 the social media, and then I hit send now! Only 15 minutes late. Only 15 minutes late. Well, 13. 13 minutes late according to my clock. It's not terrible. Sorry, you guys. I unplugged all sorts of stuff for Denver. Oh, yeah. Yeah, and then, and stole cables and they were, there are things in my suitcase still and my computer was turned off and I had to re-log into things. And I was just like, wow, this is not what I was ready for because I haven't been in my office since before I left. I haven't. I worked in the kitchen today because it was warm there. It's cold everywhere else. I know it's cold other places. But do you know what time it is? Three, two... This is TWIS, This Week in Science, episode number 644. Recorded on Wednesday, November 8th, 2017. Regenerating and transplanting. I'm Dr. Kiki and today we will fill your heads with a multiple explosions, clumsy mammoths, and murder. But first... Disclaimer, disclaimer, disclaimer. Tonight's show is not for the faint of heart. Although Halloween has passed, there are still plenty of things going bump in the night. What exactly is making the sounds you hear outside your window in the dark? Could it be an undead supernova stirring in its starry grave? Or maybe it's a mindless mammoth meandering after midnight. Are you frozen out of fear? Or because a frightful fungus is forcing you not to flee. And while there may be a killer or two out there, wait to hear about the one lurking much nearer. But not to worry, it's not all the stuff of nightmares ahead. We have science stories, all sorts. Here on This Week in Science, coming up next. I've got the kind of mind that can't get enough. I wanna learn everything. I wanna fill it all up with new discoveries that happen every day of the week. There's only one place to go to find the knowledge I seek. I wanna know what's happening. What's happening. What's happening this week in science. What's happening. What's happening. What's happening this week in science. Yes! Science to Kiki and Blair. And a great science to you too, Justin, Blair, and everyone out there. Welcome to another episode of This Week in Science. We're back once again with all the science that we can fit into this show. And that is the truth. That's the truth. I feel like I just did this. It's just deja vu. It's deja vu. Yeah, we had a show in the middle of all this. Went to Entomology 2017 in Denver, Colorado and had a live show on Monday. So we are doubling up the shows this week. So much fun, everyone. But we covered insect news on Monday. This time it's gonna be all over the place with science from everywhere. I've got stories about a sequential supernova. Cellular regeneration and some new skin. Justin, what do you have? I've got a murder mystery. Evolutionary growth spurts and artificially sweet and septic tanks. Yum, ew. No, Blair, what's in the animal corner? Well, I have some clumsy mammoths. I have very fast sperm and sheep. Sheep? Sheep, okay, all right. Don't be sheepish or, you know, you gotta listen to twists. Don't be sheepish. But if you want to be like a sheep, follow the herd of those who are listening to twists. Before we jump into the show, I want to remind everyone that you can subscribe to the Twist podcast on iTunes in the Google Play podcast portal, Stitcher, Spreaker, TuneIn, all the great places that there are podcasts. You can pretty much find us if you look for us this week in science. We're also findable, searchable on YouTube and Facebook. And you can just find us at twist.org. But now it's time. Oh, for me to remind you about our calendars. We are still taking orders for calendars. So if you go to twist.org, you can click on the calendar link for the 2018 Blair's Animal Corner calendar. It's a black and white calendar this year because it's for you to fill in with beautiful colors. You can do that if you head to twist.org and you're interested in the calendar. Someday you might get one if you order one and then you would get to color it. And there's so many great things in the calendar. But you'll have to see for yourself. Right now it's time for the science. We're going to get into it a little bit. Oh my goodness, you guys. Did you read about the skin replacement this week? This is amazing, an amazing story. There was a young boy, Syrian refugee at the age of seven years old. He has a disease called junctional epidermolysis bolosa. And what this means is that the cells on the exterior of your epidermis do not connect the proteins that link it to the supporting cells underneath the basal layer of cells of the epidermis. Those connecting proteins have malformations or they just don't form at all. And so the top layer of skin just kind of floats on top of the rest of the dermis. And when bumped or bruised or scratched, it forms horrible blisters because it's not anchored down. And so it just comes up off of the rest of the skin. This boy, going through the trauma of becoming a refugee in the first place, he had an extreme reaction. He lost almost all of his skin. He lost almost all of his skin. And the picture is just heartbreaking of this red figure. He's not covered in skin. He lost it. And doctors called a researcher and said, we know you've done some work before, these doctors in Germany where the family had run to. And they contacted a specialist, Michelle DeLuca, of the University of Modena and Reggio Emilia in Italy. And he has done small tests before with small patches of skin, using autologous, meaning cells or from the person. So using autologous, transfected