 Welcome to this week's episode of This Week in Science brought to you 10 minutes, 20 minutes later than planned because I hit the go live button, but nothing went live. So we've been doing the show without you. I'm very sorry, but we're here now and I'm very glad that you're here as well. I mean, for all those things that would have been edited out of the podcast already, Rachel is probably very thankful. So, to remind everybody as we get into this episode, if you love the live show, you love us warts and all. This is the, all the stuff we talk and we do take one, take two, take three technical glitches and all. And then our podcast editor, Rachel goes through and tries to clean things up for our podcast. So not everything that is seen here will be in the final podcast version or for that matter in the final radio version that goes out to KDBS 90.3 FM in Davis. Internet is doing all right tonight. I hope your internet is treating you well as we get into our evening of intimate science discussion because there are some intimacies ahead. Grab yourself a glass of whatever your favorite beverage is, get comfortable and get ready for the science because we are starting for real. In three, two, this is twist. This week in science episode number 905 recorded on Wednesday, December 14th, 2022. Welcome to the science monkey house. Don't feed the animals. I'm Dr. Kiki and tonight on the show, we will fill your head with goals, chaperones, and snakes. But first. Disclaimer, disclaimer, disclaimer. It finally happened. A technology that has been 20 years away for the past 80 years is now just 20 years away. Fusion power has produced more energy than it took to produce and it gained in an experiment that one day could allow humans to use near limitless power supplies that do not produce greenhouse gases or contribute to global warming. And while this technology holds great, while it is likely to be the best long-term solution to curbing global warming, it isn't commercially viable just yet. But finally, the solution is on the horizon. Thanks to those who study nuclear science, to those who loved their classes, to the crazy teachers who wear their glasses. It's going great and it's only getting better. You're doing all right. You're making the grades. The future's so bright. We all gotta wear shades here on this week in science. Coming up next. ["I've Got to Be Kind of Mine"] I've got to be kind of mine. I can't get enough. I want to learn everything. I want new discoveries that happen every day of the week. There's only one place to go to find the knowledge I seek. I want to know. Good science, you Kiki and Blair. And a good science to you too, Justin Blair and also welcome back Blair and everyone out there. Welcome to another episode of This Week in Science. We are back again as we do every week. Come together to discuss science news, science advancements, science fun, all of our curiosities. We're so glad that you're here to join us as we love to talk with you about all these things. But as we jump into the show, the first thing I do need to get out of the way is happy birthday to you, to you. Happy birthday, Blair and Justin. Thank you. Thank you, Kiki. Happy birthday to you, yes. It was Blair and Justin's birthdays, both different days, but one right after another. These are our December babies. And we are so glad that they are here with us. And I hope you both had a wonderful birthday. I did. I really did. Good. And I hope that our audience has reached out with messages of bon anniversaire and whatever other wonderful, joyful messages of happy birthday-ness that they can. Yes, happy birthday, happy birthday, happy birthday. What I want for my birthday is for everybody to buy the twist calendar. So that's what I ask of our listeners as a birthday present. Plus, then you'll know when Justin and my birthdays and Kiki's birthday will be next year. It's the same date as this year, but just it's on there. It happens every year. It's on the calendars. It's great. There are two options to purchase the calendars. You can download a printed version from Zazzle, which doesn't have all the holidays, the special holidays on it. But there is a PDF that you can download, high quality, good res. I might be fixing some of the dates on it because as I discovered, was informed last week, there are a few things that we missed. Yeah, yeah, we don't need to bring that one up again. That was embarrassing. I know, but if you download that one now, it'll probably be a collector's item later. I am sure of it. But anyway. Oh man, you need to message me about that. I am very furious. We'll fix it. We got this. We'll take care of it. But the calendars, they're ready over on twist.org If you want to click the twist.org, go to twist.org, click on links, order the calendar of your choice. We've got some great science holidays in there and maybe adding some as the days come. But we're here to talk about science with lots of science news ahead. I have stories like Justin disclaimed about NIF's ignition advancement and the excitement around that. We're going to talk about that a little bit and talk a little bit about the realities surrounding that. I also have cell control for invaders. I've got some chaperones for folding, microbial motivators, and I've also got the sixth sense. And so do you. I'm going to learn more about it. Justin, what do you have? I've got the European Union is writing climate checks. It has no intention of caching, apparently. CLL cancer cure trial results. Just good news, lady fat edition. And slime mold technology. We always love it. And we brought the same story too. I brought the, I brought the, I had brought the motivation, I was working on the motivation story too. The get microbiome one. That's going to be, that's a fun story. I like that one. Well, then we will definitely have things to talk about. I think it's, I think it's my favorite story this week so far. So far from, from at least of what I've read. I mean, it's a bit gutsy to think that microbes could motivate us. Yes, I am poorly punning. Blair, what is the, in the animal corner? Oh my goodness. Well, I have a story about taboo snake organs and also traveling with friends. But before that, in the short stories, I'm going to talk about microplastics and jaguars. I don't like microplastics. I do like jaguars. Let's, let's have it all though. We're going to, we're going to put it all in here. So as we jump into the show, I want to remind you all that if you are watching live, thank you for watching live, but you can find us all over the place, wherever podcast podcasts are found. We are this week in science, also twists. And you can find us on your favorite platform. We stream live weekly eight PM ish Pacific time on Wednesdays on YouTube, Facebook and Twitch. And we are twist science on Twitch, Twitter and Instagram. But if all of this is a bit much, you can find show notes and all of this other information over at our website, twist.org where there are also calendars. Now it's time for the science news. Okay. Big science story this week. I mean, the Artemis mission landed, made it back to earth safely. Ta-da! We went around the moon, we came back. Let's do it again now. Okay. That's the big story for NASA. That's great. But- For NASA. I know. I'm really like- But we sent something around the moon and brought it home again. Yeah, that's fine. It's great, we did that. Okay, just waiting. I don't used to send humans there. It's whatever, it's fine. No humans yet, but we're on, we're on path. It's good, it's good. However, the National Ignition Facility at Lawrence Livermore National Laboratory has announced that it has actually surpassed one of the preordained experimental end points for ignition. And so this is one of the important aspects of like research where when you go into a research study, you set an end point. When do we know that we have done what we are trying to do? And researchers a long time ago said, okay, we're gonna set a certain amount of energy output per laser energy input that we will mark as our, that's our threshold for having achieved ignition. So last year, big announcement from NIF. Oh, 0.7 megajoules, blah, blah, blah. Great, we had ignition at this small amount. They had ignition, it was higher than the amount that was put in. So similar to what they did this year, but much less. So what they did this year is that they put in 2.05 megajoules of laser light into a small chamber. Lots of lasers, like all these lasers that have been divided up and all of them converged on a single point. The Hallrom, which is the gold and other metal container that contains the deuterium that eventually we're trying to fuse together. We're getting these atoms to fuse together. So the Hallrom is the container that holds it all together and it gets smushed and all the atoms go and then to smash together because of all this energy coming in and I'm not, I can't explode. So it might as well just fuse. So anyway, 3.15 megajoules of fusion energy came out of this particular laser shot that was performed on the 5th of December and on Tuesday yesterday, as we were recording a week after, but yesterday they held a press conference in which the energy secretary, Jennifer Granholm of the Office of Science and Technology Policy and or Department of Energy and other officials from Office of Science and Technology Policy and others came through and made a big announcement saying we've done it. We've achieved fusion, we put more energy in than what we got out. The thing is, the thing is, they still haven't really gotten out, excuse me, I had to sneeze, they still haven't really gotten out the full energy that was actually put in to power the lasers. Wait, what? Because I thought that was the whole point of the announcement is that they got more out than they put in. No, they break even, even I would be happy. The end energy of the laser fired on the hall from, yes, they got more energy out, but there's a whole bunch of energy from the grid that goes into powering the laser in the first place. And so they put about 300 megajoules of energy in initially just to power the lasers that were then focused on the hall from, which ended up resulting in the three-ish megajoules out. Man, I thought you were just gonna say it wasn't scalable. This is a way worse problem. Although I guess this maybe is solved by scale because there is a point at which if you set up a grid to power lasers at a grander scale, it might actually, it might not be one-to-one, right? You might be able to use less energy per laser if you do want. I heard it sound a lot like step one steel underwear, step three make profit. What's step two? Bye-bye. Exactly. So, okay, potential, so the real thing that they're trying to do is to maintain testing of our nuclear stockpile. And to have achieved ignition in this perspective makes what they're doing at the National Ignition Facility very successful because they can more successfully test atomic aspects of our nuclear stockpile and make sure that things are not deteriorating too much, maintain what we've got. There's a lot of testing that goes into understanding what we've got sitting around right now. Just waiting for it. Okay. Yeah, blah, blah, blah, blah, blah, blah. Jesus. Jesus, I wanna know why it is we need a more limitless power system to power our unlimited fuel system there for the future. And if it's gonna be like, how did they do this? Oh, well, you know, they used a whole coal power plant right there on the nuclear facility. Like, this is, now I'm very disappointed. See what you do is it's disappointing. It is disappointing. No, no, no. It's not, it's not. Look. To power the fusion lasers, to then make fusion power. But here's the thing. They did the ignition experiment, but it was not sustained. It's not sustainable. This is not the kind of thing. It was a single thing. It wasn't like, oh, now we have ongoing fusion that can be used to continually like nuclear plants are used to do heat, water, provide power, you know, do all these things. Additionally, they think that they can make it more efficient by upgrading the lasers, by creating more efficient pathways by maybe making the whole realm itself more efficient. But they think they can routinely one day make laser pulses of 2.6 to three megajoules to help initiate higher gain reactions. And these are more words. These are more words. I'm still hearing we've created a highly inefficient, unsustainable power source. Yep. Yeah, so. So that point in the middle though, it is the thing that they needed to prove of concept at least it says, hey, this works. Now they have to figure out how to make all of the rest of it work. Yeah, and the question is really with what they've got going with the laser, how much more can they push it? How much power can they actually get out of it? When you're putting in 300 megajoules and getting three out is, that's a loss. That's a loss. It's a loss. And how do we end up with a gain? And so this is the first time that, apparently any of these kinds of ignition facilities or fusion facilities has had this kind of a gain. So that is why it is so promising. But I honestly think when we're looking at the things, the platforms that are going to be used in application, we're probably going to be looking at the stellarators, the Tokamax, things like Eater, those other plasma based fusion generators that are not necessarily limited to the supply of the fusion fuel and the specific inputs of the lasers. So I think there is going to be an interesting next couple of decades. This is, you know, it's promising, but at the same time, it's what the big thing I want to keep everybody in our audience aware of is this is not yet peer reviewed. This is not published data. It probably won't get published for several months. They're not even done analyzing all the results. This is science by press release because we have a major struggle coming up with our Congress and the upcoming budget debates. So there's a big, big play here. This is where science and politics and policy come very close together and it is proving usefulness. And the media circus around this, breakthrough, possibilities, hopefulness. Is this going to be in time to actually help us fight climate change? No, of