A new generation of radiotherapies for cancer, and why we sigh

Interactive Transcript

spk_0 This is the Science Podcast for October 2, 2025.

spk_0 I'm Sarah Cressby.

spk_0 First this week, staff writer Robert Service joins us to talk about a boom in nuclear medicine

spk_0 for cancer, for more powerful radio isotopes to improve precision and cell targeting.

spk_0 Next on the show, why we sigh?

spk_0 Researcher Maria Clara Nova Silva discusses how deep breaths cause tiny rearrangements

spk_0 at the special interface where air needs lungs, keeping them healthy and flexible.

spk_0 Now we have Robert Service.

spk_0 He wrote a story this week on a search in radio pharmaceuticals research or radioactive drugs

spk_0 for cancer.

spk_0 Hi Bob, welcome back to the podcast.

spk_0 Thank you so much.

spk_0 You know, I might have started this with why now, but that is like the whole story.

spk_0 There is so much going on right now with radio pharmaceuticals, whether it's sourcing where

spk_0 you know, the radioactive particles are coming from, the kinds of drugs they're making with

spk_0 it.

spk_0 There's ongoing clinical trials.

spk_0 There's so much happening.

spk_0 We're going to get into all of that.

spk_0 Let's start with how these drugs work and how the targeting works.

spk_0 I think this example that kind of started things off with iodine is a really good place

spk_0 to kind of get people oriented.

spk_0 Of course, yeah.

spk_0 Radiation in chemotherapy and cancer treatment has a very long history, 100 years.

spk_0 In most radiation treatment still today is done by external beam radiation.

spk_0 That's where they target a beam of radioactivity out of cancer or something like that.

spk_0 But what we're talking about here are radio pharmaceuticals.

spk_0 So what they do is they link an atom of a radioactive particle that's going to decase,

spk_0 which means that it's going to shed particles naturally as it decays into another product.

spk_0 In that radiation, what you can do is you can target it to cancer cells.

spk_0 So they bind specifically just ideally only to cancer cells.

spk_0 And that radiation hopefully will then kill the cells.

spk_0 The history of the use of radioactive iodine started out a long time ago, back in the

spk_0 1940s when a researcher at MIT realized that thyroid cells naturally take up iodine

spk_0 and he wanted to treat patients that had overactive thyroid.

spk_0 His thinking was that if he used radiation that concentrated in the thyroid,

spk_0 some of the cells might be killed by the radiation and then thyroid levels of the thyroid

spk_0 hormones would drop back to normal.

spk_0 So the experiment worked and he worked on it for quite some time and showed that about

spk_0 80% of his patients showed improvement of the radioactivity was concentrating in the thyroid

spk_0 because thyroid cells naturally sift out iodine in order to do their job.

spk_0 And that's the activity that targeting, it was part of the function of that organ.

spk_0 But now we're talking about cancer cells.

spk_0 So they have very different identities.

spk_0 They have different molecules on their surfaces and you have to target them if you want to get

spk_0 radiation to them.

spk_0 So what are some of the ways you could target a cancer cell growing in the body that's

spk_0 not going to just preferentially take up your radioactive material?

spk_0 So I'll fast forward the story then to the late 1990s when people realized that you could

spk_0 make this link between targeting specific molecules on the surface of cancer cells and then

spk_0 tie them to radioactive compounds.

spk_0 There's a lot of different ways they tried to target cancer.

spk_0 But they did try to say, okay, if we can find out something unique about these cancer

spk_0 cells, then we can target it with a molecule, attach a radiation to it and you're good to

spk_0 go, right?

spk_0 That was that concept back in the day.

spk_0 That was the concept and it certainly has been shown to work.

spk_0 The key is this locking key mechanism that biology uses extensively.

spk_0 And so a lot of cells have unique receptors on the surface of their cells and that is true

spk_0 with cancer cells as well as normal cells.

spk_0 So in many cancers, you get a strong upregulation of certain kinds of surface receptors.

spk_0 That's the lock.

