World’s tiniest pacemaker could revolutionize heart surgery
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Welcome back to The Nature Podcast. This week, the world's tiniest pacemaker. And a link between shingles and dementia. I'm Sharmini Bandel. And I'm Noah Baker.

First up on the show, a pacemaker that's smaller than a grain of rice. After someone's had cardiac surgery, one potential risk during recovery is a slow or abnormal heartbeat. To prevent this, surgeons will implant a temporary pacemaker, which ensures that the heart beats normally.

But while pacemakers like this are life-saving devices, they can be cumbersome. And there's also the issue of having to surgically remove them after a few weeks when the patient is better, which could end up damaging the heart. But now a team of researchers writing in Nature have designed a new kind of pacemaker, which is incredibly small, self-powered, and doesn't require invasive removal.

Reporter Anand Jagatia spoke to lead author John Rogers about the device and started by asking how conventional pacemakers actually work. A pacemaker consists of two components. One is an electronic system that can generate electrical pulses. There's typically power supply, a battery. The other part is kind of the business end. That's the electrode structure that directly interfaces to the cardiac muscle to deliver that electrical stimulation.

Those electrical pulses initiate contractions of the cardiomyocytes, the cells within the heart that are responsible for the cardiac cycle. But there are electrical wires that lead from those electrodes to an external power supply through the surface of the skin. You also have to monitor the heart rate during that recovery so you know whether you need to pace it or not.

So you have wires designed to monitor cardiac function. So it becomes a somewhat clumsy collection of hardware that's cumbersome for the patient from a practical sense during that recovery process.

And so this is where your research comes in. So you've come up with a completely different approach to designing a pacemaker that gets around a lot of these problems. Yeah, that's right. So this particular opportunity was brought to us from cardiac surgeons. And so it was really their vision for a fully implantable, wirelessly controlled temporary pacemaker that will just melt away inside the body after it's no longer needed, just naturally resorb in the body.

So can you tell us about your design then? So there are pictures in the paper and this thing is absolutely tiny, right? Yeah. So I think it's the world's smallest pacemaker comparable to a sesame seed. So it's two very small pieces of metal, essentially little metal pads that contact the cardiac tissue directly. But they're selected such that when they're in contact with the surrounding biofluids that are present in the cardiac muscle, they form a battery.

So because the fluid that it will be bathed in, I guess, inside the body will have ions in it, that naturally can create essentially a rudimentary battery. So you don't need to have a separate power supply. It can draw its own power just through this clever electronics. Exactly. Now, the next question is, how do you control it? So the other half of the device is actually a

light-controlled switch that's sensitive to wavelengths that penetrate biological tissue. So it's that deep red wavelength of light. And so we place an LED on the surface of the skin just above the heart.

And when we turn that light on, enough of that light penetrates the tissue, illuminates this very tiny pacemaker to turn that switch on, leading to its ability to discharge electrical current into the surface of the heart.

So we can just flash the LED on and off. And the frequency with which we're flashing that light on and off sets the pacing rate. And then basically you can just decide, right? Depending on the needs of the patient, you could have some sort of sensor that would pace as needed. Yeah. So that's kind of the other component of the overall system. It's a

skin mounted patch that includes not only this source of light, but it also has a sensor that can determine whether the heart rate drops below that threshold value. And if so, it automatically brings the heart rate back up to a normal level. And you said at the start that one of the aims was to have this reabsorbed by the body when it

is no longer needed. So what materials have you decided to make the device out of and how does that sort of bioresorption process happen? Typically, these devices will dissolve completely over like a nine to 12 month timeframe. The kinds of materials that we use for these electrodes, we like molybdenum and magnesium.

Now, the light-controlled switch is actually silicon. So silicon, like magnesium, is a recommended part of a daily diet. You'll see it in a vitamin tablet, for example, both of those elements, molybdenum also in many cases. Now, they're mounted in a bioresorbable polymer.

And they, you know, resorb in the body. And we've done all kinds of studies to establish there's no adverse effect associated with those materials or the products of their dissolution. And because this device is so tiny, the size of a sesame seed, you can do some pretty clever things with it, including how you get it into the patient in the first place.