course, definitely not. In fact, the bright spot was if we have this unlimited power source 20 years, 30 years away, all the more reason to dump carbon fuels and preserve the planet, you know, keep it in good shape because we got a, you know, we got a bright future. So let's not ruin it by getting all out of shape and sickly when we get to that unlimited power thing. But now I'm like looking at this and like, how did they only get three jewels out of the, how many did you say, 200 and 300, something that they put into it? How did they only get three out? Like, I think that would, that's like, if somebody told me, it's like, I'm going to give you 300 jewels of laser power and I want you to only be able to have, have three of it go somewhere. Like, I wouldn't know how to, to dampen. I wouldn't know how to lose that much energy. You know what I mean? Like, if I just fired that at a kettle of water, I would produce more energy than they got out of this experiment. Like, I'm missing. Yeah, they got 1% of the 300 mega jewels from the grid. 1%. Like, if I went into the backyard with a magnifying glass and a couple of bundles of sticks, I could start, I could create more energy right there than apparently they could do without, something's not right. I don't, I don't quite understand. Actually, everything is right. They have been iterating and they have been developing and they haven't, they have been making advances. They thought they could make these advances more quickly and they did not. The hope of- Meanwhile, yeah. Meanwhile, NASA, we actually went around the moon. And like, we launched, went around the moon and came back home, meanwhile, you earned 300. A couple, a couple billion dollars. Into three. No big deal. Oh, if it, no, it probably didn't even cost that. Like, going around the moon was like, it compared to like losing 299% of the energy that they put into the project. I know it's iterations, you're right. The breakthroughs happen in small steps in science. We need to fund the science for the iterations or we will never get to the point of the real application. It needs to happen. The dream is that one day we will see this become sustainable. We will see actual positive gain from the energy that's put in. The dream is that one day we will miniaturize these plants so they're not as big as the facility at the National Ignition Facility that will have smaller, more localized plants that could be used in local regions. These are possibilities. They are still in the future. This was a significant step. It's, I am just underwhelmed by the need for the press circus around it and the words like breakthrough. Yes. Endless power. The media circus is what is like, can we just talk about the fact that they made a significant step? That's great. But we are nowhere near where we want it to be. Media doesn't live in gray areas, so that's very... That's where I'm at. Speaking of media's circuses and dreaming, dream thinking, the European Union, Paris Agreement, climate targets are also in this same category. Studied by a European economics think tank, Bruegel, I guess is what they're called, they found that the EU's Paris Agreement, climate targets will not be met with the current fiscal policies that are in place. Oh, these many, many years after signing off. The EU had set a target of reducing greenhouse gases by 55% by 2030. And that's 55% reduction from 1990 levels, which we're much above those right now. So it's gone the wrong way. So their plan was to eliminate them entirely by 2050. Lead author of this study, this paper, this analysis, Professor Darvis explains that the target is currently an unrealistic ambition. Concluding that total green investments must be increased by 2% of GDP annually to get near this goal. Publishing in the peer-reviewed journal Climate Policy, they propose a European green pact should be introduced, involving better trade policies and a higher price on emissions, as well as public green investments and public financing and support for green, for private green investments as well. If they have any hope of actually meeting their climate objectives, these green investments need to be increased significantly. They looked at national energy and climate plans of EU countries for overall climate-related investments, everything in there from tax incentives to subsidies that are being proposed between 2021 and 2030. Teams set a proposal, including a green golden rule that would allow green investments to be funded by deficits without counting them in any fiscal rules. So European Union has some, the United States can be like, oh, we need money, we're gonna raise our debt sale, we're gonna just borrow from wherever our fake money comes from. And we can just accumulate a big deficit. EU countries aren't allowed to do that under their collective agreement like stuff. So there's deficit rules, expenditure rules, stuff that they, rules that those countries in the European Union all have to play by. So what they're proposing is that you exclude any green investment from the fiscal rules of deficit spending. That would provide individual countries the ability to borrow money, which is again, pretty much fake, borrow money from the future to fund the research and technologies and the investments today, so that there's a future that can still make money for things that governments do, I guess. So excluding green investments from all types of fiscal rules would provide these incentives to undertake. And additional recommendations to policy makers within this suggested fiscal pack include clearly defining what constitutes emission-reducing climate investments and monitoring the compliance, so. Less greenwashing? That's a whole gray area. There's a lot of greenwashing that goes on. And so if you've got money that's being directed towards greening or green economy sustainable energy or sustainable land agriculture use, and it's not, how do you know if you don't have a clear definition? Right now, they kind of don't. They also say another thing you could do and talk about saving money so that you can spend it on sustainable technologies. Eliminate fossil fuel subsidies. We still have these? Why are we still subsidizing one of the wealthiest industries on the planet? Because people don't like high gas prices and the high gas prices are made up, so. Yeah, so is all of this inflation too. It's like, oh, and now the inflation went down. What prices went down? What? Nothing. None of it. It's not how that works. The only, it only goes up regardless of where, yeah. So, yeah, so they've got, they've gave a bunch of economic things. And this is quoting Darvish again, our proposed green fiscal pact is the most promising option to address the tension between conflicting needs of fiscal consolidation and increased green investments. So, it's published in, again, Journal of Climate Policy if you wanna go look at their proposal, but, yeah, based on, and it's not the first time we've looked at this, we've heard from people who added up all of the land that countries said they were gonna set aside to grow trees to counter carbon. And it's half the farmland of the planet, you know? There's a lot of, there's a lot of media circus. There's a lot of publicly good sounding things that are being said. And people are buying it and thinking that we're making progress when it looks like we're really not, at least not as quickly as we need to be. As long as they're replanting Cabernet Vines up in Portland and Washington, I'm gonna be totally fine working into the future. As long as what? Sorry, I had a mistake. Last week, we were talking about Chardonnay moving up into England. I was just saying, you know, as it gets drier and hotter up in the Pacific Northwest, we could start having Cabernet Vines up here. And that was, I would be very happy. Every place is going to have different issues. Portland's the new Napa. It could be. But yeah, this is, it's important to define climate investments more specifically and to, I mean, really we have to get away from the, oh, look, I'm planting trees. Isn't that great? You know, the political compromise for our economy and the way that we work our economy has been this carbon trading system that everybody's so excited about, but that's not all gonna work. So there needs to be. Which is how all economy, I get why economists think this way, because economists, all money is fake. And how do you know, oh, where's, we're out of money over here? Oh, here, we'll lend you all this money. Oh, where'd that money come from? Don't worry, oh, we can spend this money. Hey, hey, hey, we're all out of money. Okay, oh, money shows up. Oh, where'd that money come from? Don't ask, it doesn't matter. They're used to just moving the solution around. And it's, so. That's not how it's gonna work this time. Planting trees isn't a bad thing. There just should be like mass mobilization of arborists in nurseries that are spanning giant, every major warehouse should have indoor lights growing trees if they're at all serious about the two trillion trees that they plan on planting in the next 10 years or whatever. And don't buy offsets and actually reduce your fossil fuel use. Would be the better thing to do. But that's just me. But it is, planting trees is going to be important because we are seeing massive die-offs in trees. News this week talked of what they're calling Bermageddon in Oregon, where they have counted some 100 million acres. I don't, I'm, and I'm not looking at the story right now. So that number is probably incorrect. It's, no, it's huge. It's a very. It's a, yeah. It's a frighteningly staggering number. It's a significant, staggering number of furs that are dying or dead, brown. They've done surveys of Oregon from the air to count the trees and see what's out there. And the fir trees are dying. Man, and that's their whole thing. They're ever greens. That's the whole thing that they do, is they stay green. They're not, and they're not anymore. And they're dying. And what we've talked about before, Blair, is how trees move. But this is part of their dying off here. Hopefully they will be able to move elsewhere to survive better. But maybe they can only do that really well with human support. So Justin's idea of. Yeah, cause it can't happen fast enough otherwise. Yeah. Right, yeah. So maybe that is part of it. Maybe we do need to have organizations that involve arborists who understand ecology, who understand ecologists who are working in different areas and saying, and seeing how things are changing to help things along. I, anyone who's ever built a terrarium, you know what it takes to try and keep those things alive. So we have to help our planet along in that way. Give me a budget. I'll get 5,000 poorly paid volunteers. We'll set up a bunch of yurts and get these mobile tree seedling plants. We'll just go. We'll just travel like Johnny Appletree traveling band. We'll just travel around the country, around the world, just planting trees as we go. You gotta make sure you plant male trees and female trees and they're genetically diverse so that, you know, they don't have a genetic thought on that. Yeah, yeah, yeah. There's gonna be a lot of breeders involved in this traveling road show. Also, we're gonna have to use local soils so that the microbes are the right thing. But the thing is, look at what are you gonna get? Where do you get a hundred million acres of tree? You could hit up every tree. But what you do is you chop down the trees that are doing it, you know what I'm saying. Oh, dear, it's a deep issue. Put the cabernet vines in. Just put the cabernet vines in now. Just start them. Get me my cabernet. But, you know, trees don't only grow by themselves. They need males and females and others and are jaguars the same? Oh yeah, it turns out they're not so solitary. That's basically the whole story. It's just, you know, jaguars, tigers, leopards, they're these stereotypical big wild cats that are solitary creatures. They don't like to be around other individuals and that's their whole deal, right? Well. It sounds like me. Yeah. I think you share your space with some individuals. I know, I growl at them a lot. Mm, fair enough. Oh, that's terrifying. Well, this study from the Venezuelan Institute for Scientific Research and their partners have found novel evidence of wild male jaguars forming coalitions and collaborating with each other to secure prey, improve chances of mating, and defend or expand their territories. So essentially this is just a study that demonstrates that wild cats that we consider solitary may exhibit social behaviors, like some of the social cats we are aware of, like cheetahs, lions, now also these jaguars. So it just, you know, I could say a lot more things, but that's basically all this study is really telling you is this is another situation where maybe because people only ever saw one at a time, maybe because they were projecting onto these animals because they're like these strong wild hunting things, right? Maybe also because they'd only been observing them during mating season when it was jaguars fighting over females or, you know. Could have been young ones looking for a territory that are lost and so they come across humans more often. Also, this could all be new because of habitat fragmentation. I did not see that mentioned in this study at all, but certainly jaguar territory is smaller than it once was. So is this a recent development or has it always been this way? I don't know, but seems like we need to challenge our expectations for wild cats. I don't know, knowing cats in general, there is a bit of, they're independent, yet they're also social. And so, yeah. We need more stories like these to understand, especially as we're looking at species that are potentially going to be very endangered because of habitat fragmentation and hunting and other pressures. You know, how are we going to allow them to survive? How do we help them? Right, yep. Yeah. Well, what about when there's an invader? What do you do then? Destroy? Oh, I don't know. Right, right, normally. Okay, so our body cells, eukaryotic cells, right? We have tons of organelles that used to be invasive bacteria, but that turned into symbiotic banked bacteria, and now they're just part of ourselves. It's