skin cells, stem cells. So they took a sample. This doctor, Michelle DeLuca said, okay, I'm in. They took a sample of stem cells from the remaining skin on this little boy's body and were able to grow the stem cells to create sheets of new skin. And they used a viral vector to introduce the proper genes that not contain mutations into those stem cells. They grew the skin and then they transplanted it onto the boy's body over a period of three surgeries to do it. Two years later, this little boy has skin. And it's not sloughing off. It's not forming blisters. They fixed it. They fixed it. This is an amazing, amazing story. And this gives so much... The implications for this are huge in terms of treating burn victims, not having to take skin from other people, being able to use a sample from the damaged individual, being able to grow those cells. If it's just a burn, you can just replace the skin. But if it's a mutation, if it's something wrong genetically, the idea that it can potentially be repaired is fascinating. One of the other really interesting things about this study is that there's a big question as to how the stem cells work in this skin, in skin regeneration. And so they're wondering if the renewal, if there's a large population of these progenitor stem cells that all produce new skin cells and create the skin, or if there are individual, a smaller subset of these individual stem cells that create regeneration. And so the difference, it was hypothesized that if it's a large population of progenitor cells, if you sample the regenerated skin for genetic profiling, you'll find thousands of little mutations and differences because it would be all these different cells potentially contributing to the regenerative process. The other alternative hypothesis is that if it's an individual, smaller group of cells, then you'd have only in the tens to the hundreds of these differences between the profiles of the cells in the skin. And that's what they found. So this confirms an idea of how the skin regenerates that we never have been able to confirm before also. So there are individual stem cells that were able to be transfected, to get new genes put into them. And those individual stem cells are the ones that have continued to go on and continue to grow new skin for this little boy. So is this something that could replace skin transplant in the future? Potentially. I mean, if you can grow your own skin, you don't need to take it from a donor. Yeah. Or, you know, face transplants for people that have gotten acid on the face or something like that or a burn. That would really change things if you don't have to worry about rejection. Absolutely. What a game changer that would be. Yeah. So that's where that that's where they're working. And yeah, the skin graft is this it's working. They're figuring it out. Now, the skin is a bit different from other parts of the body and has its own quirks that other parts of the body don't have. And so maybe skin is amenable to the more amenable to this kind of therapy than other organs, organ systems in the body. But even so, this is a huge step forward. And they say now the boy is going to continue to receive regular checkups for problems. But right now he's back to school. He's exercising and he started to play soccer. Nice. That's amazing. That's a kid that had no hope for a normal life. He was now. He was going to die. He had no skin and a severe bacterial infection because he didn't have any skin. It was a systemic infection. And the parents basically said, let's try this because we have no other hope of our child surviving. And so they had a it was a special compensation or dispensation for them to even be able to do this experimental process on the child in the first place. But it worked. Transgenic stem cells regenerating an entire epidermis. You know, and maybe it's something this is something that'll work really well on young kids. Maybe it won't work so well on older individuals. But it's a step in the right direction. Absolutely. Amazing. Yeah. Amazing. Yeah. So I've been reading about this this week. And I've just been so excited about it. It's science. It's thrilling. And it has the potential to help so many other thrilling things, though, happen out in the universe when you look in the universe. And we've talked before about supernovas. Right. What do you know about supernovas? What do you know? What do you know? Well, they're the they're the candlelight, the one a candlelight that we use to kind of tell how far away things are because they glow with a certain radiance. They are an exploded star that didn't turn into a black hole because it wasn't big enough. Mm hmm. Unless unless they do, which I think we talked about a while, that might still happen later. Yeah. So they are the standard candle and they have this super stars go supernova at the end of their life if they are big enough. They must be much larger than our own son. There's they're usually somewhere between five to 50 or five to 75 times larger than our own son. You need a certain mass of hydrogen to be able to create the bright explosion that occurs during during a supernova. So researchers a few years ago, a couple years back using the intermediate to Palomar transient factory. They're using this telescope at the Palomar Observatory near San Diego. And they saw what they thought was just a plain old regular type to supernova about 500 million light years from our planet. Not a big deal. It's like, oh, a supernova. All