spk_0 So for example, in prostate cancer, something called PMSA gets strongly upregulated.

spk_0 So people develop targeting agents that specifically seek out those receptors or on neuroendocrine

spk_0 tumors.

spk_0 There's a different one called the somatostatin receptor and on and on and on down the list.

spk_0 Molecular biologists and biochemists for decades have been laying the groundwork by finding

spk_0 these specific receptors on cancer cells that is now enabled a new generation of cancer

spk_0 therapies to come about.

spk_0 The field is very hot right now, but it's been a slow burn for a few decades.

spk_0 What have been some kind of big hurdles?

spk_0 Why has it been so hard to come up with radio drugs that can go to trials?

spk_0 There are a number of different problems.

spk_0 One is that just even developing the sources for these compounds is difficult because what

spk_0 you want to do in oncology for radiopharmaceuticals is have something that will produce radiation,

spk_0 strong radiation for a very short period of time.

spk_0 So hours, days at most weeks, typically, because you want the patients to get the benefit

spk_0 of killing the cancer cells, but then not have the radiation damage anything else in the

spk_0 body.

spk_0 And so what it means is that these drugs can't be stockpiled.

spk_0 They're all very short-lived.

spk_0 So you have to produce the radioactive isotopes, ship them to a place that's then going to

spk_0 link them to a targeting agent, then ship them again to hospitals around the world, get

spk_0 all your patients ready to go and line up and then deliver the radio isotope therapy and

spk_0 then monitor them.

spk_0 So there's a lot to manage there that is not in the conventional drug pipeline.

spk_0 This is a supply chain that has a timer on it.

spk_0 And also everybody along the line has to be able to deal with radioactive materials.

spk_0 Absolutely.

spk_0 So there's more costs and potentially not necessarily any more benefit, although that

spk_0 now we're starting to see, you know, those benefits, gain steam.

spk_0 At least one has been approved, but then now we're starting to see that there isn't

spk_0 enough of this radioactive material to go around for all the clinical trials that people

spk_0 want to do.

spk_0 As you can imagine, every single radio isotope is unique and it has to have its own supply

spk_0 chain.

spk_0 Right now, there are many isotopes that have a perfectly healthy supply chain and they're

spk_0 being made in abundance and everything is fine.

spk_0 So for example, one of the recently approved drugs is a drug called Lutophera.

spk_0 It's from Novartis, Lutitium 177 is the radio isotope.

spk_0 It has a quite healthy supply chain and for manufacturing Lutitium.

spk_0 But one of the things people are trying to do now is replace Lutitium with a different

spk_0 radio isotope called actinium 225.

spk_0 And actinium 225 has a rickety supply chain, I would say.

spk_0 It's not used commonly in clinical medicine yet.

spk_0 And so there's a lot of efforts to build that supply chain to actually find new ways to

spk_0 make actinium to make it in larger quantities to ship it, all that kind of thing.

spk_0 And what are some of the different properties that researchers are exploring?

spk_0 Why change from one isotope to another?

spk_0 So each isotope has its own sort of set of characteristics.

spk_0 And the most common one that people think about is its half-life.

spk_0 So this is how much of that isotope will decay in X number of hours or days or weeks or

spk_0 eons.

spk_0 So some half-lives are extremely long, but the medical isotopes that are favored are again,

spk_0 like we said, short.

spk_0 So Lutitium, I believe, is six and a half days for a half-life.

spk_0 So that means in six and a half days, half of that radiation will be gone.

spk_0 It's like you're shipping ice cubes around.

spk_0 So these things are melting as you go.

spk_0 Yeah. And where are you going to cite your plant so that you can get it out the door,

spk_0 get it to the pharmaceutical plant, then get it to the hospitals or the clinics where

spk_0 this is being tested.

spk_0 It's very much a logistics issue.

spk_0 Very much.

spk_0 Besides half-life, there's also two different kinds of decay that you can consider for

spk_0 reuactotreatment, alpha and beta.