like, hey, look, look at these cool organelles we have. How did they come about? Oh, well, they actually used to be their own living things, but they got subsumes. How did they get controlled? How did that happen? So researchers publishing in the journal Current Biology would describe how there are certain proteins in the flagellate control of cell division process of bacteria, and so as these researchers from the Institute of Microbial Cell Biology at Heinrich-Hein University, Dusseldorf, they were specifically looking at the flagellate angomonis dinii, which has a bacterium that has only been incorporated relatively recently as opposed to mitochondria, which ourselves took up probably about one and a half to two billion years ago or chloroplasts that are involved in photosynthesis, same idea, like these are billions of years ago these bacteria were incorporated, made symbiotic, and turned into eventually became organelles. So what happens over time is the bacteria come in and then they're like, oh, I give you something, you give me something, maybe I don't need all the genes that I've got, and so their genome gets reduced. But how did this happen? The researchers looking at this particular flagellate that lives in the intestines of insects. So we're talking about like multi-layered invasiveness going on here. This is like bacteria inside of bacteria inside of bacteria. Anyway, what they found is that this particular invasive or incorporated bacterium into the flagellate was between 40 and 120 million years ago, so not as long ago. It supplies the host with vitamins and metabolites that helps the flagellate do its flagellation and everything's great, great symbiosis going on. And so they wanted to find out exactly what was going on with the control of this endosymbiont. How it's not completely an organelle yet, it's still more of a symbiont. It's not completely integrated, but cell division occurs synchronously so that when the flagellate organism divides, so does this endosymbiont. So they've gotten to the larger organism has a control pattern that's able to take the smaller endosymbiont and go, you're gonna divide with me now too and I'll take you with me and then their babies or their split-offs, the budding and all the things that they do. Yeah, that's a pretty insane interaction. Cubbies. Yeah. And so what they found is that there were particular proteins that form a ring around the division site. They looked at the protein composition and they found that there are a lot of proteins from the host cell that get transferred to this endosymbiont, this once invasive, but now helpful bacterium. And they would predict the function of two of them because they matched known protein sequences, one of them is similar to dynamin, which polymerizes contractile helical chains and another one is peptidoglycan hydrolase, which breaks down cell walls. And so in mitochondria and chloroplasts, these dynamin-like proteins, they form a ring around the organelle division site and they contract and they aid, they make the fission of the organelles happen as well and the peptidoglycan hydrolase enzyme is like, yeah, I wanna break down your cell walls and we're gonna get in there, we're squeezing you and I'm eating you and you're gonna divide whether or not you want to. And so what their work has basically shown is that there is this ring around these of proteins that the larger organisms have been able to take advantage of and they use it to control those invasive symbiotic cells that they want to get to and they use that, they use their protein tools to control them and to help them. So the simian doesn't reproduce on its own anymore? No. Right, the symbiont is- It's completely reliant on the host to take an over reproduction. That's a very interesting relationship. Yeah, so the symbiont is like, I don't really need all these things anymore. I don't need this now, yeah. That sounds like a virus. It does a bit, but yeah, but it is hijacking the cellular controls, right, for reproduction. But in this particular case, it's useful. It just don't, yeah. Yeah, you got this big powerhouse right next to you that's doing all this stuff anyway. So then whose idea is it? Like, or is it just, is it a case of just matching up? Is it related enough? Is it related enough somehow, evolutionarily, that the same proteins were already triggering this reproduction? And so then when they started hanging out close together when the big one went off, it did the other, the small one as well, the symbiont as well, it's, ah, yeah, it's very interesting. How does that relationship start? How does that process begin? How does, right, because at some point, the process was just, yeah. Yeah, at some point they're just hanging out near each other. Eventually, one engulfs the other and then the relationship begins where they're really helping each other out and the one that's been engulfed says, I don't need these genes anymore because you're doing that and the one that has done the engulfing also gets rid of a few genes it doesn't necessarily need anymore, but not to the same extent. And so it's still an interesting battle of the genomes, right? If you come from the selfish gene aspect of things, if it is the genes prerogative to reproduce, which is the better strategy? But it's sort of like then, what are those birds that have the other birds raised their eggs? It's a cuckoo. It's cuckoo, but is it, what's the, is there? It's a nest parasite. Yeah, a nest parasite. A rude parasite, yeah. Because essentially too, like if you, it's also, it could be a strategy or a benefit to your genes to have a bigger, stronger or a more efficient system out there doing all of your reproduction for you. So I don't know. Who's being selfish and who's just being opportunistic there? These are the interesting questions. Is there a difference? These are the fascinating questions of biology, I think. Justin, tell me about some cancer cures. Take us, take us to some cures. That works. That works, yeah. Does it work? Okay, let's see, what do we got? Well, it takes three different drugs. They got three drug combination, which currently seems to be winning the battle against chronic lymphatic leukemia, CLL. They had a broad group of patients in a clinical trial that went into remission. Good news. Then they had a phase two clinical trial that they focused on high risk forms of the disease, ones that are gonna be more aggressive and have a more quicker detrimental effect on the humans. And they found that it was really effective there. And so now they're getting ready for phase three. This is out of that Dana-Farber Cancer Institute, the investigators are doing it so far. All their trials have looked amazing. The initial cohort of the trial, again, this was the any type of subtype of CLL, which is, I have that and it's, and I've got like the, don't worry about it. You're gonna die of old age before, CLL does anything to you, versus people who will get diagnosed and in the olden days would be dead within two or three years. It has a wide range of aggressives and it depends on some genes and chromosome differences and what kind of a disease it is. So the first one, they just, anybody, any form of CLL, and they found that this three drug regimen, I'm not gonna try to say the drugs, I'll try to say, Acula, Brutinib, Venetokalax, and Obi-Nudu, Zumab. It sounds like I made that up, but that's really the name. This is, they produced a deeper mission in 89% of the participants. In the phase two, which is exclusively patients who are in the high-risk CLL, or the more aggressive form, they found deeper mission rates of 83%. And we're talking deeper mission, this is only 68 patients altogether, but what that means is in that high-risk group, after 35 months, they did a follow-up, 83% of those high-risk patients had undetectable disease in their blood, no detectable CLL in their bone marrow, and 45% were considered complete remission, like there was no indication that they even had had it. Wow. Yeah. Wow. Now, some other technologies that have been out, CART-T has had similar sorts of results where it's put this cancer into complete remission, but that's a very high-tech, somewhat dangerous, there have been some catastrophic small percentage where people die from it. Yeah. And it's extremely expensive. This is, this one here is a targeted drug and antibody therapy and another targeted agent working together for 16 years of use that's produced this pretty amazing result. So this is specifically in high-risk patients. So what is high-risk as opposed to like, is it high-risk is like, you're at the point where this is going to cause you to die within a certain amount of time or? So high-risk means that it's going to, the progression of white blood cells that are basically zombies or smeared cells so that they, is what it's going to look like in lab where they're either not going to do their job but they're going to get produced in 10, 20 times the amount that a healthy individual would have, that that process is going to happen really quick. You're going to get a doubling and a doubling and a doubling within three month periods, three, six. It's going to go up very fast. And so you're more likely to get sick. You're more likely to get sick, you're more likely to get the immunocompromised situations happening because you're going to have a body full of white blood cells that aren't actually working. And it's a very confusing part to the body and your body's not even causing problems. So it showed really high, it showed a really high effectiveness for even the high-risk, even more effectiveness for the lower risk, the slower moving. And after three years, 93% of participants were alive with no advance of the disease. That 7% too, now to be fair, usually you don't get CLL until you're pretty old. It's very common to be over 65 years old before this gets diagnosed. So with the average age over 65, no doubt, that 7% might have died, something else. Yeah, there's other stuff, yeah. Yeah, so they're next, and so they're going to keep applying this, they're going to try to apply this to other forms of CLL, maybe off of CLL and look at some other things that might work. But so far going into phase three, looking pretty effective. Yeah, so phase three studies are usually much larger, sample sizes, you're looking at big control groups and really looking at comparisons of how well it works. So that's where we'll really see if this is something, it is a real result, right? I think it likely is just that there's been, because I tracked this one a little bit because when you get a disease, you look it up every once in a while and say, hey, what's going on with? How's it going? Yeah, so there's actually a bunch of treatments out there. If this was 10 years ago, there's this and there's a handful of other treatments that are being specifically targeted to how the CLL, which is a small spectrum of diseases that CLL, small spectrum of causes of CLL, they've now targeted what those different causes are and they treat them differently. And it's almost, I'd call it an almost 100% treatable disease already, but not to the point of complete remission, removal, non-detection, like this is doing. Right. Yeah. They've been able to knock it down and control it for most people at this point. And yeah, it's lovely to see that there's, and this doesn't sound as expensive as the CAR T one. That CAR T one, it sounded really expensive. But again, that one was curing people in 48 hours where they were cancer-free. So just another cancer going down. Not a potential future maybe. This is again, this is cancer cures that are on the scene already, making their way through these trials, kicking cancer's butt left and right. Yeah, there was a really good result from an mRNA cancer trial this week as well. So, similar to the mRNA vaccine that we've been using for COVID, they've been studying that for treating various cancers and there was a very promising result this week on that front also. So yeah, let's kick cancer's butt left and right. I love that. Yeah. It's about time. But then we got to figure out what we're gonna, the extra people we have on it. We'll figure that out. That's a good problem to have. Yeah. So we already have too many. What's a few more? It's no big deal. People aren't having as many kids anymore and apparently the Y chromosome's gonna disappear even though that's very contested. But you don't have worries. No worries. Birth rates are growing down all over the world. We're gonna manage ourselves. Y chromosome is going to disappear. Yeah, I can't. No, just, shh, shh. What? It's not really gonna, this is a story that rears its head like every couple of years. Yeah, I remember seeing this before. It's silly. It's not yet. No, the Y chromosome is not disappearing anytime soon. So Y chromosome individuals of the world do not despair. However, let's talk about, don't despair. Let's talk about a really, really, really cool discovery that could give us new information as to how proteins fold. This comes out of the Department of Energy's Slack National Accelerator Laboratory, which used to be a linear collider. They don't do the linear collider stuff so much anymore, but they do lots of high energy physics and really, really cool imagery, high resolution real-time imagery of proteins and cells and lots of stuff. And so this study itself is like a decade in the making because of the work that's gone into it. And the researchers that have been involved in this from the Slack National Accelerator Laboratory in Stanford University, we're looking at a particular machine within cells that's called TRIC, T-R-I-C, and TRIC directs the folding of tubulin. Tubulin is, oh, there goes my light. Woo! What just happened? I don't know. Are you all right? You just got so excited about tubulin, you lost it. Hold on one second. What is this? Somebody's in the chat. I said, I heard that make no way. Do you know there's more people with red hair alive today than have ever been on the planet before? That's true just about everything people watch. Yeah, yeah, yeah. Yeah. Also like, I doubt it's going away. I mean, the ender towels were around a long time ago. They had the red hair. That is one of those things that hopefully