Yeah, it's so small, actually, you can inject it into the body just with a syringe. The other thing is because these devices are so small, you can pace the heart in very sophisticated ways that rely not just on a single pacemaker, but a multiplicity of them. And so we demonstrated you could actually pulse the right and left ventricles

in a timed manner that offers a greater level of control over the cardiac cycle than would be possible with just a single pacemaker. But you can even go beyond that. You can take these devices, you can just sprinkle them around. You know, you could do half dozen, a dozen of these things and each one controlled by a different wavelength. So we're pretty excited about that because that really takes you into a whole new realm of control over the cardiac rhythm.

What sort of stage are you at with this? So you've come up with the design, you've manufactured the device and you've tested it in cardiac tissue? Yeah, we have. So there are small animal models that we've used for initial testing, but larger animals as well that have anatomy that's more analogous to the human cardiac system. But we've also taken hearts from organ donors.

to demonstrate that these very tiny pacemakers can capture the cardiac rhythm even at a human scale. So we have not tested in living humans, which is a little bit into the future, as you might imagine. And just thinking about the way that you could use this more broadly, could you use the underlying technology in humans?

other aspects of healthcare? Yeah, I think this is a powerful technology for cardiac patients, but really you can think about it more broadly as a very tiny light-controlled wireless stimulator. I mean, there are deep brain stimulators used to treat symptoms of Parkinson's disease or electrical stimulators that are used to restore some level of vision in vision-impaired individuals. So I think it's a technology that we hope or we believe will have

broad-ranging implications beyond those related to cardiac patients. That was Anand Jagatia speaking with John Rogers from Northwestern University in the US. For more on that story, check out the show notes for a link to the paper. Coming up, evidence that being vaccinated against shingles could lower someone's risk of developing dementia. Right now though, it's the research highlights with Dan Fox.

Global warming is causing lakes to lose oxygen. In recent decades, the levels of dissolved oxygen in many watery environments like rivers and oceans has declined. Now, by using a machine learning model along with existing measurements of lake oxygen, a team of researchers have been able to assess the changes in more than 15,000 lakes worldwide.

They found that between 2003 and 2023, 83% showed a drop in the amount of dissolved oxygen. The main cause, especially for temperate lakes, was that as water warms, the amount of oxygen that can be dissolved in it drops. Changes in oxygen levels are stressing nearly all the world's lakes, with fish growth and food consumption declining in these ecosystems.

Read that research in full in Science Advances. An analysis of eating habits over 30 years has confirmed that for healthy aging, you really should finish your vegetables. Researchers used data from studies that followed more than 105,000 people between 1986 and 2016.

They saw that only 9.3% of the participants achieved healthy aging, defined by the lack of 11 major chronic diseases and no impairment in cognitive, physical or mental function by the age of 70. The authors concluded that a diet of plant-rich foods that includes a moderate amount of healthy animal-based foods is associated with the highest likelihood of healthy aging.

They suggest that these data can be used to improve recommendations for living longer and healthier. Tuck into that research in Nature Medicine. Dementia is one of the leading causes of death among older people. Deaths due to Alzheimer's disease, the most common cause of dementia, have nearly doubled in the past 30 years. But progress in understanding and treating the causes of dementia has been slow.

This week in Nature, however, a team show evidence that getting a vaccine, one designed to prevent a common viral infection, appears to lessen the risk of someone developing dementia and so could represent a cost-effective way to prevent or delay the condition. The infection is called shingles and it's caused by a type of herpes virus.

This is a virus that causes chickenpox in children, but it can remain dormant within neurons before reappearing later in life and causing a painful infection. Now, there's some evidence of an association between a herpesvirus infection and an increased risk of developing dementia. And because effective vaccines against shingles do exist, this led researchers to investigate whether they could reduce this dementia risk. But this has been hard to test.

because there are a multitude of compounding factors and difficulties comparing outcomes in people who had or had not received a shingles vaccine. For example, things like diet and levels of physical activity could differ between these two groups and are also thought to play an important role in dementia risk. To try and overcome this, a team have used a huge collection of anonymised health records called the SAIL databank,

which contains detailed information about people in the country of Wales and their interactions with healthcare systems. Now, the way a shingles vaccine was rolled out in Wales created a natural experiment that this team could use to get around these compounding factors and allow them to investigate the vaccine's possible effects on dementia risk.