spk_0 So beta emitters include elements or isotopes like Lutitium 177.

spk_0 And these emit energetic electrons and positrons.

spk_0 They're quite good if you need that radiation to travel a certain distance,

spk_0 because it doesn't get absorbed right away in tissues.

spk_0 That means it might be good for a larger tumor or diffuse tumors or things like that.

spk_0 Whereas alpha decay emits neutrons and protons.

spk_0 And these pack a lot more punch.

spk_0 So not only do you get more energy coming out of these decay products,

spk_0 they also get absorbed quite quickly so they don't travel very far.

spk_0 There's more experience in the community with beta emitters.

spk_0 There's a lot of effort now going on to develop alpha emitting versions of previous drugs

spk_0 or entirely new drugs.

spk_0 And the thinking there is is that if you really can isolate the radioactivity

spk_0 very locally just to tumor cells, then you can really do a lot more damage.

spk_0 You get this whole cluster of radiation damage to the DNA in those cells

spk_0 and they just can't recover.

spk_0 We have a bunch of different variables here now.

spk_0 We have the half life of the radioactive material, the strength,

spk_0 the kind of particles it delivers, how powerful they are, how far they travel.

spk_0 And we also have how it's targeted.

spk_0 What kind of different targeting techniques are researchers looking into

spk_0 to get this radiation right next to cancer cells?

spk_0 There's a lot going on here.

spk_0 And of course, this builds on the basic research of cell biologists and molecular biologists

spk_0 and oncologists that they've been doing for decades.

spk_0 So there's a lot of exploration going on

spk_0 and defining those molecules that are unique on the surfaces of different types of cancer cells.

spk_0 I mentioned the PMSA.

spk_0 That's the protein that gets up-regulated on the surface of prostate cancer cells.

spk_0 Well, it turns out normal cells have PMSA as well, not as much for sure.

spk_0 But that means that you might end up getting some damage to normal tissue.

spk_0 So people are developing compounds to target different receptors in prostate cancer cells

spk_0 called ACP3.

spk_0 And those are less abundant on normal cells.

spk_0 And this story gets played out again and again and again as researchers consistently try

spk_0 to home in on just those molecules that are on cancer cells.

spk_0 There's also this idea that the linker between the targeting portion of the drug and the radioactive

spk_0 payload, the linker can be more than just structural, that it can have a function.

spk_0 Right. So what you want in a drug at the end of the day is something that will kill cancer cells,

spk_0 but not harm your normal tissues.

spk_0 Any drug is going to, even if it's a directed compound, will hopefully send most of its therapeutic

spk_0 power towards the cancer. But there's going to be some atoms or some molecules of this stuff

spk_0 that don't make it there. Those have to get clear out of the body and then when the

spk_0 radiopharmaceutical has finished its job, tissues process it and also have to get those out of

spk_0 the body. Folks are coming up with these novel linkers that they've recognized that certain cells

spk_0 in the kidney, for example, have unique enzymes that will cut very short protein fragments called

spk_0 peptides between two very specific amino acids that these peptides contain. And so what they do is

spk_0 they put a linker with just those two peptides in it. So that way, when the radiopharmaceutical

spk_0 reaches those kidney cells, it will clip them apart and just begin cutting this thing apart to make

spk_0 it easier to get rid of from the body. They're easier to break down because you put this little

spk_0 recognition, cut me here, cut me here. I'm going to get out of here a little bit quicker if you kind

spk_0 of guide the way. That's it exactly. Circling back to the production of the isotopes,

spk_0 researchers are trying new ways of creating these radioactive particles. Can you talk a little bit

spk_0 about some of those efforts? Absolutely. And I want to set this up with a story about how it's

spk_0 currently done because at Oak Ridge National Lab, back in the 1960s, they had an effort to produce

spk_0 nuclear reactors that use thorium and it ended up not being a project that got pushed forward in

spk_0 the United States, but they wound up with a bunch of thorium that they had to house at Oak Ridge.