will be edited from the show. But the thing about the ender towels that people gotta always remember is that they had a very large territory. They probably had every kind of skin color hair. They were probably just as diverse as the current modern humans in that respect. Well, even more so than the fact there are still redheads now as, you know, I mean, it's conserved. Redheads, very conserved. Come on, come on. Anyway, tell us about protein folding, Kiki. I'm so excited about protein folding. What are these slackers doing? You're talking about slackers. The tubulans. You're talking about slackers. They had a litter accelerator and then they stopped using it because they're slackers. They're like, ah, it's too hard to set it up. Let's try some other science. Ooh, but they've got high energy stuff. So they're like, let's look at super high, make high resolution movies of things that are happening inside cells. So where once upon a time you had to like freeze a section of a cell to try and get the, you know, the crystallized structure of a protein to see what it looked like and to be able to get that structure. Now they can actually start, they can take movies. They take these picture by picture, frame by frame, high resolution images and once upon a time the idea was, okay, you've got a chain of amino acids. The amino acids are like there in the body of the cell, right? You know, they go through the ribosome. They get turned into this chain of amino acids and then ta-da, electromagnetic or electrostatic forces and other attractive forces say fold together in this way and then the protein just can't help it. It folds together in the way that it folds together. Over the years, we have realized that there are guiding chaperone proteins which are very creatively called chaperonins and one of these chaperone proteins is called TRIC. And TRIC is the chaperone protein that is involved in just kind of guiding tubulin on its way to becoming the microstructural, one of the microstructural proteins inside of cells. So that it's like this tubulin is like it makes up the scaffolding that's inside cells. And so it's a very important protein. When they went in and actually looked at it through this, through the system at Slack, being able to take these very high cryo-electromagnetic images going back and forth between biochemical, biophysical tests, the imagery that they were able to get. They were able to determine that TRIC is actually like a chamber and there are these chaperones, a lot of them are like chambers. They're like little dressing chambers actually. And the protein, the amino acid chain goes into the chaperone and then the doors close. And when the doors open of the chaperone, the proteins there all structured the way the protein should be. And so they were like, what's happening inside the chaperone? What is happening when the doors close? So what they discovered is that inside the chamber that TRIC creates is that there's actually a lot of like little fibrils on the interior that are all electrostatically charged. And they kind of are like little helping hands that help tell the protein to go where it needs to go. And there are up to about 10% of the proteins in our cells as well as those plants and animals that get help from chambers like these in folding into their final states. So not all of the proteins in our bodies do, but 10%. So there's a few of them. And so there's an interesting aspect to this which is what's going on inside of these chambers? How are the chambers and the quote is folding spaghetti into flowers? How are these chambers basically helping the origami happen? They're these little barrels and they have eight different subunits internally. They form two stacked rings. There's a long skinny strand of tubulin protein that delivers into the opening of the chamber by a helper molecule that in this article from newsmedical.net is shaped like a jellyfish. Then the chamber's lid closes, the folding happens, the lid opens, and then it comes out. They were able to determine that internally there are four intermediate steps that occur in folding human protein tubulin and they are all directed by the inner walls. Of the chamber that is trick. One end hooks, one end of this amino acid chain hooks into the inner chamber. The other end attaches in another spot and then there are folds that happen and the folding is directed by the electrostatic charges of those little wobbly, wobbly electrostatic tails that dangle off the inner wall and they hold and they nurture the protein into doing what it's supposed to do and getting where it needs to be. So the chaperone must be specific to a specific protein. Right, so this is an interesting question, right? So there are a number of different chaperones and the question now is what role do these different chaperones play in things like misfolding of proteins like those that may be responsible for Alzheimer's or Parkinson's disease or Huntington's disorder and how can we potentially target the chaperone themselves as opposed to mutations within the amino acid chains themselves. So it's a new discovery, like totally new idea that yes, some proteins do just go, I'm short, I'm great, I'm just gonna fold the way I wanna fold but others need a little helping hand and there are chaperones for them. Instruction or the assembly of a protein as a strand, there's little bits that are gonna be attracted to other bits and segments in it that's gonna allow it to fold naturally, right? But it could get distracted. Bonds, there's bonds within, there's bonds within this structure that are designed to connect or to attract, to hold it together. Where does the specificity of this, like where does the chaperone come from? Is it getting printed off and then separated by an enzyme when the protein is printed made by the ribosome? Is the chaperone also being printed at the same time? Or because if it's- I have no idea. These are great questions. It's somewhere completely else. Yeah, if it's complete, if it's somehow- It's a multi, it is itself a multi-part protein, right? Stacked rings that have been put together. It's a complex protein itself. So where did it come from? Turtles all the way down. Yeah. Oh gosh, the human, whatever, I don't even know if it was in a human. Body, this biology is complicated, man. It is, it's messy. Biology is complicated and messy, but what I think is very interesting about this is that what it probably does is because of some of the bonds that need to occur to create the tubulin protein-final structure, perhaps there are energetic barriers that need to be overcome. And because of the structure of the chaperone, it's able to more easily allow the energy that's needed to be accessed. But is this happening in the, where is this happening? Where is this taking place? Is this in the- This is in the, not the nucleus. Could be the iodoporatus or the- No, this is in the cell body. This is in the cell, there's nucleus cell body. So it's already- Yeah, this is post ribosome. Yeah, but hmm. Free floating, except I got a chaperone. Yeah, fascinating new ideas though in how these proteins get folded. And also- It sounds like it's sort of like the whole phrase of fix it in post that we do when we do our live show. It's like the Rachel of biology. It's like, yeah, yeah, well, here's the proof. We made, yeah, we didn't really put it all together in order or anything, but it's not in particular. And then the editor comes by after, he's like, oh, they did it again. They did it again. All right, let's fix it. Yeah, it's more presentable. Yeah, is asking the good question is not how is this happening but why is this happening this way? So yeah, why did this particular system come to be? Why is it only 10% of our proteins that are chaperoned in this particular way? What is special about those particular 10% of proteins? How can we use this information? And what does it mean for all of those AI programs that are like, I can predict a protein structure. So yeah, a really fascinating question you just hit there is where's that 10%, is that 10% of those proteins, are they, what do you call it? They have a greater conserved longevity throughout the history of organism or are these the more newcomers? Yeah, I mean, more complex you might think is newer but maybe this, like, oh, are these helpers ancient or are these helpers a new thing that's come along and evolved? Self-folding proteins are the newest thing instead. Yeah, yeah, like which one came first? I feel like the self-folders are tie themselves. I feel like the self-folders are actually somehow be old but it seems like less complicated. It seems very less complicated. But it'd be interesting to track the evolution of this too. Yeah, yeah, so very interesting discovery, a long time and a lot of collaboration to allow this to even happen. Advancement of technology that made this possible is one of the biggest aspects of it. Like, 10 years ago, we could not have made this discovery. And really only four elements of tweaking a protein to get it in the right shape. I played those folded games. You had a whole myriad of tools and pulling it away. If you had to do something in four moves or with four tools, it'd be tough, it'd be tough. They're very tough. They've done it, wow. Where do I need this and do I need to sing now? What, singing in the microplastics? Is that where you're gonna sing? It's raining microplastics, is that like an, was that ABBA? Oh no. No. Anyway, it's raining. Why is it raining microplastics and do I need an umbrella? More specifically, it's not even raining microplastics, it's just in the air. This is a study from University of Auckland. They calculated 74 metric tons of microplastics dropping out of the atmosphere onto the city annually, which is the equivalent of more than three million plastic bottles falling from the sky. So this is not the- It's just on one city. Yeah, in New Zealand, not even like a, great, it's not New York, right? It's anyway, the thing that's interesting about this is not that there's microplastics in the air, this has actually been figured out before, but that their new method of measuring microplastics in the air they think are as more accurate and unfortunately contains way more microplastics than previously measured. So in previous studies, they found 771, I am missing the tons? No, I don't know. The 771 was their metric for London, 275 in Hamburg and 110 in Paris, but this new metric for Auckland was 4,885. This is the mean number of airborne microplastics in a square meter in a day. There's that, that's what it is. So it is just the base number, 771, 275, 110 in Paris. So obviously Auckland doesn't have 40 times as many microplastics in the air as Paris. What's happening is the method for measuring microplastics is not the method. Right, so it's the method for measuring it is more specific and catches specifically nanoplastics, which previous methods did not. And so that goes into the measurement. And so of course this means it's way worse than we thought, it's just, there's just plastic everywhere. You're part plastic, there's no way around it at this point. I think it's a big relevation to know that plastic and microplastics are just a normal part of nature that we just didn't know about all of this time. Or, stop using plastics. They think a big part of the way that airborne microplastics end up in the air is from breaking waves. So it's still originally started in the ocean in this theory, but then it ended up air rated and hangs in the air because it's so small. And so that can carry it to remote places far away from water, even though, you know, it's not wet. But basically, yeah, I just wanted to let everybody know you're breathing in microplastics. There's nothing you could do about it, except we can reduce how much microplastics are in the air moving forward. So please use less plastic, thank you, goodnight. I mean, that's really, that is really the solution. Can we use less, we use too much plastic. It's too much. Can we put pressure on manufacturers? I feel like the second half of this century is going to be all about undoing the past century and a half worth of damage to the planet. And just, it's gonna be like, okay, we had other plans for this half a century, but we're just gonna spend the next 50 years cleaning. I feel like it's really only the last 50 years are the biggest contributors to what's going on here. I feel like, you know, we need to teach ourselves to clean up our messes. Once upon a time, plastic was the most amazing advancement that was going to make everyone's life. It's revolutionized healthcare. The amount of plastic used in healthcare is insane. Can we just have them use it? Just them. We don't need the plastic bottles for our water. Oh, yeah, water bottles, we gotta have those. I really, really love my big old metal, metal truck. We just need to take out people. Just need to learn how to clean it up. Tiki, how much of that was lead? Shush. I'm sure it was for jet microplastics. Lead is definitely. Remember when you used to be able to take your toy car and draw on a wall with. I do recall. You remember when you used to be able to take mercury out of the thermometer and just play with it. Yeah, just play with it all day long. So we learned, and this is just part of life, right? Sometimes things are revolutionary, but they're not necessarily so great. And so we need to take stock of that and accept it and move forward. Our Lord is saying don't forget makeup. And there was another story this week about a group of chemists who have created a plant-based shiny glitter that is biodegradable. So it could be used in makeup. It could be used as glitter for parties and all sorts of things. Not metal-based, not plastic-based. Very cool. Brand new kind of glitter. We'll see when and if it mix it out. Biodegradable things on my body anyway. So sign me up. As long as there's no allergic reaction, I'm happy. My goodness. Well, this was a fun first half of the show. We saw so many conversations, so much good news. Quick science news, huh? Quick. This was the quick science news segment. This is The Seekin' Science. Thank you so much for joining us for another episode. We are really glad that you're here. And while you're here, please