Reporter Benjamin Thompson spoke to one of the team, Pascal Geldsetzer, who explained more about how this worked. What we need in medicine to show that a new medication or a vaccine works is a randomised clinical trial. And so we might take a thousand study participants,

throw a coin and then assign them to either getting the vaccine or no vaccine. And the power of this is that we know on average these two groups must be similar to each other because all that's different for them is whether the coin landed on heads or tails, right? So in Wales we have a really similar situation because of the way in which they rolled out the vaccine. So they said

If at the start date of the program, which happened to be 1st September 2013, you had your 80th birthday prior to that date, you were ineligible and you remained ineligible for life. Well, if you had it just after, you were eligible.

And so this is really beautiful because it's essentially just like a randomized clinical trial because, again, you've got two groups that must be on average similar to each other, the vaccine eligible and vaccine ineligible group, because all that's different for them is whether they were born just a few days earlier or a few days later. So if someone turned 80 just before this date, they were in one group, while if they turned 80 just after, they were in the other. So you compared these two groups and to look at the effects of...

being offered this vaccine for shingles and in some cases taking it and what this had on these different groups and their chances of developing dementia after several years? Exactly, yes. So our primary follow-up period is seven years and we just look at whether there are new dementia diagnoses and how these differ between these two groups. And what did you find then? So we just see this strong protective effect

And we estimate that roughly one in five new dementia diagnoses over the seven year period are averted through shingles vaccination. So you're seeing this drop then between the two groups, but not everybody who was offered a vaccine took one. So is this one in five? Is this extrapolated out into a whole population? Absolutely. So.

Only roughly half of those who were eligible went to get vaccinated. So we can adjust for that. We can essentially scale the effect sizes to get at the effect of actual vaccination rather than just eligibility. And so you're seeing then this relative drop in what, 20% between the two groups. I mean, when you saw that, what were your first thoughts when these numbers came out of the computer?

We were just extremely excited because if this really truly is a causal effect, then this would be hugely important for population health, dementia care, and also for at least a subset of dementia, what the causes actually are. And the effect size here is much larger than for any other interventions that we currently have for delaying or preventing dementia.

And getting to the root cause of what's going on is, of course, important. At the minute, you've got this kind of correlative effect between the two, but working out what the actual causation might be is tough. But in your paper, you've had some thoughts and done some statistical analysis as to what might be going on. Yes, of course, we are limited by the fact that we're working with electronic health record data here. So I

I think we are able to plausibly get at causal effects for the effect of shingles vaccination on dementia. But what exactly the causal mechanism is, is of course a different research question and a very tough one to answer. So we're only able to provide suggestive evidence here. And essentially what we're showing is that

a reduction in reactivations of the chickenpox virus is a plausible mechanism. But it could also be that it's a broader immune mechanism that's elicited by the vaccine that has benefits for the dementia disease process. So this would be a virus-independent mechanism, if you like. Both could be at play to some degree. We don't know which one it is.

And do you think this is a one-off? Do you think this is something that was only seen in Wales? There's something intangible about it? This...

protective effect we're seeing in a variety of other data sets as well. So that's what I've been investing in over the last two years is trying to replicate these findings. And we see this effect in other data sets from the UK. We see this also in other countries that have rolled out the vaccine in a similar way. So it's a really exciting body of evidence, I think, that's being generated there. I mean, of course, people are going to look at your paper and

potentially be quite excited about it but there are other questions I think one of the ones that stood out to me is that there really seems to be a difference in your paper you talk about between men and women the effect of this potential protection against dementia is

strong in the records of women you looked at, but was potentially negligible in some cases in the men. Yeah, so we can't exclude a meaningful beneficial effect among men as well, just because of the width of our confidence interval. So essentially, the statistical precision with which we can estimate our effect