right, let's look at it. And they kept observing and they're like, wait, that's a lot brighter than a normal supernova. Oh, look, it's dimming now. That's great. And then they said, oh, wait, it's getting brighter again. And then, oh, whoa, it's getting dim again. What? Wait, it's this thing is just ongoing. It's that this has been an ongoing fluctuation for over 600 days. They continue to observe it and it is not acting at all like a normal supernova. This supernova that they have called IPTF14 HLS. Catchy. Very catchy, always catchy with the naming of these things. Yeah, it has been fluctuating and has gone supernova at least twice in the time, or apparently supernova as we look at the brightness, but it shouldn't have enough hydrogen anymore to continue doing this. So I don't really know what is going on. And it also turns out that in an old picture by the Palomar Observatory from 1954 that it looked like there was a supernova in the exact same position as this star. Wait a second. What if this isn't a supernova then? That's exactly it. What they're thinking is that there are hypotheses that there are much larger stars that are absolutely massive somewhere on the order of like 95 to 130 times the mass of our sun. So massive stars and that because they have so much mass and then there is a they get really hot and they convert gamma rays into electrons and also into antimatter. And so they think that it's this antimatter positrons that get produced that somehow keep triggering partial explosions. And so they have a it's not a because they're large. The brightness appears to be a supernova, but then it's not a complete explosion. It doesn't blow off all the mass. And so there's still some stuff there recombining and then little mini novice mini novice that look like regular novice because it's in a really big star. Yeah. So this is one idea that people have proposed historically. But some there are some things that don't add up for this also. So they're kind of wondering maybe it's not even one of these large supernovas that maybe there's something else going on. Anyway, the researchers are going to continue observing the star, the location in space. They do say it is finally fading compared to where it has been. And so maybe that means that it's done, but they're going to keep looking because if it exploded in 1954, that means that they just have to keep looking because there could be some much longer term process that's underway that will rewrite our ideas about how large stars and their lives. I wonder if it's something that's like an in-betweener. Yeah. Like just below the threshold of just going black hole. So where it's going supernova and then it's like I'm being drawn back into my own gravity and then there's another supernova, although not as big maybe because some of the energy got away. But then I'm still so massive that I'm pulling everything back. But now I'm definitely not going to go to the black hole because I've been expending all this energy. One more. There we go. There we go. Let's do it again. Yeah. So we'll keep looking at the nimbly named IPTF-14 HLS and see whether or not it does come back again, whether further explosions, whether it collapses into a black hole even because if it's that big, it's probably going to go black hole at some point. Or what if there is a stage where we just keep going supernova forever? Like you're just too big to escape. Too big to fail. Yeah. Too big to or too big not to keep failing over and over again. I don't know. I don't know what success is to a star. You're already a star. How can you be more successful than that? You just keep recapturing your own energy from that gravity but still not enough to implode upon yourself. Yeah. Anyway. Interesting. Yes. So it's the star that will not die. The Palomar Observatory is going to keep looking at it to see what it means. What does it all mean? At this point, they don't know. This is a week in science. Justin, tell me a story, please. Oh, yeah. I should have one. Oh. And now for murder mystery. There's a killer hiding in the darkness. Lurking under your skin. Lurking and waiting. And then lurking some more. Then taking a quick break but then right back to more lurking. Thankfully, this lurking killer works for you. It means cells called killer cells target unwanted bacteria that invade the body's cells. But just how they dispose of these malignant microbes is the mystery of this murder. Bacteria, as we've talked about quite a bit on the show, can involve resistances to things. Antibiotics, they work for a while and then the microbe goes, I know what you're doing, changes its targeted defenses or attacks and then it survives. Yep. There have not been able to survive the killer cells. Not very easily. Not very rarely able to invade these killer cells. This has caused researchers to become interested in finding out the exact mechanism that killer cells use to destroy bacterial invaders. One way that killer cells can trigger bacterial death is by inflicting oxidative damage. So you just stick some oxygen in there, I guess. But how do they kill cells in environments without oxygen? So in this time, researchers have caught killer cells red-handed in the act of microbial murder. Observing them as they systematically kill three strains of microbes, e. coli and the bacteria responsible for causing listeria and infection and tuberculosis to process inflicts bacterial cell death regardless of whether the environment contains oxygen or not. Their findings published