spk_0 One of the decay products of thorium is actinium 225 and actinium 225 is one of the most promising

spk_0 medical isotopes there is. So for the last 25 years, researchers at Oak Ridge have had what they

spk_0 call thorium cows that they essentially milk. These are vials of thorium that produce actinium

spk_0 225. They harvest the actinium 225 from these. They do this year round and all their work, all their

spk_0 producers less than a grain of sand of actinium every year. That's enough to treat hundreds of

spk_0 patients, which is great, but if all the actinium drugs that are being developed succeed,

spk_0 they're going to need millions of doses, right? And so they need a vastly upscale. So how do they

spk_0 go about doing that? Well, there's a bunch of different methods I won't go into, but one of them

spk_0 as a new reactor, it's called a linear accelerator that's, it has been built and is now being commissioned

spk_0 in Utah. Linear accelerators have been used to produce medical isotopes for some time, but what

spk_0 makes us when unique is they've come up with a new way to do it more efficiently. So they've redesigned

spk_0 the front end of it with a what they call an ion source that creates a much richer beam of ions

spk_0 that they can then fire at targets that then produce the medical isotopes. They can make 40 different

spk_0 compounds or so. Again, they can make them in a relatively large supply. And so it has a lot of

spk_0 prospects for eating in all kinds of treatments, including actinium based drugs. The main thing to

spk_0 underscore here is that there's a lot of excitement in the nuclear medicine field because for a number

spk_0 of years and decades, I think practitioners in the field have felt like progress has been held

spk_0 down by a lot of the challenges. And now there's been enough positive results and frankly, commercial

spk_0 success that then drives the market forward and encourages other companies to get involved because

spk_0 this call can't just be academic work. You've got to be able to scale this up in ways that can produce

spk_0 enough of these compounds to help millions of patients. There's been enough progress on both of those

spk_0 sides now to create a lot of enthusiasm, not just in the academic community, but also in the commercial

spk_0 landscape as well. Thank you so much, Bob. You're welcome. Robert Service is a staff writer for science.

spk_0 You can find a link to the story we talked about at Science.org slash podcast.

spk_0 Next up, we hear about the role of sying in long health.

spk_0 Imagine two curious minds collide and a new idea is born. This is particles of thought from the

spk_0 producers of Nova. I'm Haqim Oluşey. Science really is about putting forth bold ideas and then

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spk_0 Let it all out. We sigh sometimes to release stress, sometimes to express exasperation,

spk_0 and sometimes it turns out to reconfigure our lungs. This week in science advances Maria Clara

spk_0 Noviah Silva wrote about measuring the effects of size on the internal mechanics of lungs. Hi Maria,

spk_0 welcome to science podcast. Hi, thank you very much. Yeah, I really enjoyed that sigh. I actually

spk_0 a lot of pleasure from briefly started. Whoa. Yes. So is there a definition of sying of

spk_0 size that you're working with here for the scientific paper? Yeah. So basically what we usually do

spk_0 is that we take tidal breath. So this means that usually we have this given volume that is not so high

spk_0 that we are putting in and out of our lungs. And when we take a sigh, this means that this volume

spk_0 is larger. So we are putting more air, we are expanding our lungs, and then we are reconpressing.

spk_0 We do it both voluntarily and involuntarily. And my dog also sighs. Exactly. Dogs are pretty good

spk_0 at sighing. So I guess I shouldn't be surprised that it serves some kind of physiological purpose.

spk_0 But what made you look to see if this was important for health, important for our lungs?

spk_0 This work was started around 13 years ago. Basically, my supervisor was discussing with a medical

spk_0 doctor. And he said that our pulmonary compliance, which is how easily we can expand our lungs.

spk_0 He noticed that when you are under mechanical ventilation, for example, and we don't have the

spk_0 size every once in a while that we unconsciously take, this pulmonary compliance is gradually

spk_0 decreases. So this means that it's harder to expand our lungs. And once we take these deep breaths,

spk_0 it actually gets reset. It gets back to normal. From an interfacial properties point of view,

spk_0 the difference between a tidal breath and a sigh is just how much area you are changing.