But yes, the effects were stronger among women than men, which is actually something that has been observed fairly consistently in the literature on off-target or non-specific effects of vaccines. But it could also be due to chickenpox virus-specific pathways. As we know, shingles is more common in women. There may be differences in the way that dementia develops between women and men as well. That's also...

a growing area of interest in the dementia field. And we know that there are important immune system differences between women and men, with women, for example, often responding to vaccines with higher antibody responses than men. And dementia, I mean, it's such an insidious disease as well, and it can take...

a very, very long time to develop. You've followed the people in your study via their health records for quite a long time, seven years. Is there the chance that whatever effect this vaccine is having, it's potentially just delaying things? And really, if you'd looked at eight years, nine years, 10 years, you would have seen really quite a similar outcome? Yes, I think it's possible. We can't really say that we're preventing dementia or delaying dementia. We don't know. But

In these older age groups, there is actually not that much of a difference between these two concepts, right? If I delay dementia onset long enough in an 80-year-old, a good proportion of them will die from other causes before they develop dementia. So we have effectively different...

prevent dementia. So delaying dementia would also be a hugely important and beneficial finding, I think, for dementia care and population health. And I've laid out a few that I'm sure you have some other questions you're interested in as well. What other things are you looking to investigate? Because you've looked at a vaccine, I guess there's multiple types. Yeah, so absolutely. I think it's a very important question as to whether the effects that we're seeing are specific to the life attenuated shingles vaccine. So the old vaccine

that was rolled out back in 2013 in Wales. If with the newer vaccine, these effects are at least as strong, then it becomes more plausible that the effect mechanism that we're seeing is through a reduction in reactivations of the chickenpox virus. But if it's more of a broader immune mechanism that's independent of the virus, then it may well be specific to the lipogenesis vaccine.

And what else are you interested in, Pascal? I mean, you're presenting your evidence. What are you hoping comes out of this work? I hope that there will be a lot of interest in the dementia research community around singles vaccination, vaccines in general and dementia. And I also hope, and that's an effort that I'm trying to currently raise funds for, is a randomized clinical trial.

We want to use the lipotenuret, the old vaccine that's no longer being manufactured, to more conclusively test the effect of shingles vaccination on dementia and cognition. That was Pascal Geldsetzer from Stanford University in the US.

To read Pascal's paper, look out for a link in the show notes. Finally on the show, it's time for the briefing chat, where we discuss a couple of articles that have been highlighted in the Nature Briefing. Sharmini, why don't you go first this week? What have you been reading about? So I've been reading this Arts Technica article. It's about a paper in science.

that some people might not find a terribly surprising result, but is a really detailed look into a phenomenon that some people might call driving while black. Yeah, so this is the racial disparity that has been seen in many countries. It's particularly prominent in the US, where people of different racial backgrounds experience different rates of traffic stops or traffic tickets, for example.

Yeah, exactly. And there's been loads of studies that have looked into, you know, is there racial discrimination in traffic enforcement officers, whether they're stopping people, giving them speeding tickets, how much they're giving them fines for, and whether there's a difference between drivers who are white and drivers of other ethnicities. The trouble with this is where you're getting your data from and what possible sort of biases there are in the data. So a lot of studies of this have looked at data from drivers

the police stops. So you're taking data from like, who have they stopped? And then they filled out a form about who's been stopped, where, why, and sort of how much a fine was. But that sort of only gives you

part of the picture. It kind of excludes the people who weren't stopped at all. And it doesn't actually tell you whether the people were speeding or how much, although people have also used speed cameras to try and work that out as well. Okay, so these additional granular data are things that these researchers are trying to gather. How are they going about gathering it? Where are they getting it from? The data is coming from...

Lyft. That's Lyft spelled L-Y-F-T. So this is one of those ride sharing platforms. So there's Uber, there's Lyft. It's what people might use instead of a taxi. And it matches up drivers who have the app with passengers who want to Lyft somewhere. And the key thing about this data is that when a driver is giving someone a Lyft, they're also pinging passengers.