in Cell reveal that killer cells act to program a complete internal breakdown and cell death. So you've got this, this catalyst goes in there and starts tearing stuff up. Researchers from Boston Children's Hospital and Wister Institute and University of Michigan used an equally systematic approach to make this discovery. This is a quotey voice of Judy Lieberman. We took three bacteria that are very different and to see which proteins were destroyed by killer protein levels before, during and after they were attacked. Judy Lieberman, by the way, MD, PhD, Boston Children's Program of Cellular Molecular Medicine is a co-senior author of the study. Proteins, of course, very important in life. They direct the use of nutrients and production of cellular machinery that bacteria need to survive and each strain of bacteria has about 3,000 proteins involved. About 5 to 10% of those proteins were slashed by the killer cells during this death inducing enzyme activity. This enzyme uses Granzyme B, Lieberman says. If you made a list of the proteins that bacteria absolutely needed to survive, it would be a small list. Interestingly, it seems to be the identical list that Granzyme B is hitting. This is the hit list that Granzyme B is using is the absolute most critical proteins for the bacteria. So our killer is pretty targeted. Really, really it's like all it's all like shots to the heart or headshots or something. It's a wonderful infographic that goes with this story that imagines little monkeys, those little monkey wrenches getting in the way of the process. To deliver the fatal blow, Granzyme B the killer cells seek out surface markers on the body's cell surfaces that might indicate a bacterial invader is taking up residence inside the cell. Killer cells then latch on to the infected cell and use an enzyme to create a small pore in the cell surface through which they inject Granzyme B. Once Granzyme B gets into the cell, it passes into the invading bacterium and essentially destroys the critical proteins for that cell survival as well as its ribosomes. Amazing. There is a war going on in your body with assassin cells, killer cells going and targeting and killing things you don't want to be in you. Good. I am glad. I'm glad that I have that Granzyme B is there. No matter how many times their researchers exposed the bacteria to it, they did not develop resistance to its attack. I suppose if you're that successful one it's hard to come up with resistance to it. If a bacteria only sees it once and it's successful there's no retooling possible. Yeah, and it's also if Granzyme B is going after these survival proteins one of the strategies is you go after these proteins that are essential for the bacteria to survive. If you break those, if you're able to disrupt those that's not something that the bacteria are going to get mutations in. Those places are not hot places for mutations because if they mutate there, they'll probably die. If you've killed off a whole population like selection has allowed for a certain variation of the genetic population to survive without those critical proteins. Exactly. Because the proteins are so critical that evolution, natural selection doesn't even really act on them anymore anyway. If anything, it's doing everything it can to preserve them. To make sure that they're there every time. Exactly. This is cool. I love the idea. The proteins maybe or the targets of Granzyme B and then maybe we can get new antimicrobial drugs. Maybe this will lead to a new class of antibiotics. Granzyme B I like the name of it but it makes me think of an old granny hip-hop artist. I'm Granzyme B. And I'm here to say I cannot bacteria in a savage way. Good job. You guys are awesome picking it up. That's a fun story. Hey, it's this week in science, but do you know what time it is? What time is it? I think I do. It's time to get Blair's Animal Cornered with Blair. Music I have a lovely story about mammoths. I know... about this story. Yeah, I know Justin loves his mammoths and they are rather majestic creatures. That is, unless they happen to be male. Researchers who have sexed 98 woolly mammoth specimens collected from various parts of Siberia discovered an odd trend despite being a mammal and therefore most likely a 50-50 female-to-male sex ratio. Never take a couple points. Seven out of every 10 specimens they found were male. This creates a bit of a question mark in the fossil record. Why were males being preserved left and right and females not? Well, it is highly likely, says the Swedish Museum of Natural History, that the remains that are found in Siberia these days have been preserved because they were buried, thus protected from weathering. So why are males being buried more than females? Well they hypothesize that males were falling through lake ice in winter or getting stuck in bogs. Unexperienced male mammoths more often travel alone, and the hypothesis is that they got themselves killed by falling into natural traps that made their preservation more likely. They were surprised they were looking into this because there was no apparent reason that you would find in the fossil record a bias towards one side of the sex ratio, and so they really had to kind of put on their thinking cap. So everything they have found about William M.S. to this point makes it sound like their social structure was similar to modern elephants, with herds of females and young elephants led by an experienced adult female at the head of that kind of group. In