spk_0 This is actually a key point for us. And this is why we decided to investigate why is this

spk_0 important in an interfacial property kind of perspective? I think this is super interesting.

spk_0 So if you're on a breathing machine, we saw this a lot with COVID. This happens if you're in

spk_0 the hospital and you're not able to breathe on your own. There's a machine that's saying,

spk_0 have some air. We're taking it back out. Have some air. We're taking it back out. But that is not

spk_0 going to sigh for you. And there might be some relationship you suspected between sighing and

spk_0 kind of like this reduced capacity to like flex and bring in air in the lungs under mechanical

spk_0 ventilation. We need to take a side trip now, though, to kind of what is happening at the

spk_0 interface of the lungs and the air. So if we think about our lungs, right, it's a very complicated

spk_0 structure. And the smallest one we have is the audio light. And inside of our audio light,

spk_0 we have this very thin liquid layer. And this creates liquid air interface. We are constantly

spk_0 expanding and compressing this area. The things that are in bulk, which is below the interface,

spk_0 all the molecules are surrounded by themselves. But at the interface, they are being

spk_0 contact with the air in this case. So there is this tangential pool between the molecules

spk_0 that will basically define how large is this surface tension. Basically, this shows us how

spk_0 difficult, how much energy costs to increase this interfacial area. Because if the molecules

spk_0 really like to be together, then it's worse for them to be in contact with the air. So if we only

spk_0 had watering inside of your life, the cost of expanding them would be enormous. That's a lot of

spk_0 surface tension, right? Exactly. The water molecules want to hang out together. They don't want to let

spk_0 air through. And so this is where we get surfactant. Exactly. There's this layer of surfactant.

spk_0 Can you talk about what this miracle film is? So this is where the surfactants come,

spk_0 because basically they have, I don't know if I should get into the details of that.

spk_0 It has a mixture of molecules that kind of break that surface tension and kind of the mixture,

spk_0 what supplies, what you need in order to have nice, compliant lungs. Exactly. So basically,

spk_0 we will have lipids and proteins. And they will form a film at our interface in normal

spk_0 context. This can either be a monolayer, which is only one layer of molecules, or it can be in our

spk_0 case for the long surfactant, something that has multi layers. So we have this top part that has

spk_0 some heterogeneously distributed multi layers. I first came into contact with surfactant, because

spk_0 this is something that is lacking in babies that are born really early. And it's very difficult to

spk_0 get their lungs to inflate and deflate to use laben's terms, because there's nothing in there to

spk_0 kind of break the surface tension. This is a big cause of health problems in these premature

spk_0 infants. And surfactants really change the game for neonatal care. If the baby is born too early,

spk_0 there's not enough time for this surfactant to be produced. The baby will have this huge

spk_0 interfacial area, but there's nothing to regulate it and to give the optimal properties.

spk_0 So this is why it has this difficult to breathe. They're not doing the air water interface when

spk_0 they're in utero, right? Exactly. They're not having a deal with that. Yeah, exactly. But then

spk_0 the main point is that for these disease, there is the solution. This is called the surfactant

spk_0 replacement therapy. And what happens is that they extract surfactant from the lungs of animals.

spk_0 And actually, this is what we used in our study. And this is what we called, we assume that it was

spk_0 a relevant mimic of what we have in the lungs. And this is what they give to

spk_0 neonatals that don't have the surfactant. It's quite a well established treatment. And if I may add

spk_0 some, I mean, of course, this we cannot say for sure. But one of the things we saw in our study,

spk_0 and also other people have seen in literature, is that we need to kind of pre-condition the

spk_0 interface. And of course, this is something that I needed to be tested in vivo. But if we think

spk_0 about when we are being delivered, right, we are giving birth to the babies need to expand their

spk_0 lungs and they have this first crying. So what this first crying is what it takes to pre-condition

spk_0 our lungs. And what if this is what we need to really get the surface stress lower and really

spk_0 set the conditions right? Because right before the big cry is the big inhale. Exactly.