take a moment to head over to twist.org and check out our 2023 Twist Blair's Animal Corner calendars. They are available through Zazzle or as a PDF download. You can print it yourself wherever you are. Beautiful, high-quality PDF that you can print wherever you are. But you gotta go to twist to be able to access it. And, you know, Blair's request. Buy a calendar for her birthday. I mean, for you for her birthday. This is something that we enjoy doing every single year and your support in this project really does help us keep doing it. And honestly, Blair's art this year is just fantastic. The Lego art is beautiful. It's lovely. You don't wanna miss it. All right. Also tell a friend about twists and tell a friend about our calendars. These are things you should share. Do not keep it to yourself. Do not. This is not a secret. This is not This Week in Secrets. Okay. This is This Week in Sharing. That's what we are. Okay. Anyway, back to the show. It's time for that part of the show that we do love to call, what is it called? Oh yeah, Blair's Animal Corner. With Blair. Buy pet, milliped, no pet at all. If you wanna hear about animals, she's your bro. Except for giant pandas and squirrels. What's your gap, Blair? I have the mystery of snake, female genitalia. Number one, didn't know it was a mystery. Yeah, okay, number one. Yes, let's start there, shall we? So this is based on a widespread issue in biology, human biology and zoology where male genitalia is studied extensively. And female genitalia is not. Specifically the existence of and the function of a clitoris on female animals. It's just not studied. So as you might imagine, I am here to tell you snakes have clitorises. And this is breaking news. Since the 1800s, we've known that male lizards and snakes have a dual sex organ called a hemi penis, which is basically a two-headed penis. But it wasn't until in 1995 that a German herpetologist who is researching monitor lizards first described something maybe like a female sex organ on a lizard. And there's a bunch of ideas about what this could have been. Previous ideas were that they might have be a scent gland because it's near the cloaca, which is where waste comes out and where sex organs come out or go in, depending. But so there was an idea it was a scent gland. There was an idea it was just an underdeveloped version of a hemi penis, which is also what a clitoris is in a lot of ways. Anyway, and then there was also a theory that it was there to stimulate males. Oh, of course. Which is a hilarious jump to take before looking at whether there's biological signs that there's female stimulation going on with that organ. So this finding is, hey, looks like it's a clitoris. And in fact, it's a hemi clitoris, there's two. So it mimics how the hemi-penes work, right? And all of their study makes it look like it works just like or very similar to a mammal clitoris. So it has a rectile tissue, it swells with blood, it has nerve bundles. And so all of that indicates tactile sensitivity and potential use in sexual stimulation, which, now let's talk about sexual stimulation in female animals. There are reasons for that. There's one there and we're not. Obviously, like the base level one is if it's pleasurable in any way, that extends the length of copulation, which extends the likelihood of fertilization and successful reproduction. So baseline, if it's not painful, if it's actually pleasurable, then they'll keep going and they might do it again later, right? So there's an evolutionary reason to that being the case. But also there's a lot of theories about stimulation to females during copulation being related to lubrication, which prevents damage to female anatomy, specifically from spiny hemi-penes. So if they're spiny, if you have better lubrication, then you're less likely to get injured, less likely to get infected, less likely to die or have complications related to your reproduction. So there's a lot of benefits to this. There's not a lot of studies done on the clitoris in the animal kingdom or in humans. And it's because this whole kind of topic of female pleasure in sex is a taboo still somehow. Is it? Is it? Oh, it is embedded. It is embedded in the history of science, yes. I mean, just peek on the Twitter, even before a few weeks ago, there were lots of people saying that it didn't exist at all. So it's still a misunderstood subject, and it's still a taboo subject that a lot of scientists don't go looking to do studies on these kinds of things because it's not as well respected as other particular things they could study, including male anatomy. So it's a very interesting thing that I think this is the second or third study I've done in some way on the study of the clitoris in animals and how it's all still very, very new. And I hope that we continue to look at it because reproduction is the basis of the mechanism of evolution. And it's like the whole reason. It's propagation of species. We exist. And so, yeah, so it's understanding one half of the story that we never talk about. We talk about, okay, so males are trying to spread their seed. It's like they're trying to get as many females pregnant as possible most of the time so they can have reproductive success. And we're talking about how females are just kind of like the receptacle in the oven. But there's this whole other side of it that's about female pleasure in sex and how that is actually part of a successful species. And I can't wait to hear more. I don't know. I think that's all very secondary. Really. Two. Because the one overwhelmingly consistent theme throughout is that life is not about us. It's about egg. It's all about egg. Egg making more eggs. Right, but this is exactly that, right? This is the egg. That's it. Yeah, yeah, yeah, protect the egg. Yeah, protect the egg. This is where the egg is. So if a clitoris increases the likelihood of egg getting fertilized, this is key to that. I 100% agree. And if it increases the likelihood of the safety of that egg for any reason, that is important as well. What I will additionally. All about making more egg. Good egg successful egg. What happens after egg? This whole life and drama that we play out here on Planet Earth. Oh, interactions. It's all part of making more egg. It's all egg. It's all about egg. It's all within that matters. I think you're agreeing with me, Justin. I think I am. I know, but I couldn't just say it. It started as an argument, but it sounded like you actually agreed with me. It's fine. No, I totally agreed with you. I just didn't want it to, you know, because we're out here in the world of drama and everything, but it's all about egg. It's the most important thing. And in reality, it's all about genes. Right, right. And the genes that contribute to having a functioning clitoris could be a more successful gene that's then, yes, absolutely. That's what it's about. But reptiles. So we're not talking about mammals. No. This is a new family. Like, this in itself, I think, is massive. Yeah, so there's this whole idea now that Squamata, lizards, and snakes, they could all have them, which, yeah, why aren't we looking? They're not that small. The smallest ones are like a millimeter. We look at stuff smaller than that in biology all the time. That's why we're just not looking. You're not looking. If you're not looking, you don't see it, yeah. Yeah, it's the first. Yeah, I'm going to go, they look, now I'm curious to see if they have nipples. All right, well, they don't have those. They don't have nipples, no. They do have nipples. Have you looked? I don't know. I don't know. Now we need to look. Yeah, they have this visual limb. But this is another reversal of a kind of an age-old theory that a lot of animal sex is non-consensual. There's a theory that a lot of it is kind of not a universal consensual thing. Who wants to be a duck? I don't want to be a duck. Right, nope. But if we find out that female ducks have a clitoris and there is stimulation happening, then there is... It kind of flips the script a little bit. I think this is really interesting. And there's this narrative that, you know, sex is not always pleasurable and the animal can do it, which I'm sure in some cases is true, but the existence of this structure and the need to look for this structure more and more and more, it has the potential to change the narrative for how sex works in the animal kingdom. And I am very excited to see what happens. If there weren't a drive, if there weren't something that kept the, I'd like to do this again, especially for organisms that exist for multiple years. I feel like I'm getting the talk. I feel like I'm getting the talk. I feel like this is the, I'm finally getting the talk. This is not the birds and the bees, this is the snakes and the seas, the clitorises. Yeah, exactly. Anyway, moving on, sometimes animals will move great distances for various things, including, I suppose, sex. But when they do, when they migrate, we have obviously spent hours and hours and hours on this show, cumulatively, over the years, talking about how the heck animals migrate, how they find their way, how is it possible, lots of theories, landmarks, stars, sun, magnetic fields, new research offers a clue onto how migrating animals get to where they need to go when other signals fail. Even if they are using, yeah, go ahead. I know what they did. They didn't throw away their old, like, map books. Thomas' Guide? The Thomas' Guides, yes. Yes, exactly. So, but if you lost your Thomas' Guide, if there's a sun spot and you lost the magnetic field or there's other conflicting signals like humans, gosh, and our electronic devices, or if the sun goes down and you are using the sun or the stars go down and the sun comes up and you are using the stars. In any of those cases, you could start to lose your way. And so, researchers wanted to do an animal model to figure out if they are using multiple signals at once. That's one hypothesis. The another idea is that they are consulting their magnetic compass, custom. They're consulting their magnetic compass to use other ways of navigating, like smell or landmark. So all of these current theories are basically like, it's and. So you might have a main way of navigating, but you also use this other stuff when your main way fails. But this new hypothesis that they wanted to test was that perhaps it's because they stick together. And while one individual's sense of direction may fail, if they have others with them that still know where they're going, they can kind of lean on each other throughout the travel, the flight, the swim, whatever it may be. And kind of by the law of averages, if you have a large enough group, you can always have some people that know where they're going or some animals. And then they get to their destination safely. So they created this computer model. They simulated virtual groups of migrating animals and they analyzed how different navigation tactics affected their performance. They began their journey with a bunch of animals spread over a wide area. They encountered others along the route and started moving together. And they balanced between two competing impulses, one to band together and stay with the group or two to head towards a specific destination. So if the group is kind of going away from where you think the destination is, what are you gonna do? And then they gave everybody a degree of error. So sometimes your sense of direction is gonna get messed up. And when they simulated animals where they made more mistakes regarding their magnetic map, the ones that stuck with neighbors reached their destination. Those that didn't care about staying together didn't make it. Even when their magnetic compass sent them the wrong way, more than 70% of animals still made at home just by staying with the others in their group and following the lead. So for, this is interesting to me. So on screen right now, I've got an image of monarch butterflies, which we know very well for their migratory ability, but butterflies are not long-lived organisms. Yeah, they don't make the whole trip. Right, and they often they don't make, they don't, they don't live more than a year, right? So these are insects that, their whole purpose is fly, reproduce. You don't have like birds who have potentially migrated the same route year after year after year and have some memory of it. So this is what I find very interesting is how can you still have, everybody's magnetic compass is going off. You're not, something's gotten in the way, solar flare, whatever it is. Right. How do they end up going where they are supposed to go if they've never been there before? Yeah, I understand birds, but I don't understand the butterflies. I was thinking about how when you put a larger and larger and larger group of humans together and ask them questions, they become more and more wrong. The more humans are, they make worse and worse decisions. Oh, come on, group think it's really good. I mean, it leads to riots and stuff, it's awesome. Yeah, yeah, but this is the opposite. Somehow, this is somebody veers off course and they're like, no, no, no, I think it's this way, we're gonna keep going this way. And then it's somehow, but this is the thing, this is the other thing they noticed about the study, is that the smaller the groups get, the worse they are at keeping course. If a hypothetical population drop by 50%, this is similar to what monarchs have experienced in the last decade, fewer of the remaining individuals, about 37% fewer, made it to their destination. So this is really important to consider for population dynamics and impacts on migrating species. Is there a way to keep them on course, knowing that they might have a harder time with a lower population? Yeah, but yes, you're right, Kiki, there's a mechanism here that I don't totally get other than just like, there's so many of them that they stay the course just inherently and being such a large group. It's hard, it doesn't really make sense. And not another course, it doesn't make sense. So yeah, I'm fascinated by this. So I mean, we talk about groupthink and the possibility for negative behaviors, but we also know that there have been economic models built off of human behavior and prediction models. In fact, there