Lyft, the company, with their location data every 10 seconds. So what this means is that these researchers know who the drivers are, where they are, where they're driving, and whether they are in fact breaking the speed limit in a particular area. Okay, so that's the kind of key here to get that kind of granularity of data out.

What are the trends that they're seeing as they start to do analyses of the information that's coming back to them? Well, the big and maybe unsurprising headline is that what the paper has termed minority groups, so in this case, Asian and Pacific Islander, black and Hispanic people, tend to get more tickets. And when they do get tickets, they tend to pay higher fines, which is what other studies have found. But what this group is doing is accounting for other factors that could be causing that. So, for example,

You know, you could say from the traffic data, well, maybe these minority people are speeding more. Maybe they're more unsafe drivers in general. There are factors like the fact that they might be driving in a different kind of neighbourhood. That neighbourhood, it might be a more policed neighbourhood. There might be more stops. They might be younger or older. They might be driving different types of cars. Lots of sort of confounding factors which...

do or could influence whether a police officer is going to stop someone. So what this team have been able to do is take all these other factors, some of them they've looked for the factors themselves, sort of come up with some ideas about what could be confounding. They've also used machine learning to see if an AI could deduce any possible confounding factors. And they've basically...

said if you look at the sort of equivalence of a minority driver and a white driver in the same situation, there is a difference that they think can only be accounted for by bias from the officer. And this is bias to the extent that

minority Lyft drivers were about 30% more likely to be pulled over and cited for speeding between sort of 24 and 33% compared to a white driver. And once cited, they were also likely to receive higher fines. So between maybe 23 and 34% higher fines again than white drivers.

Right. It's always interesting to me that we do feel as a society that we need this level of sort of proof, I suppose, something that we can see quite clearly in the data, i.e. more finds that don't match the racial makeup, for example, or the demographic makeup of an area. But we need to be completely sure that it's not just because the bias is real. And it's important as well, because it does come back to

sort of policy implications what you can actually do about this. There's a perspective article in Science alongside this paper that is really focusing on, well, okay, once we've got this data, how do we apply it to policy to sort of help make things better? And one of the things they mention is that you can potentially bring a legal challenge if you can, to some extent, prove that there's discrimination, prove that it's like everything else is equal except for the race of the driver.

So it is important to be able to prove this. And they also did look in general in their data with Lyft data between the white drivers and the minority drivers and found that there wasn't a significant difference in the frequency of speeding or in their sort of proxy for problematic driving. So they kind of tried to deduce how many accidents people were having.

Now, Lyft drivers are in particular sort of incentivized not to speed, certainly while they're working for Lyft. But

But still, yeah, that's an interesting result that there isn't a difference in speeding and there is in traffic enforcement. Right. I mean, I wonder whether or not this kind of study is going to be the final piece of information that's needed for policymakers to take this disparity that's been seen and say, hey, it's real. We've controlled for all of this now. It's quite clear that this is something that we can see from our data. So we now need to make some change on a policy level. Now, you mentioned the perspective article, which discussed...

how change might be made. Do you think, or does anyone in the article suggest that there may be any investigation or any changes made about how traffic enforcements work? Well, this is just the paper being published at the moment. I think the perspective article is kind of putting the point forward that the researchers, when they're looking at this kind of data and analysing it, need to be analysing it in a way that would support traffic

policy changes through whatever means. But also, I just want to say there is another sort of even more tangible reason than sort of traffic fines, why this kind of discrimination that these people are showing exists here, certainly in Florida, is going to have a sort of

Increased impact on minority drivers, which is most car insurance policy providers, change the price depending on how many traffic violations you're cited for, which suggests as a sort of extra bonus that minorities in US states where they are legally required to have car insurance might also face this additional burden of actually just paying more to be able to drive.