contrast, male elephants that were not part of a group of elephants, forget what the collective noun for that is, those other males lived in bachelor groups or alone. And because they were by themselves or in bachelor groups, you know how big a group of bachelors are, they were more likely to engage in risk-taking behavior. Without the benefit of living in a herd led by an experienced female, male mammoths may have had a higher risk of dying in natural traps such as bogs, crevices, or lakes. So that is just a hypothesis. Of course, we can't know exactly that all of these kind of conclusions that we drew are correct, but it is a good idea knowing what we know about elephants. What makes this particularly interesting to me, though, is that having a sex bias in the fossil record, this is something that we haven't really heard of before, but that's because you don't always do a gender test on fossil specimens of ancient species unless you need to. And so a lot of the studies that they were doing on these mammoth fossils, they needed to have the sex data to continue on. So this was kind of a stop point that they needed to get to before they could continue with their data, and that's when they stumbled across this weird bias. So the question is, now that we know that fossil groups are not necessarily proportionally representative of a random sample of a population, does that change some of the conclusions that we've drawn about other fossil species in the past? It definitely could. The first thing I thought in this story is like, one, maybe being mammals, the males are much heavier and so are more likely to fall through ice, but I think your point was much more likely the lone wolf aspect when you're with a pack of herd of mammoths, a gaggle of mammoths are roaming about, a mud of mammoths, I'm wondering about. There's probably some wisdom in the crowd. You may have some matriarchs, one or two, in that group of women who are females that are going around that have a little bit more experience, have seen a male mammoth fall through the ice and know when you hear those cracks, we've got to go the other way. So it could be a little bit of the community sort of hive think together, figuring out things and sensing danger. Well, hive think isn't usually matriarchal, it usually is node based. Well, yeah, so the hive is not the right way to do it. Yeah, so the idea is that when left to their own devices, these younger mammoths were foolhardy and made risky decisions, which is something that we see in animals quite often is that the younger animals, when they're not with another group to watch the rest of the group's decision making behaviors and their kind of their thought processes, if you want to call them that, then they do tend to make fatal decisions, which also is kind of the name of the game in natural selection, right, the mammoth that doesn't step on the thin ice survives to have babies. So that's the other question. Are we getting all of the failure mammoths in the fossil record? And therefore, is that a disproportionate representation because we're getting all of the bad genes or we've only got the dumb mammoths. We only see those hominins that were eaten by lions. Well, that's different because hominins were preserved differently because some of them had burial rituals and so it's very different. Only saw the ones that did get eaten by lions, we may have a different picture. But also, Justin, I want to mention that if you wanted to clone the mammoth from some of these fossils, you would get the dumb ones. So that's right. Your idea of taking mammoths into the future with your Dr. Justin's mammoth park, it's going to be full of dumb mammoths. Super dumb mammoths that will fall down constantly. Unlucky. We'll just call them unlucky. Just walking into walls and fences all the time, falling over their own tusks. What am I doing? I don't know. Oh my gosh. Yeah, the fossil record, who knows? So speaking of males, let's talk about sperm. All righty, let's do. It's been a while since I've talked about sperm on the show, but there's this very interesting article that came out last week from the University of Otago and University of Canterbury looking at male salmon sperm, male sperm. Of course. Salmon sperm, swimming speed, and what they found was that males can adjust their sperm swimming speed when their social status or sperm competition risk changes. Let me say that again. They can adjust. Males can adjust their sperm swimming speed dependent on competition in less than 48 hours. Interesting. Yeah. So, what they found was. This is very important because these are what do you call, spawn breeders, right? Correct. Correct. What is it? It's not spawn. Is it spawn? No, it's not spawning. Yeah, spawning. Uh-huh. Where they. Broadcast spawners. Broadcast spawning. Yep. So these guys aren't quite broadcast spawners. Broadcast spawners are like urchins that just spit it all out and hope the current takes it. With salmon, the females will lay their eggs and the males actually direct the kind of the stream at the eggs. So it's not quite a broadcast spawn, but it does mean that multiple males can deposit in the same general area where there are lots of eggs. So that's why swimming speed is so important. And swimming speed usually is the defining characteristic for a successful sperm in the salmon. Yeah, you get there first, you win. Yep. Who's fastest? Right. Yeah. And so the way they actually found that out was they raced sperm from two males to see who fertilized