spk_0 It's the big breath. And yeah, so I mean, it's interesting to think about even though it's not

spk_0 for sure. With neonatal care with babies that are born prematurely, they can be given their

spk_0 surfactant as medicine. And that will help them breathe. But there are cases like what you talk about

spk_0 in the paper, where with what happened during COVID, where more and more surfactant didn't seem to

spk_0 be helping. This was very important when we had COVID. There was this thing called ARDS,

spk_0 acute respiratory distress syndrome. It's somewhat similar to this other disease. In this case,

spk_0 you can have a lung injury and this will trigger some lung inflammation and so on. And basically,

spk_0 your surfactant can be inactivated. And you add more and you add more and it does it solve the

spk_0 problem. For this disease, there's not really a treatment. It still has a very high mortality rate

spk_0 associated. So one of our main motivations was of course, I mean, we are not

spk_0 dwelling into the disease part. But in order to understand how the disease conditions are changing,

spk_0 we have to understand how it works in a healthy condition. We now have established a lot of ground.

spk_0 We've established the existence of surfactants and the compliance of the lungs,

spk_0 like how willing they are to inflate and deflate and that can change. It's affected by illness.

spk_0 What you want to know was where does sying fit into all of this. And so how did you start to

spk_0 to ask that question? What kind of experiments did you do? One key point for us was that,

spk_0 I mean, in the literature, it's often mentioned these multilayers that I was talking to you about

spk_0 before. And it's interesting because if we only take into account what I was telling you the surface

spk_0 tension, this is a property that is purely thermodynamical. This is something that is a state

spk_0 variable at constant temperature. It will only depend at how much molecules you have of

spk_0 this refracting at your interface at the surface concentration. And all these matters of sying and

spk_0 how fast you're breathing and the breathing deformation and this microstructure is not taken into account.

spk_0 Of course, we are not the first to study lung surfactant. This has been going on since many many many years.

spk_0 But our point was then to take this into a new framework. How can we take into account the

spk_0 breathing deformation and how can we take into account this microstructure? How are you able to

spk_0 measure the influence of the microstructure? What's going on with the surfactant and what happens

spk_0 when you change how much volume is going in and out of the lungs? So what we did actually was to

spk_0 measure what we call the surface stress. For this, we also studied how different amounts of area

spk_0 change is impacting this surface stress. So basically, we applied different amounts and we saw how

spk_0 this changed. And of course, we have to relate this to how the interface looks. And to do that, we did

spk_0 also some structural characterization. This was done in two ways. First was through neutral

spk_0 reflectometry. And in this way, we have more real structural characterization, what is below the

spk_0 interface. But also, we did some compositional analysis. So you're doing this very fine analysis

spk_0 of the surface. And you're seeing different things with different stresses. So what is

spk_0 sighing change about all these stats that you're gathering? So our lungs reflectant mixture. It has

spk_0 a very broad composition, right? We have different lipids and we have different proteins. Basically,

spk_0 the lipids we can classify in two ways. We have saturated lipids and unsaturated. The main difference

spk_0 between them is that the saturated they can handle compression very well. This means that they can

spk_0 pack super well. On the other hand, the unsaturated lipids because they have this double bond,

spk_0 their chains will be kind of tilted. So this means that if you compress them, they will not handle

spk_0 this as well as the saturated lipids, right? So there was already an ongoing discussion that

spk_0 it's very likely that these saturated lipids are enriched at the interface so that you can handle

spk_0 this compression. Of course, the proteins are there to likely regulate these dynamics,

spk_0 but it was not very known how this enrichment was achieved and how much or if it was necessary.

spk_0 So what we discovered through our experiments is that when you take these deep breaths,

spk_0 everyone's in a while, what happens is that you have a restructuring of the interface.

spk_0 So this means that if you look at our new term reflectometry data, if we are only

spk_0 apply tidal breaths to that average in our nothing special, smaller area deformations,

spk_0 it looks very similar to what you have if you are not doing anything at your interface.