So what have you been reading for us this week? So I've been reading an article in Nature, which is about some research that's come out about a perennial topic in science publishing, which is paying for peer review. Should we pay for peer review? Should the science journal industry in general be paying for peer reviewers? And that's just never been the standard. And that's not entirely...

because people didn't want to pay. There are good reasons, right, why people think maybe you shouldn't pay for peer reviews. Yeah, so for a long time, it has sort of been an expectation in the scientific community that when you publish papers, you have your paper reviewed by a panel of your peers and that process is done pro bono. So that process is done for free for your papers, but then you offer your services as a researcher to review others' work to make sure that there is this sort of

symbiotic relationship within science and society. Now, that can, however, rub people up the wrong way, because it can mean that you have for-profit publishers that are making money from publishing research that are relying on free labour being done in the form of reviews by the scientific community,

And yet the flip side of that is that there is a concern that if reviewers are paid, then that might incentivize people to follow the money rather than follow the quality. And so it could decrease the quality of the reviews that are being given. Yeah. So if people are sort of purely financially motivated...

They could be just sort of like, oh, yeah, yeah, I'll just I'll just scribble out a quick review, get my money, not really thinking about it. Maybe trying to pack them all in, maybe just sort of signing things off. Precisely. And so I guess what's happening now in this particular story is that there have been two studies that have investigated what would actually happen if you did pay for peer review. What would happen to the quality of research and would it have any benefits?

to the process in general. And so that's what's being covered here. There are two different experiments that have been done by two different journals that have tried this and they found relatively positive results. It's so interesting, isn't it? Because, you know, there is a lot of things that people do get paid for and we don't say, hmm, well, you're not completely unbiased because you're receiving money from it. So it's good to have some actual initial data on the difference between it. So how were the studies done and what did they find?

So the first experiment was done in a journal called Critical Care Medicine, and it started in September 2023. And they asked 715 researchers to review papers and offered...

roughly half of them a $250 incentive to do that. And then they looked at what came back. They looked at the quality of what came back and they looked at the speed at which it came back. And what they found was a modest benefit. So they found that 53% of researchers accepted the invitation when they were offered payment and 48% accepted it when they didn't get offered payment. So a very slight increase in the number of people that accepted the invitation. And they also found that on average, people that were paid...

delivered their review a day earlier than people that were unpaid. So they were slightly quicker to do so. And then overall, they found that there was no change in the quality of the reviews that came back as far as the journal editors were concerned. And so they saw this modest increase.

which is one thing. However, the other example that's discussed in this story is from Biology Open, which is another publisher, and they found a much larger effect, but with much fewer reviewers. So again, look at that as you will when it comes to your p-values. What they did is that they offered a £600 retainer for people to review up to three papers per quarter, or they offered £220 – this is Great British Pounds here – per review for papers. And

And they treated their reviewers essentially like contractors. And under that scheme, the editors would send freelancer reviewers an invitation to review. They had to accept it or decline it within one business day. And then once accepted, they had four days to submit their peer review. So it was really trying to increase the speed with which they do this. And they found much more dramatic impact.

So their paid reviewers came into the journal much more quickly than unpaid ones. So the average turnaround time for paid reviewers was 4.6 business days, but it was 38 days compared to reports that didn't get payments. So it was a really drastic increase in the speed with which these reviews were turned around.

And again, editors found no difference between the quality of the paid and unpaid reports here. It's a nice result to say, because you could also assume that like, oh, well, if someone's being paid for a peer review, maybe they'll do a better job. It could go either way. I suppose it's a good outcome that researchers who are writing peer reviews don't seem to be varying their quality depending on whether they get paid or not.

But the speed, it does make a lot of sense. I mean, I must say, if you were paying me, I would do your work faster than if you weren't. So I mean, in the critical care medicine example, the researchers did say they thought that their modest improvement suggested that the incentive wasn't huge, and that there are still clearly incentives around caring for the community around, around an obligation, I suppose, to the scientific community to do this. But

There are other researchers quoted in this study that have said, you know what, when you employ someone with a contract, a contract has conditions and you have control over that. And so therefore, if you're employing someone with a contract and one of those conditions is that the review is of a certain quality, then that would be something that could in theory be enforced by the journals that are paying it. Otherwise, you don't get paid anymore. And so...