are predictive betting sites where based on surveys of large numbers of people, you can put your money on the next election or various aspects of what's going on in our society. And these ideas of the knowledge of the crowd, the wisdom of the crowd have worked very well in these, in many situations. So I wonder, this is wisdom of the crowd, but how does it come about? Why does it work? And yeah. I mean, my guess with very little understanding is that whatever signals are failing for some individuals do not fail for all in that moment. And so you might have a slightly better sniffer than someone next to you. And so you can hold on to a sent queue that somebody else has lost and would veer off course. Or there you have natural selection at play, right? Right, right. Yeah, or your inner ear still knows where to go based on the magnetic field because yours is more attuned than somebody else's goes haywire, right? This is what I'm guessing based on the context of this information, but we don't know. This needs to be tested and modeled further to really know what the mechanism is. Yeah, and I think it, you know, I'm gonna guess it's different for different kinds of species, but it is interesting to see that it might be something that works for generally applied across species. The wisdom of the crowds. So ask for directions. Is ultimately what I would say here. Stick with me. Yeah, stick with your friends, travel with friends, or if you don't know where you're going, ask for directions. Someone around you probably knows. Someone might know. This is This Week in Science. Hopefully we know things we can take you in the right direction towards. Justin, what would you like to talk about? I have got just good news. The science news segment that volunteers to sniff the expired milk cartons of unpopular subjects in the search for uncurtled outcomes or still good enough to use for one more day. It's just good news. Lady fat edition. Ladies more so than men tend to deposit fat on hips, buttocks, and the backs of arms. So-called subcutaneous fat. While many may attempt to reduce these areas of cutting, it turns out they might not be so extra after all. As it appears, they have a protective factor against brain inflammation, reducing problems like dementia and stroke, according to this report. So males tend to get greater fat deposits around major organs inside the abdominal cavity, which is known to be far more inflammatory. And for menopause, males are much higher risk for inflammation related problems that things like heart attack and stroke are much higher amongst men. Men don't have menopause. I mean, they might have men who take pause, so thank you for the clarification. Yes, so women before menopause have much lower risks of these inflammation related problems, but it levels out postmenopause. They catch up. And part of what also happens is fat starts to redistribute a little bit. They start to take on fat deposit areas that look more like what takes place in men. In this study, they were looking at how, specifically they were looking at the brain, a couple of brain regions, to learn more about how brains become inflamed. And they looked at increases in the location of the fat, as well as levels of sex hormones and compared to brain inflammation in male versus female mice at different time intervals as they grew fatter and fatter on a high fat diet. So, since like people, the female mice tend to have more subcutaneous fat and less visceral fat, then it's a reason that the distinctive fat patterns might be part of the reason for the protection from inflammation, the female before menopause. So they found no indicators of brain inflammation or insulin resistance, which also increases inflammation, can lead to diabetes, until after these female mice reached menopause at about 48 weeks, menstruation stops, fat positioning in the females starts to shift, becomes more like the males. When they compared the impact of a high fat diet, which is correlated related to body-wide inflammation, mice in both sexes, following surgery, similar to leg perception, to remove the subcutaneous fat, it did nothing to directly end any of the astragibals. So they had them on this fat diet and some of them, then they got the subcutaneous fat removed and sex levels stayed the same. But the subcutaneous fat loss increased brain inflammation in the females without changing any of the sex hormones. So that shows at least a correlation between these specific fat deposits and a decrease in inflammation, or a managing of it of some sort. Bottom line, female brain inflammation looked much more like the males after removing subcutaneous fat, including increased levels of classic inflammation promoters of certain signaling proteins. This is all according to Dr. Alexis Amsterdam, neuroscientist at the University of Georgia. So this is quoting, when we took subcutaneous fat out of the equation, all of a sudden the female brain started to exhibit inflammation the way the male brains do and the females gained more visceral fat or the internal organ fat. It kind of shunted everything towards that other storage location. The transition occurred over about three months, which if you were to make a correlation to humans would be several years of human time. By comparison, it was only after menopause that the females who did not have subcutaneous fat removed but did still eat the high fat diet started to show brain inflammation similar to the males. So again, this is tying in two different ways that they looked at this fat storage deposit rearrangement seeming to correlate with the brain inflammation. So it's sounding to me like this is another case of it's all about egg, because if this is happening right up until menopause, then you're protecting the brain from inflation when you're a baby bus. It's all about egg. Basically, yeah. Exactly, exactly. Yeah, we need to make sure, and apparently it doesn't matter what the men. Men can get inflammation, get a stroke, they can die, whatever. They don't have egg. They're not the important ones. Interestingly though, they removed subcutaneous fat from mice that they had on a separate low fat diet, and they removed the fat in early age, and they developed a little more visceral fat and a little more inflammation in the fat, but they saw no evidence of inflammation in the brain, which is a little bit counter to the rest of their findings. So their take on messages is like, don't get liposuction and then eat a high fat diet. Yeah, that's not gonna help, exactly. Eating, moderation, moderation's key possibly, and also you're not a mouse. You're not a mouse. But you're not a mouse, but I think this also has implications for potentially the sex differences that we see in the onset of various neurodegenerative diseases and other issues, and like you mentioned, stroke and other issues that maybe lead to the premature deaths of men before women. And another reason to do separate studies, so that you're not just studying inflammation in the brain in humans, you have to separate this out to the kind of hormones you have in your body to kind of indicate it might be different, right? And treatments might be different because of that. And in the meantime, while you've got it, flaunt it because it's good for your brain. Yeah, so yeah, they're saying also, pointing out in this that BMI, body mass index, is dividing weight by height, which is commonly used to indicate if it's over weight. Garbage, not indicating the proper kind of fat. It's not a very meaningful tool. It's nothing. Yeah. She says, Strangheny goes on to say here, we can't just say obesity. We have to start talking about where the fat is, because that's the critical element here. There's still a lot of correlation here. It seems like not a whole lot of specifics about mechanism. Yeah. The studies looked specifically at the hippocampus and the hypothalamus of the brain, hypothalamus, which controls metabolism and exhibits changes with inflammation from obesity. That also helps control, can just develop body-wide as a result. The first Center for Learning Memory, regulated by signals associated with those pathologies, but doesn't have any direct control over them. Gravitance indicates estrogen may not explain the protection females have, at least not alone. Next, they won't want a better defined dose. And yeah, so just good news for you ladies having a hard time losing subcutaneous features. Your diet fails may actually be good for your brain. Might be preserving a healthy life. And in other news. Hey, have you ever had a piece of technology break like a phone or a watch or electronic device? Or maybe it didn't break, maybe just a new version came out. Just a new version. You're like, ah, it's time to upgrade. No planned obsolescence stopped working because the new version came out. So apparently a lot of people, they throw away their old electronics. And this is leading to something like 40 million tons of electronic waste each year. With this in mind, University of Chicago scientists made a watch that was alive. They made a watch, a somewhat smart watch with an integrated slime mold. The researchers created a watch that not only works. That not only works. Actually, sorry, they created a watch that only, it has a function that only works when the electrically conductive single celled slime mold is healthy and it requires the user to provide it food and care to keep it healthy. Excuse me, I got to feed my watch. Not just mind it, feed it. They then test how this device affected the wearer's attitude towards the technology. So the watches were designed to tell time. That was by itself standalone. And then they also had a feature that measured the wearer's heart rate. But that second feature, that heart rate measuring feature only functioned when the slime mold was healthy, well-fed and bridging that to conductivity connection. So slime below blob is placed. I found a picture of it. This is wild. Are you ready to share it? I want to see that. Yeah, I'm gonna. I don't have the picture. So they tested how this thing works. They took the blob and they placed it in an enclosure within the watch. User must regularly feed it a mixture of water and oats to induce its growth. Oats. Oats. When the slime mold reaches. I mean, that's when I try to feed myself. Okay, easy. When the slime mold. Little for me, little for you. Is healthy enough and it grows and it reaches the other side of the enclosure. That's the electrical circuit that activates the heart rate monitors. Now your heart rate's being monitored with this organism. The organism can also enter a dormant state if you don't feed it. And then in that dormant state, it can apparently be revived again after days, months, or perhaps even years later. So while this makes tech less user friendly in some ways, it is also requiring the user to be more friendly towards the tech. They conducted a study with five participants who wore the watch for two weeks. Over the weeks, the users cared for the slime mold until the heart rate monitoring was enabled. And then researchers asked participants to stop feeding the organism, causing it to dry out and disrupt the heart rate function. That the study participants updated journals about feelings about their device and answered questions and interviews. Researchers found a high level of attachment to the watch. With some users saying it felt like a pet, some named it, even putting their partners in charge of feeding the watch when they could not. Oh dear. That's the first thing I thought. If I was told to not feed my watch, it would be very hard to do that. Like, whoa, I'm gonna feed it still. I love people in the chat who are- Yeah, they had emotional responses. Yeah, Paul Disney and the marked are responding and saying this is kind of like Tamagotchi's. The Tamagotchi toys that used to be those digital pets that you'd have to feed and take care of, and but this is actually a piece of tech that is not just a pet, but something that can work with you as a piece of useful technology. Yep, and so some of these actually said they felt a much bigger connection to this than they had with playing with virtual pets. Like, they were, the emotional response when the study participants were told to neglect the organism were ones of guilt and grief. We're not, we're not reading this. So the papers published in the 35th annual ACM Symposium on User Interface Software and Technology, but part of I guess the brainchild behind this, partly this is just a fun thing to do, I think. Interesting experiment, social experiment kind of a thing. But kind of the idea is if you could get people to feel more attached to their, or sentimentally attached to their tech, maybe they'd throw it away less. Maybe they would go in for the repair. Maybe they would keep it longer. Well, it's not just the repair. If they thought of it as a pet. Well, it's also, I mean, as we mentioned at the beginning of this, the planned obsolescence, aspect of things is a huge issue. And if the technology is being updated in a way that makes it hard for you to continue to take care of it, I mean, that's something, I love this idea. Yes, I think we should find ways for people to connect more with their technology in this kind of way. I think using biology and technology together is a fascinating way to make it work. And perhaps it's more sustainable. I mean, if you're using components like slime mold to conduct electricity as opposed to precious metals, maybe this is better. I don't know. The researchers are making no claims about practicality. Oh, yeah, no, this is not. They're not saying, hey, slime mold is the future of tech in any way. What they're saying is, if you can build an emotional bond separate from the one-way user need, give me the information, use my tech thing. People like, oh, I can't get rid of slimy. Slimy's been with me since middle school. I gotta keep my iPhone 6 a little longer. I just can't throw it out. Or even if I don't use it anymore. I killed my watch. Even if I don't use my smartwatch anymore, I'm gonna at least keep feeding it. It'll have it on the bedside, and it'll give it a little bit of water and oats, and it'll still have it. I don't need it for the heart monitor anymore, but maybe I'll pass it