spk_0 The structure is quite similar, but once you apply a deep breath, every once in a while,

spk_0 what happens is that this structure becomes enlarged. And if now you compare this with our

spk_0 other compositional analysis and also our difference in area strain amounts that we did

spk_0 in the surface stress characterization, we saw that indeed it seems to be enriching in the

spk_0 saturated lipids. So it seems that this large area deformations are necessary to enrich the

spk_0 interface so that these unsaturated lipids are allocated in these multilayer structures.

spk_0 Okay, so the ones you don't want, the one with the doubles bands, the wiggly ones,

spk_0 yes, they're being kind of repressed, they're being shunted aside so that you can enrich

spk_0 with the saturated. It's not that we don't need the unsaturated lipids, they are also important.

spk_0 They need both. Right, this mechanism is very interesting, it seems to be all regulated by

spk_0 these proteins. And they are present in very small amounts, but still they have such an important

spk_0 function in the long-suffactant case. I think I understand the reset that happens when you

spk_0 sigh, it gives you a more desirable distribution of saturated fats. Exactly, it doesn't delete anything,

spk_0 it doesn't stop or increase the production of anything, it's just more of a rearrangement.

spk_0 This suggests that sighing is good for us and that if you're going back to the

spk_0 mechanical ventilation that we kind of started with, does there need to be more sighing?

spk_0 Or does it need to be some kind of sighing in those situations?

spk_0 Of course, we did the experiments in vitro condition, so extrapolating this today in vivo

spk_0 requires a lot of care and testing. That being said, what we saw in vitro is that if you don't apply

spk_0 this size every once in a while, is that gradually the surface stresses increase,

spk_0 it will become harder and harder and it will take more work to breathe.

spk_0 So this means that we should have a timescale of how often do we need?

spk_0 In our individual experiments, this was around 15 to 45 minutes.

spk_0 What is a person walking around in the world? How often do they sigh?

spk_0 The physiological rate is around a dozen size per hour.

spk_0 And yeah, we do this without noticing. Of course, we tested this in very controlled ways.

spk_0 It was always the same area of strain and so on.

spk_0 Of course, in the physiological manner, it's something that it's not so precise.

spk_0 So if you were going to figure it out for medical treatment, you would have to do various tests to

spk_0 make rational choices about how often to mechanically sigh.

spk_0 Yeah, that was very cool. Is there any chances could be good for anything else?

spk_0 Like, is there anybody else who should be sighing on purpose to help put their lung out?

spk_0 Yeah, so maybe not the sighing per se.

spk_0 But if we think about now this interface in this new framework, with the stress,

spk_0 with this microstructure that is important, I was telling you before about this other disease,

spk_0 this ARDS. Currently, how people usually look at it, we have to give more surfactant.

spk_0 We have to revert this inactivation. But now what we are saying is that maybe the amount of

spk_0 surfactant is not the only thing we have to care about, but also restructuring this interface.

spk_0 We have to keep it in the way that these multilayers can properly work and that these timescails

spk_0 are also reversed. So I think in the context of disease, this can also be an interesting thing to

spk_0 think about. Thank you, Maria. This has been really fascinating. Thank you very much. It was a pleasure

spk_0 to meet you. Maria Clara Novaia Silva is a doctoral student at ETH Zurich. You can find a link to

spk_0 the science advances paper we discussed at Science.org slash podcast.

spk_0 That concludes this edition of the Science podcast. If you have any comments or suggestions

spk_0 right to us at Science podcast at aaaas.org. To find us on podcasting apps,

spk_0 search for Science magazine or listen on our website Science.org slash podcast. This show was

spk_0 edited by me Sarah Cresby and Kevin McClain. We had production help from POTAGE. Our music is by

spk_0 Jeffrey Cook and Wenquay Wen on behalf of Science and its publisher Triple A.S. Thanks for joining us.

A new generation of radiotherapies for cancer, and why we sigh

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