It's an ongoing question and it's an ongoing debate within the community. But these early pieces of research are suggesting that perhaps this might be a way forward. And actually, the Biology Open study was so successful that they've decided to extend this model to all of their students.

specific subject areas that they publish under up until the end of 2025 using a discretionary fund that they have to do so, so they can gather more data because they found it of such advantage to have this increased turnaround time. Yeah, I mean, if speed is an issue...

then that's a huge sort of increase in your turnover of getting peer reviews. But of course, this is being done in the context where it's not the norm. So some of the concerns people have could still arise if we're switching to a world in which peer

being paid is the norm and that sort of might give different kinds of incentives. Absolutely. I mean, one of the advantages that was put forward by the managing editor of Biology Open was that one of the reasons it's been so helpful is that in some cases it's been very hard to secure reviewers at all. And so this has allowed editors to secure their reviewers, but what

whether or not that benefit would disappear if all reviews were then paid for again and so there wasn't this sort of difference is a question mark. There's also the very big question mark of at the moment these experiments I suppose have been funded by discretionary funds but in the long term if this was the case that is going to increase the cost to publishing for the publishing companies and so the expectation is that that money will come from somewhere it could maybe come from

efficiency savings, but the likelihood is it's probably more likely to be factored into things like article processing charges. And that is already what could possibly be the case with Biology Open, according to this article, is that it may need to increase its article processing charge to factor in this increase in cost for publishing papers. And that comes down to then another controversy, which you kind of touched on earlier, and which we've reported on before, which is

the scientific community's feelings about who should be paying for the publishing, who's getting the money for the publication of scientific research.

whether these article processing fees are too much, especially with the increase of open access publishing as well. So it sounds like this might be something we're going to be touching on again in years to come. I certainly think this is an issue that has been around for a long time. And I should add that there have been lots and lots of other initiatives that existed to try to get around this concern. You know, there have been publishers that have offered things like tokens, if you are a reviewer, which you can use cash in to reduce the cost of

publishing yourself as one method to try to incentivize reviewers. So, I mean, there are other things that could happen, but it's certainly not a debate that's going away. And it's not a debate that Nature itself will not be thinking about quite a lot as a publisher itself. And so as time goes on, I am sure that there is going to be more about this on the podcast. Well, watch this space.

listeners. And another thing you should watch is your email inboxes for your copy of The Nature Briefing, an email newsletter. And we're going to be putting a link, as always, in the show notes to where you can sign up for The Nature Briefing. But before we sign off, I have to say there's something that you won't be seeing or hearing a lot in the years to come. And that is Noah Baker, because this is in fact your last week at Nature. It is indeed. This is my last podcast. I was trying to look back

Over my time here, I've been here for longer than I care to admit. It's more than a decade. At what number the first podcast I appeared on was, and I can't find it, actually. I should be able to find it. That's maybe concerning for me. But I do remember the first piece I reported on was about the Neame ice shelf in Greenland and an ice cause. I remember that very, very clearly, that particular episode. And now...

many hundreds of episodes later, my time at Nature has ended. But I'm hoping that I will be appearing on the show every so often as a freelancer. So maybe my voice will occasionally pop up still. I'd like to keep working with these wonderful people. It'll be a special treat for the listeners when we get a bonus guest voice of Noah Baker. And yes, we're all going to miss you tons, actually, because yes, it has been...

has been a long time, end of an era, but you've done a wonderful job contributing to nature's multimedia coverage and we shall certainly miss you.

But I shall leave that there. We'll have some leaving drinks of our own where we can expand upon that more later this week. But to all the listeners, thank you so much. That is all for this week. If you want to keep in touch, don't forget you can follow us. We're on X, we're on Blue Sky, or you can email us if you like. We're podcast at nature.com. I'm Sharmini Bandel. And I'm Noah Baker. And to everyone that's listening, to you listening right now, and to everyone at Nature, thank you so much for my time. It's been brilliant. Keep listening to these brilliant people.

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