down to my kids, and then the slime mold will be in the family for generations. Oh, just let that mean starter for the sourdough, yep. And Eric Napp is saying the 130-year-old pocket watch I got from my grandfather is not getting thrown away anytime soon. That's beautiful. Yeah, you can pass down this combination heirloom organism and tech memorabilia generationally passed down. And I don't know how long a slime mold can live. I was just gonna ask that. Well, maybe it's a long time. However long it continues to be fed, it's an ongoing organism, right? I have a couple of stories to bring us into the end of our show. Talk about, we're talking about slime mode. Slime mode? I mean, maybe you might be in slime mode when you're feeling stuck to your couch and you haven't showered and you're just unmotivated to get up and exercise or do anything that would be physically challenging. And you're like, oh, I just can't get, I can't do it. I'm in slime mode. I heard there's some pandemic term, I guess. It's like goblin mode or something like that. I learned recently, yeah. Regardless, researchers at a number of universities have found that two bacterial species, eubacterium rectale, guess where that one's found, and coprachoccus eutectus. Also same. Yeah. The same. Guess where these are found. They're found in your gut, everybody. They produce metabolites known as fatty acid amides. These fatty acid amide metabolites go on in the gut to stimulate receptors called CB1. These are cannabinoid, endocannabinoid receptors on gut embedded sensory nerves. Guess where those gut embedded sensory nerves go? To the brain, actually, they connect to the brain via the spinal cord and in a region, specifically known as the ventral striatum. They don't just go up like vagal nerve and go do-do-do brain stuff. They go to a very specific area, the ventral striatum, which is important to releasing dopamine. Mm. Which, this all happens, this whole process, this cascade that I just talked about, happens during exercise. Dopamine gets released during exercise and in their work that was on mice, not on humans. They had mice without bacteria, mice with bacteria. They found that mice that had these bacteria seemed to have more of a runner's high when they were exercising. More dopamine was released while they were exercising than mice that did not have these bacteria. And so they're attributing the presence of certain gut bacterial species in the performance of, or the activity. Of higher active animals. So these are- So we finally have a probiotic that is a sure-fire diet mechanism that motivates the whole body to exercise. So maybe do more exercise. So you'll never know if you don't exercise the first time though, right? So if you do and you go, uh, this is terrible, then you don't have it. You don't have enough of this microbi... So we don't know. Yeah, so really they did machine learning, looking at attributes of mice to see like, okay, why do we have some mice that like running more than other mice? And they really could only account for a little teeny tiny percentage of it through genetics. The genetics really were not the part that made the difference. It was bacteria in the gut that made the difference to those that wanted to run and those that didn't want. So now what we don't know is, do we put more of these bacteria in the gut and then that leads to this pathway? So would it be the kind of thing that we could do specialized fecal transplants or probiotics that somehow get into the gut to populate the gut with these bacteria? Is it something that can, is it that you exercise and you create an environment in your gut that allows for these populations of bacteria to exist in a way that leads to wanting to exercise more? But regardless, we don't know if there's a pathway like this in people, but in mice, it appears that microbes motivate. And maybe this is the pill that we all need. Dr. Justin's not a real doctor, poo pills for what else yet. Won't help you with this. I don't have these metabolites. I don't have the metabolites. I used to. Oh, wait, Justin, you're selling your poop? I don't think I ever realized that. Oh, well, I don't know. Where am I gonna go get other people's poop? That's disgusting. No, I'm not gonna get any retouching anybody else's poop. You know. And it may or may not be in pill form and there's no guarantees, but. No guarantees. So this is like, if I had this, I would have had this in my youth because I used to run. I used to love running. I used to run like extra laps in the physical education classes. I did the track team and I ran. I ran and I ran and I ran. I just loved it and I wanted to keep moving. And then at some point, that stopped. You lost your bacteria. Your motivation went away. I think I, you know, one of the times in life where you got antibiotics or whatever, maybe it knocked it out. So I need days. So I need somebody else's poop pills to fix Dr. Justin's, not a real doctor poop pills system because yeah, no, this is, that's, I mean, I love the fact that they looked at, they went through and they looked at the genetics and they looked at diet and they looked at all these other things and the only thing that trended, the only thing. The biggest thing. The biggest thing that made the difference between the mouse that was out there running on the little mouse treadmill. That's what I have a picture of them all on little treadmills and that's, I don't know how they. They're little running wheels, you know, they get in their red. The mouse out there running on the, yeah, running on the wheel and it's going and going and going in the biggest factor that they could tell them the differences to the mice that didn't do it. They got microbiome. That's just awesome. It's fascinating. And the researchers, one study co-author, J. Nicholas Beatley, who's associate professor of biology at University of Pennsylvania School of Arts and Sciences says the gut to brain motivation pathway might have evolved to connect nutrient availability and the state of the gut bacterial population to the readiness to engage in prolonged physical activity. This line of research could develop into a whole new branch of exercise physiology. You know, it's also interesting is, because they say the genetics played only a tiny part in this, I'm thinking about all of the professional athletes in this day and age who have two parents who were athletes. Now, you think, oh, of course, two genetics, two athletic genetic, you know, that's why you get another genetic athlete or is it the family microbiome? That is being present like that. Those are the poo pills we need. Yeah, we gotta go find some athletes. It's like, I just, no, I don't want an autograph. No, actually it's not, I don't need a gang. I don't need a jersey. I don't need an autograph. I have a slightly different request. You seem motivated to exercise. You're always out there training and running and just small, small thing I need from you, but just buy some poop. Okay, moving on from the, This is my favorite story, though, by the way. It really is. Yeah, it's a great, I love it. It's a great story, right? Yeah. And all those athletes who spend a lifetime athleteing, where are they hanging out? In the locker room and the trainer and the gym, surround with all these other, they're sharing microbiome all over the place. So somebody in there has got the good microbiome by the end of a season of sharing tight spaces and working together and eating together and all this. They end up sharing a bunch of microbiome and then the team gets better. It's like, hey, we're way better than we were at the beginning of the year. Everybody's done a lot of work. It's because that one or two people in there had the right microbiome. It's not, so CrossFit, it's not a cult. It's the microbes. Yeah. Because everybody's going to the CrossFit gym and they're sharing the microbes and they're all like, oh, now I need to come back and do more CrossFit. Well, that's why the first class, if you don't have the microbes, the first couple of classes are like, oh, this is tough, I can't do it. But then after you've been in there breathing their air and smelling their, you get sharing their microbiome, then all of a sudden you're like, hey, I can't wait to go exercise. You're like, I got really into it. I'm fit, that's enough. It's because you drink from the drinking fountain. You know, that's what happened. You went and worked out on that one piece of equipment where nobody toweled off. That's what did it. So that's what they were doing at the gym when you got the athletes in there. Okay, nobody towel off. We wanna make sure we spread this stuff. No, no, no, no, no, no, no spreading. No, no, we're not, anyway. Let's talk about the sixth, sixth sense. And I'm not talking about like the movie, not talking about some dead people. I see dead people, yeah. No, no, I'm not talking about ESP or not talking about ghosts and talking with dead people. No, I'm talking about proprioception. That is really our one, two, three, four, five, sixth sense. So you've got the normal five senses and then we've got the sense of where our body is in states. And I think I talked a little bit about a study related to this last week also, but researchers at the Max Delbrouk Center publishing in Nature Communications this week have been interested in the idea of the sixth sense, whose job it is to collect information from our joints and our muscles and our posture and where we are in space and then tell our central nervous system about that. And it allows us to do things like navigate in darker spaces than maybe our eyes would normally allow us to do because you've become familiar with the layout of your house. Okay, so I'm highly limited in my sixth sense then. Oh, I am the person who runs into doorways all the time. Yes, but that's the thing. Some people are less able in their proprioceptive abilities than others. Some people do not really have proprioception. So if you closed your eyes and tried to take a sip of your coffee in the morning, would the coffee cup reach your mouth? Yeah, I think it would hit my teeth. I'm done. I usually like clink right into my teeth. Yeah. And so these researchers, they have published this article in Nature Communications to better understand how what they are looking at, which are called proprioceptive sensory neurons actually work. And so these proprioceptive sensory neurons are located in the dorsal root ganglia of the spinal cord and the dorsal root ganglia of the spinal cord. Like the bottom part and they're a place where from the body, from all your muscles, all the nerves come in and they come into this little nerve center before they go into the spinal cord itself and then head up toward your brain. They're connected by long nerve fibers and they are attached to these muscle spindles, which stretch when you move, Golgi tendon organs, which again, when the stretching happens, they go, oh, signal, signal, signal, send it to the spinal cord. And they're supposed to be registering all this movement, relaxation, tension, throughout every muscle of your body. And they have to connect precisely because if they're not connecting precisely, then your proprioception is going to be off. And so they started looking for molecular markers that would differentiate certain proprioceptive sensory neurons for different parts of the body. So different neurons that would go to the abdomen, the back, your legs, your arms, and figure out what markers in the RNA are in there that are like, hi, I'm an abdomen proprioceptive sensory neuron. Oh, I belong to the back. And they were able to show that these genes are active at the embryonic stage. They're active for a while after birth and that there are programs that move along, deciding whether or not they're gonna actually innervate different parts of the body or not, whether or not these particular cell body sensors, the cell bodies of these sensory neurons decide to actually connect to stuff. The idea eventually is that once they understand how these proprioceptive sensory neurons work is that when you lose the function of a limb or even to give additional abilities to the functioning of a limb, we can build prostheses that then could potentially connect to these proprioceptive sensory neurons in a much more valuable way, in a more effective way. So they can use light to turn, right now, optogenetics to turn these on or off in groups or individually and they're able to get a lot more information about this stuff but I have scoliosis, my spine is a little bit crooked but and so this particular statement really kind of hit me a little bit is that one thing that researchers in Israel have discovered is that if the proprioception isn't functioning properly, the skeleton isn't going to form properly and so scoliosis possibly is a result of improper proprioception during growth so that the proprioceptive sensory neurons are not necessarily acting in the right way to be able to allow the spine so that there's even balance of the muscles that help support the spine and so that the scoliosis forms isn't necessarily only a disformation, a distortion of the spine itself but also controlled by dysfunction within these sensory proprioceptive neurons and so from forever, forever now this is why I'm going to blame every time what I'm going to blame every time I walk into a door frame. You should. Yeah but the definitely interesting aspect of this is the potential to be able to understand how our nerves are connecting to the various parts of our bodies and then how the signals are being transmitted along and how different cells decide that they are going to connect or not connect where they connect and what that means for the development of organisms and functioning bodily systems. Your sixth sense, yes. Yeah I hadn't thought about it at all in this sort of terms I have a, what do you call it, sciatica. Every once in a while I get a little bit of a lower back pain inflammation or something and what happens is there's a nerve that's getting squished it's getting mistreated somehow and then the back muscles tighten around it because they're trying to protect that nerve but by tightening they're squishing up more and it's this vicious cycle. But anyway the sciatica runs