on in the pandemic, the UK government reportedly ordered loads of antibody tests that we mentioned earlier on and then later on, had to sort of backtrack and say, ‘Oh, actually, we've found out that they don't really work.’ To what extent are all these various new tests actually meeting standards? Are they being validated? Are they being approved? What percentage of these antigen tests that we're talking about have actually been demonstrated in a reliable and robust way to be accurate to the levels that they say that they're accurate?

Richard Van Noorden

I mean, once you get to the point of a regulator approving the test, even if it's for emergency use, they've normally shown some kind of promising accuracy. The thing is that often a lot of money is given out to develop these tests before you know the answer. But we are getting some good news. So, in the UK, there was a lot of press about this company, DnaNudge, that made this quick 90-minute PCR test. And the UK government gave them £160 million, and there were a lot of very sceptical articles about this pointing out that we don't really have any numbers, and that was true. And then last week, they showed in a peer-reviewed study that they were very specific and 94% sensitive, so avoiding false negatives. And so, it turned out really well in that case. That test is not going to be the answer in itself. It requires this machine, which means that you can only put sort of one test in at any one time, and it means you can only have a few dozen of these tests a day on any one machine. So, it'd be really useful for a hospital where you need a quick confirmation, and it will help. There are lots of other tests like that in the pipeline. There's lots of trials being run, lots of money being given out, and inevitably, some of them are more hype than reality, but a lot of them are starting to work, and we will see more of these tests being rolled out. It's just going to be really important to understand how good they are and what they're telling you.

Host: Benjamin Thompson

So, it seems like we're getting horses for courses then. This test works best in this situation and that one works best in that situation, that sort of thing.

Richard Van Noorden

Yeah, absolutely. And I mean, also, I don't know if we're able to think beyond COVID right now, but all of this work is going to pay dividends for other kinds of viruses and diseases that emerge all over the world because we've had an absolute explosion in portable tests. And, in fact, some of the new tests have been expanded from earlier research on things like Zika virus, where it was really important to get a quick idea in the field of whether you were looking at Zika infection, and we're sort of seeing some of that carried over now to SARS-CoV-2.

Noah Baker

It's always great to see silver linings. It reminds me of something Amy Maxmen said in a podcast earlier on, which was all it takes is a pandemic to find out that we can do these things. And so, at least there’s an advantage going forward.

Richard Van Noorden

it's very encouraging to hear about all these tests. It's just also very confusing at the same time. And as I said, it probably depends more on logistics than it does on science as to whether these get rolled out quickly and efficiently and straightforwardly in whatever country you're listening to this from.

Host: Benjamin Thompson

Well, as is so often the case with what we’ve talked about on Coronapod, I guess we'll have to wait and see how this works out and what goes on. But for the time being, Richard and Noah, thank you so much for joining me.

Noah Baker

Thanks, Ben.

Richard Van Noorden

Thanks.

Host: Nick Howe

Listen out for more Coronapod next week. Coming up in this week's show, we'll find out about controlling cell death in neurodegenerative disease. That's coming up after the Research Highlights read, this week, by Dan Fox.

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Dan Fox

In a case where going green might be less environmentally friendly than it sounds, parts of the Arctic tundra have become greener, as rising temperatures let plants grow. Satellite imagery and observations from the ground suggest that the often-frozen Arctic tundra has become greener since the 1980s. Now, a team of scientists some analysed high-resolution satellite imagery and found that between 1985 and 2016, 37% of the Arctic tundra grew significantly greener. And since the turn of the century, the most northerly regions have experienced the most intense greening. This increased vegetation may disrupt the delicate ecological balance in the region and could even leave the tundra vulnerable to wildfires. Defrost the rest of that research in Nature Communications.

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Dan Fox

The leaves and stem of Dendrocnide excelsa carry what looks like an inviting fuzz, but touching it probably isn't a good idea. The fuzz is actually a coating of venom-filled needles that can cause an intense pain that sometimes lasts months. That's why it's also known as the giant stinging tree. Now, a team of researchers have analysed the venom and discovered a previously unknown family of peptides. The team have named them gympietides after gympie-gympie – the tree’s name in the Indigenous Gubbi Gubbi language. Investigation into the peptides revealed that not only that they generate pain signals, but also suppressed the mechanism that stopped those signals. The researchers who have all fallen victim to these things previously, hope their findings could spur research into an antidote. Reading that research is painless. You can find it over at Science Advances.

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Host: Nick Howe Next up on the show, reporter Ali Jennings has been investigating how particular proteins are involved in controlling cell death and the health of cells in neurodegenerative disease.