the greatest amount of eggs in a lab. Those males with the fast sperm fertilized more eggs, and the seminal fluid from males with flat sperm sped up the sperm of the other males. So this is how they were able to find out. It's not the sperm themselves that's making them faster. It's the seminal fluid that's making the sperm faster. I like to picture it, this might be too much, like a slip inside, right? So like it's just, it's a quicker delivery system. Wee! It would be like if you put lube all over a slip and slide. Yeah, exactly. It'd be a lot faster than just plain old water. So that's kind of the way it works. So they were able to identify that first of all, they could adjust the speed based on nearby competitors, but also that that adjustment was made in the seminal fluid. They don't know yet what the component of the seminal fluid is that makes it faster. But yeah, they said, we found that when males change their sperm velocity via seminal fluid, this altered the number of eggs that they fertilized relative to a rival male. In other words, the adjustment of sperm velocity altered male reproductive success and therefore fit net. But what I found so interesting about this was that it happened in 48 hours. So I'd assume, as I always do, that it's all about hormones. That's my assumption here. We don't know that yet. But that sounds like what's going on, that they, that they're testosterone kind of spikes because there's other males around competing and that in less than two days, faster sperm. Yeah, what would be doing it? What would be giving that energy boost? I mean, you'd think of it. I mean, maybe it's increasing enzymatic properties. So it basically, in that sense, would increase the metabolism by making chemical processes faster or maybe it's something that is maybe there's actually an energy source that can go into feeding the mitochondria. Yeah, I kind of just assumed it was it was purely mechanical. It could be purely mechanical. I'm just thinking of different options. Yeah, absolutely. But it could be. That's something I hadn't even thought about. I just assumed that it had to do with kind of the the physical nature of the seminal fluid that made it a quicker channel for the sperm. But you're totally right. It could be creating a chemical reaction that is causing the sperm to move faster themselves. But it is this happens in humans, too. I mean, not necessarily the speed, but the production goes up. This is one of the earliest stories that we talked about a long time ago, where men who viewed certain types of pornography were then like suddenly had higher sperm count as a result. Right. So there was something about the competition that sort of confronted them with. Well, yeah. And when you look at primates, they're the size of their storage space for the for the sperm and seminal fluid is larger in proportion to their body size when there is when there are multiple mating events when animals are not monogamous, then they they increase volume and sperm count because there's sperm competition going on. And that might be equal to or greater than the size of their brains. Hey, Kiki. So no, I've got this, but I was just looking up. I was trying to confirm my memories of how flagella work. Yes, they are powered by the proton motive force. And this is the flow of protons or hydrogen ions. The bacterial cell membrane due to a concentration gradient that's set up by the cells metabolism. So it's this could be something that increases the concentration gradient that somehow they're the seminal fluid to increase in protons. So the solution may be the solution and the solution. Yes, that's why you're the doctor. I was like, I've read something about this. And that is fascinating. And as good as your analogy was earlier about the the the lube and the slip and slide, I seem to recall actually experiencing this with Kiki at a graduation party where they had a slip and slide in the backyard and a garbage can full of lube for people to dip themselves into and then go and hit the slip and slide. And I think there was like blow up things or something at the at the end of it to kind of slow you down or. Yeah, well, we didn't want people to get hurt. Yeah. It was a very slippery slip and slide. Well, you know, safety first, were they wearing lab goggles? I wish, right? Actually, I think that might have been part of the other part was, you know, this was a graduation party. So there was a bit of imbibing. And even for those who weren't intending to participate, after a while, the entire backyard was coated in a layer of lube that made standing upright very difficult. Oh, grad school, that's right. Locatious one, it was a slippery slope indeed. Well, anyway, Sam and Sperm speed up in response to other males. That is interesting and it's very possible that it has something to do with with the proteins with that it allow hydrogen ions to build up. Who knows, find out, find out, scientists. We want to know why. Why does the flagella go faster? And that is the end of the first half of this week in science. We have more stories coming up, but right now we're going to take a break. In the second half, we will be getting to bonobos. We're going to be getting to artificial sweeteners in your septic tank. So many questions, so little time, but stay with us. This is This Week In Science. Hey, everybody, if you are watching right now, thank you so much for watching. 