down one leg it's like a weird kind of a pain but it's like just an irritating feeling runs down one of the legs. One of the things I've noticed is when that's acting up really bad I sometimes will take a step or two and my foot isn't right. My foot like will be tilted in and it's like I need an adjustment or something but I might take a slight stumble when I walk, when I'm having this but I never thought of it in this way but what it could just be that nerve pinched nerve is now mis-telling my foot where it is or mis-telling my brain where my foot is and so the foot's going out there like there's no range problem with the foot it's like not like it can't move in the right way but it's just naturally it plants itself slightly wrong. Maybe thinking that it's in the exact right place but because of the distortion because of this, what do you call it, sense? The proprioceptive sense. The proprioceptive sense. Proprioception is off so it thinks it's doing the right thing but it's wrong and that's why when I stand up sometimes when I've got that back issue going on that the first step is kind of wobbly because the foot's not planted. That's really interesting. Yeah. Yeah, I mean I think there's a lot to be said for continued physical activity that is not just like oh I'm gonna go just lift a bunch of weights or run as fast as I can but actually as you get older focusing on very specific activities related to stabilization and making sure your knees are turned forward as opposed to splayed inward or outward making sure that you are standing in a solid position on your feet. Like making sure that you are telling the muscles in your body. This is normal as opposed to letting just the deterioration of age kind of take over and then suddenly oh your foot is in that funny position. Is it like, because the question is is it in that funny position because we've been sitting in our chairs and doing computer stuff for too long and not doing very specific exercises to make sure that our muscles are telling those sensory neurons the right things. And maybe the sensory neurons are now confused about what's right and what's wrong. So which way does that go? And this gives like a whole new Yeah. Yeah, this gives a whole new level to my thinking of what yoga is doing. Because there's so much what I tell like sort of muscle memory in terms of having done poses and stuff enough times that you can, that strength and that core muscle and you think of all that stuff. Also training the body if you're doing a very uniform physical task that you do it once on this side you do it once on that side. It's probably building those positions to that sense of where body parts are for all of these poses. You do them over and over again and your body's getting better trained to know where all of those parts and pieces of you are flailing about in the world. Exactly. Stop flailing. That's a scary one. You're not flailing. It's intentional, right? Yes. Anyway, proprioception. It's important. I think this kind of information is going to be really interesting from these perspectives. How do we use this from understanding how certain developmental disorders occur and then also if you consider development all the way through into old age how do we manage it and manage our proprioceptive state all the way through old age to manage healthy aging as we get older? A lot of people with sciatica. We can do better than that. We can fix it. I don't know if they're going to fix sciatica. I got it right now. I'm like standing there. I don't want to go and get back nerve surgery or whatever. But it's an interesting thought because I did not have this when I was doing a lot of yoga. Stretching, it could be all these other things. It could be back positioning adjustment. But I'm now just going to say it's the what did you call it? The propitia. What is it? Proprioception. Proprio. Proprio. Proprio. Maybe it's just proprioception is now like I haven't mentally worked out with my body enough lately. Yeah, exactly. Concentrating, being mindful of where your body is in space and how it's moving. Exactly. Noodles is saying, is someone with neuropathy? I live this thought process every day. First priority is balance. Yeah. All right. So we can train our brains for better body health. That's a great idea. Yes. Fantastic. Helpful tips that you can take with you at the end of this twist episode. We did make it to the end just now, didn't we? Yeah. We made it to the end. We got a couple of them. It's beginning to look like the mind and body are connected in some way. It's being taken to look a lot like mind-body connection is important every single day. When you get up out of bed, you should think with your head about where you're going to put your feet today. Okay. That was the end of that. Thank you everyone for joining us for another episode of This Week in Science. We are so glad that you have all joined us. Once again, happy birthday to Blair and Justin. Thank you for all of your time and effort, and I hope you had wonderful birthdays this past week. And for everyone else out there, it is time for a few shout-outs. Shout-outs to Fada, thank you so much for helping with show notes and social media, all those wonderful descriptions and things. Additionally, Gord and Aran Lore and others for helping to take care of our chat rooms. Everyone in the chats, thank you so much for being here, for chatting, for being a part of this conversation. We love seeing your comments as we do the show. That's what this is all about. Identity 4, thank you for recording the show. Rachel, thank you so much for editing. There will be a little bit more of it tonight. Not as much as there would have been if we'd actually started when I thought we started. And as always, time to say thank you to our Patreon sponsors. Thank you, too. Teresa Smith, James Schaefer, Richard Badge, Kenton Northcote, Rick Loveman, Pierre Villazarb, John Ratnaswamy, Carl Kornfeldt, Karen Tozzi, Chris Wozniak, Dave Bunn, Beggar, Jeff Steid, Hal Snyder, Donovan Styles, aka Don Stilo, Ali Coffin, Gaurav Sharma-Raggan, Derek Schmidt, Don Munda, Stephen Albron, Darryl Meischach, Stu Paulik, Andrew Swanson, Fred S-104, Sky Luke, Paul Ronevich, Kevin Bearden, Noodles, Jack, Brian Carrington, David E. 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We will be back Wednesday, 8 p.m. Pacific Time, broadcasting live from our YouTube and Facebook channels, and from twist.org slash live. And you know what next week's show is? It's the year in review, isn't it? It's the year. Yeah, it's not just any old show. Ooh, we're taking a look. Oh, that's a big show. Back at the top 11, science stories. Top 11 stories of 2022. And while you're waiting for that, or after it airs, if you want to listen to us as a podcast, perhaps while you go over your year in review, just search for this week in Science Over Podcasts or found. If you enjoyed the show, get your friends to subscribe as well. For more information on anything you have heard here today, show notes, links to stories will be available on our website, www.twist.org You can also sign up for a newsletter. You can contact us directly. Email Kiki at Kirsten at thisweekinScience.com, Justin at twistmanina at gmail.com, or me, Blair, at BlairBazzettwist.org. Just be sure to put twist T-W-I-S in the subject line or your email will be spam-filtered into a dark room and we'll never find it because we can't, it's lost. Because Blair's bad at proprioception and so am I, and as he's done. It's gone. It's gone. It's too dark. And can they still, are we still on to Twitter? I gotta ask you a quick, because it says here that you can still hit us up. Okay. We're still on Twitter. We don't know why, but we're there. Twist Science Yes. At Dr. Kiki, we love you. We love you. We love your feedback. If there's a topic you would like us to cover or address a suggestion for an interview, a haiku that comes to you in the night, please let us know. We'll be back here next week with the year interview and we hope you'll join us again for more great science news. But if you've learned anything from this show, remember, it's all in your head. This Week in Science This Week in Science This Week in Science is the end of the world. So I'm setting up shop. Got my banner unfurled. It says the scientist is in. I'm gonna sell my advice. Show them how to stop the robot with a simple device. I'll reverse all the warming with a wave of my hand. And all it is is coming your way. So everybody listen to what I say. This Week in Science This Week in Science This Week in Science This Week in Science Science This Week in Science This Week in Science This Week in Science Science I've got one disclaimer and it shouldn't be news that what I say may not represent your views but I've done the calculations and I've got a plan. Through the science you may justände understand Not trying to threaten anything at all all we've got is an awesome Lego made calendar by Blair I'm sure you'll have a wonderful year just because you buy the calendar. How's everybody how's everybody. How are we lost to Justin? I'm slowly really fading into oblivion. We are all fading into oblivion. It is 1046 p.m. here on the Pacific Coast, and it is late. I cannot remember when we've done a show that long. We have, well, we started late. It's been a really long time. It was, yeah, two, 20, it was a really fun show, though. Yeah. I do have to say it was a very fun show. That was even without a guest. I apologize for the very long show. Kind of, yeah. I mean, it is the end of the year, and this is the last real show of the year. Next year's, next week's gonna be. I just don't know how, I don't think I can stay. I think I'm spent. No, I agree with that. I'm spent as well. I have been spent. I actually like fell asleep earlier today and took a nap. I don't take naps very, I was like, I'm really tired. It's time for a nap. Thank you, Paul. I'm glad that you, yeah, it's worth staying up for. I know you're on the West Coast. How many East coasters are still up with us right now? That's what I, oh, noodles, 146 a.m. Getting ready for, yeah, warming up for a marathon New Year's. That's right. That is right. I was just gonna wait until Justin comes back so that we can actually signite in the proper fashion. 447 p.m. Daniel Smith, you are obviously not on the East Coast. That's fantastic. She's like, can we go to bed please? Say, he's loud as bedtime. Why are you keeping me up this late? Oops, my cats have given up on me. Totally given up on me. Yeah, I think I have weird energy tonight. I realized that I get monthly migraines and so East Coast of Australia, there you are. So tonight I, last night and tonight I've tested taking a tryptin. Yeah, that's my new rescue medication. It's great, it's changed my life. Yeah, and so earlier when I was very sleepy and was very unhappy and hiding under blankets, I took a tryptin and now I'm like, hi, everything's great. There's a huge euphoria. You're like, I'm really awake, oh my gosh. I was in so much pain, I couldn't think or move and now it's gone. Yeah, yeah, that's basically what happened. Oh, yeah, so that's a new thing when you realize that maybe you've been dealing with monthly migraines as a symptom of being a female for several years. That could have been treated. Oh yeah, no, I've been getting migraines since I was in middle school and they kept saying like, oh, you need new glasses. Oh, you're wearing your hair too tight. Oh, you know, they always had a different excuse whenever I went to see a doctor. And then a couple of years ago I went to a doctor I was like, I'm pretty sure I have migraines and they're like, let's talk about it. They go, oh yeah, you have migraines, let's get you some medication. I was like, medication? What? What? Yeah, that's great. Yeah, the only reason this is a thing is because my husband has migraines as well and he's like, he's been watching me and he's like, you get, you've got migraines. I'm like, I don't have migraines. Leave me alone, this is, I just, it's just, I'm not happy once a month. I'm tired, it's fine, it's good. Oh, oh no, no. That's like a medical thing that's treatable that's not just a headache. In fact, like headache medications don't work on migraines. So no, they don't. Yeah, so it's amazing how much you can learn about yourself as you grow older and find the right resources or other people who are going through similar things. Once again, this is the stick with the others. Other people have knowledge that's valuable to you and can help you out. All right, Justin's back, say good night, Justin. Oh, that was quick. Good night, Justin. Hey, good night, Blair. Good night, Blair. Good night. Good night, everyone. Thank you so much for joining us for another episode of This Week in Science. We will be back again next week and oh my goodness, I can't believe this. Top 11 show, send us suggestions. What was your favorite story of the year? Top 11. We gotta know, we gotta put the top 11 together. Oh, this is one of my favorites. It's the second favorite show of the year, I think. I'm gonna say right now that I don't think I'm gonna put the National Ignition Facility story on my top, it's top, but I don't think top 20 maybe, top 30, but I don't think it's gonna be top 10 for me. Top 11, even. I might go with one from last week, just cause I can remember. We got it. The, I think the environmental DNA in Greenland is one that's gonna make it. Yeah, EDNA, I think, yeah. RMR saying the best story was from this week. I know it's the snakes, right? I know. Who knows snakes have nipples? That's such a strange takeaway. Justin, hold on. Don't purvey misinformation intentionally, that's not our job, that's other people's job. It's still how I'm gonna remember. They don't miss information. I don't know. Good night, everybody. See you next week. Exciting show. We're gonna have to, we're gonna have to collaborate a little bit more than- We have a lot of work to do before next week. Yeah. Yeah. Okay, everyone, take care. Stay safe, stay healthy, stay curious, and let us know what you think about the top stories of the last year. We'd love to know your ideas. We'll see you again next Wednesday, 8 p.m. Pacific time. Thank you for joining us once again. Good science to you all.