Interviewer: Ali Jennings

Junying Yuan has conquered death – a certain kind of cell death that is. In tissues suffering from neurodegenerative disease, cells often have to go through a complicated internal process in order to die. But by blocking just one enzyme involved in this process – an enzyme called RIPK1 – Junying can stop cells from dying all together. Unfortunately, this leads to another problem.

Interviewee: Junying Yuan

Because we know that neurodegenerative diseases, such as ALS, Parkinson's, Alzheimer's, are all characterised by accumulation of misfolded proteins. So, in other words, in these diseases, you not only have cell death but the protein homeostasis is also disrupted. So, it's like, if you just inhibit cell death, it's like keeping a cell alive, but they're not functional because their jammed with diseased proteins.

Interviewer: Ali Jennings

Junying and her team wanted to find a way to not only stop cell death but to also get rid of all of these diseased proteins. So, they took different kinds of molecules and applied them to cells grown in the lab to see if any molecule would have the desired effect.

Interviewee: Junying Yuan

Altogether, we screened 170,000 compounds, and basically, we came up with two hits that we call ICCB-17 and ICCB-19.

Interviewer: Ali Jennings

Both compounds stopped cell death and cleared cells of junk proteins. But finding the molecules was the easy part.

Interviewee: Junying Yuan

From there to the next step is finding how the small molecules do it, which is very difficult, because you can imagine that you threw these two compounds onto the cells. The cell has tens of thousands of proteins. How do you figure out how the compound works? It's a very challenging question.

Interviewer: Ali Jennings

To answer it, Junying went back to RIPK1, the enzyme she had originally blocked to stop cell death alone. If the new compounds she had found also stopped cell death, then maybe they worked in a similar way. Before RIPK1 can trigger cell death. It must first be attached to another protein, a protein called TRADD. So, Junying’s team analysed how her new compounds interacted with TRADD. It turns out they bound tightly together. This binding stopped TRADD from attaching to RIPK1. With no TRADD attached, RIPK1 could no longer trigger cell death. But that was only half the story. How did the compounds also encourage the clean-up of misfolded proteins? Well, it turns out that TRADD lives a double life. When it's not attached to RIPK1, TRADD can interfere with another pair of enzymes, enzymes that would normally promote a cell's self-cleaning. When Junying’s new compounds bind to TRADD, TRADD can no longer interfere with these enzymes, leaving them free to stimulate the clear-out of junk proteins. So, blocking TRADD can simultaneously stop a cell from dying and encourage it to clean itself up. But that was in cultured cells. Would it work in a living animal? The team decided to test it on a model for neurodegenerative disease, a transgenic mouse whose cells accumulate diseased tau protein.

Interviewee: Junying Yuan

So, we injected the misfolded tau into the hippocampus and that will rapidly induce the transgenic tau to aggregate, and then we treat the animal with the compound and we see that the accumulation of tau disappears.

Interviewer: Ali Jennings

So, does this mean that these molecules could be used as new therapies to treat human disease? Junying is sceptical.

Interviewee: Junying Yuan

At the same time, these are just proof of concept compounds. They can target TRADD, but they are not potent enough or stable enough in vivo, which means that we cannot use them as drug. So, a lot of work, chemistry work, medicinal chemistry, will have to be done to improve these compounds, to make them stable enough to be used as a drug. So, this is the next step.

Interviewer: Ali Jennings

But if they can improve the compound successfully, then Junying hopes they really could make it into the clinic.

Interviewee: Junying Yuan

So, if we talk about, for example, ALS, which is a sort of a typical neurodegenerative disease that has both accumulation of misfolded proteins, cell death and inflammation. So, if we have a compound that's stable enough to be in vivo, maybe ALS will be one of the diseases that can undergo clinical trial. But we still are working on how to figure out what would be the first indication for this kind of compound.

Interviewer: Ali Jennings

From first discovering how to block the enzyme RIPK1 to finding these new compounds that can help keep cells alive and healthy, this is a detective story that has taken Junying the better part of 20 years to unravel. Now, with this new discovery, Junying cannot only conquer cell death, but she's learned how to give them a better kind of life.

Host: Nick Howe

That was Ali Jennings. To find out more about Junying’s work, head over to the show notes, where you'll find a link to her paper.

Host: Benjamin Thompson

Finally on the podcast, it's time for the weekly Briefing chat, where we discuss a couple of articles that have been highlighted in the Nature Briefing. What have you got for us this week, Nick?

Host: Nick Howe

Well, Ben, this week, one thing caught my eye, which is something that I think you and I, in our jobs, are familiar with quite a lot, and that is sometimes scientific papers are kind of hard to read.

Host: Benjamin Thompson

I don't know what you're talking about, Nick Howe. Every time I'm just there, laser light clarity.

Host: Nick Howe

Well, maybe you are better at this than me. But this is an article that I was reading in Nature Index that has been talking about a few analyses that have been done on scientific papers. And in one, they've said that basically, acronyms, jargon, long sentences, they really cloud scientific research writing sometimes. And in one of the analyses, they looked at 24 million paper titles and 18 million abstracts, and in 90%, of paper titles and in 73% of abstracts, there was at least one acronym.

Host: Benjamin Thompson

Yeah, I mean, I was being flippant earlier. I will say that so often when I'm reading a paper, I will have to keep going back to the very first line where they use the long version of whatever that acronym is. If it is getting more prevalent, I mean, it begs the question, why is this? Is it because techniques are getting longer names? I mean, I don't know.

Host: Nick Howe

It’s not clear, like it's not something that was really discussed in the article, but it definitely is getting more prevalent. So, for example, in the analysis, they found that in 1956, there are around 0.4 acronyms per 100 words. Whereas today, there's about 4 acronyms per 100 words. So, it seems like it's definitely getting more prevalent, and the trouble is, like a lot of these acronyms are not common. It's not like ‘DNA’ and stuff like that, that people are familiar with. 79% of the acronyms that they looked at had been used fewer than ten times in the scientific literature, so if you've missed those ten papers, you're not going to know what the acronym even is.

Host: Benjamin Thompson

Yeah, you have to be sort of following the rabbit hole to find the original source of them. Did the authors of this report make any suggestions? Are they calling for greater clarity or something like that in papers?

Host: Nick Howe

Yeah, I mean, they point to the fact that science is something that needs to be accountable. A lot of research is funded by people's taxes, so they should be able to understand it. And also, it's not just the general public. There was a separate analysis that was discussed and in that, they found the papers with more jargon, more acronyms and that sort of thing, they actually get cited less as well. So, other scientists are not able to use those papers as well. So yeah, it's just a call for more clarity. And well, if you are clearer, you may get more citations too, so there's a little bit of an incentive there.

Host: Benjamin Thompson

Well, Nick, I've got an acronym for you, and it's BBQ. And it is, of course, the international acronym for barbecue, the art of cooking food outside on charcoal. But there's a story in Nature this week that suggests that, in some cases, at least in Europe, this charcoal might have a problematic origin.

Host: Nick Howe

Oh, right. So, has it come from like not-well-managed forests or something like that?

Host: Benjamin Thompson

Bingo. So, there is some research that's been done looking at where charcoal originates from. And what they've done is, in this case, they've analysed samples from 150 charcoal bags bought in 11 different countries, and they've used this rather nifty new microscope technique to analyse where this has come from. And the results suggest that almost half of the barbecue charcoal bought in Europe contains wood from tropical or subtropical forests, and some of it is not labelled as to what it actually is.

Host: Nick Howe

Okay, so are there not ways to check where this comes from or are these checks and balances just not working in this case?

Host: Benjamin Thompson

Well, it is quite difficult to work out what a lump of charcoal is. It doesn't smell like the tree it used to be. It certainly doesn't look like the tree it used to be. But in this case, researchers have used 3D-reflected-light microscopy, and what it does is it digitally reconstructs sections of charcoal from these kind of irregular lumps, and it creates images from which the original wood it came from can be identified. Really, really clever. And it goes down to the genus level in some cases, and this information can be used to disprove where the bag says the wood is from.

Host: Nick Howe

Oh, wow, so with this in mind and with this technique, what's going to be done about this? Are there going to be more rigorous checks to make sure that it's not coming from protected forests and things like that?

Host: Benjamin Thompson

Yeah, in some cases, the researchers found that the origin or the species of wood was labelled incorrectly. But it's kind of a difficult one because once charcoal gets into the EU, the laws that kind of protect illegally logged timber don't apply. The authors of this work, they're calling to extend these regulations to make sure that suppliers label their bags properly and stop any illegally logged charcoal from getting in.

Host: Nick Howe

Well, here's hoping that this analysis will put a spotlight on this sort of thing going on and something can be done about it. But thanks, Ben, for chatting to me. And listeners, if you'd like more stories like these then make sure you check out the Nature Briefing. We'll put a link of where to sign up and links to stories we've discussed in this week's show notes.

Host: Benjamin Thompson

That's all for this week. As always, if you want to get in touch with us, then you can reach us on Twitter – we’re @NaturePodcast – or send us an email – we’re podcast@nature.com Send us a message and we might read out on the show. I'm Benjamin Thompson.

Host: Nick Howe

And I'm Nick Howe. See you next time.