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We would have stepped the guy in. I can't believe you believe in that show. We disagree, but I still give a dance. And we are back with more this week in science. Oh, yeah, we are. And you know what I've moved to this half of the show now. You know, you know, what have you moved to this side of the show lately? That's right. I'm moving it around to see where it fits best in the show rundown. But it is time now for this weekend. What has science done for me lately? For Minion Veronica Hayes, science gave us science teachers. I was homeless for a time in high school, resulting in a myriad of issues jumping from school to school. By junior year, I was sick of being placed in remedial classes due to administration not willing to determine what the different transcripts were saying about my class rank. I went to this new school asking anyone who would listen that I needed to be placed into AP chemistry. The amazing Mrs. Ward led the charge to let me take the class with which eventually led me to pursue my PhD in physical chemistry. Yay, Mrs. Ward. Good for you, Veronica. Oh, it's a wonderful story. And Veronica, thank you so much for writing in and sharing it with us. Teachers are so important. Good teachers, teachers who listen to their students, who respect their students and really inspire them and help them to become the people that they want to be. Yeah, and what a tough time to go through and and and to fight on for your education. Yeah, and just, yeah, still want to be an AP chemistry. That's fantastic. I mean, you knew what you wanted to do. So it's amazing, Veronica, that you fought for yourself. And that was good work. Fight for yourself. Fight for your right to do science. And be proud of what you're good at, too. That's something that's such a hard thing to learn because you're told to be modest and to not oversell yourself your whole life. And sometimes you need to just say, I'm good at this. Yeah, I'm not going to I'm not going to listen to the people who are putting me down or at least not helping to lift me up. I'm not going to listen to them. I'm going to go to go around and find a way to move forward. That's what I deserve. That's what we all deserve. Thank you again, Veronica. This is just it's an inspiring story. And I hope many kids today have teachers as great as Mrs. Ward. Remember, everyone, we need you to write in with your stories to let us know what science has done for you lately. What has it done for you? What does it do for you every day? Leave us a message on Facebook. Go to facebook.com slash this week in science and you and leave us a message. Leave us a message in our message inbox. And I will fill the show this segment of the show with your stories. And we have done almost a half a year of this right now. I am just thrilled that we've had so many stories coming in. Let's keep them coming, you guys. Let's do this. Let's let's do this a whole year of it. I want it. I want it. Help me. Help me. Help me. Give me more stories, please. And now, Justin, what do you have next for me? What you got? I have a wide ranging new study of fossils. This was 311 species of hominin dating from the earliest upright species, 4.4 million years ago, right through to the modern day, you and me type humans. Followed by I said you published today in the Journal of Royal Society, Open Science Research shows that rather than steadily increasing in size, hominin bodies evolved in pulse and stasis fluctuations with some lineages shrinking even. They also suggest that sexual dimorphism, physical distinction between genders with females, typically smaller in mammals, was more prevalent in early hominin species, but then steadily kind of got ironed out over time disappeared. Hominins from four million years ago, roughly averaged 55 pounds were just over four feet tall, about 4142. That was us, like fifth graders, fourth graders. I don't even know what that is. Like, that was humans. That seems skinny, though. That seems low weight for over four feet. Yeah, yeah. With the dawn of our own defined species bracket, Homo, about two million years ago, we had a decent growth spurt of eight inches, but only added 40 pounds. Study found body size to be highly variable during earlier hominin history with a range of different shaped. We had, like, there was the gorilla-like parenthropus, more wiry grace, grass-style, they're saying, Australopithecus afferensis. So even in there, there was more variation than just these things that I'm throwing out. Scientists were surprised around one and a half million years ago. Hominins grew roughly four more inches. But didn't add any additional weight. This is about the emergence of Homo erectus. And this is possibly because of endurance hunting that we were maybe getting involved in, where we would, because we could sweat and evaporate and sweat again and keep cool, we could run long distances. So we could chase prey that was much quicker than us and eventually catch up to it, force it to run again, eventually catch up to it, force it to run again. And then it would just sort of flop over from heat exhaustion. And we didn't have to be like really physical hunters. We just pestered our prey to death. There are animals that do that now. There's humans that do that now. Well, but but there's there's quadrupedal animals that that's how they hunt now as well. Yeah, just just having a better cooling system is sometimes all you need. 500,000 years ago, an average increase of 27 pounds, but not a lot of height gets packed on, possibly because we begin moving to cooler climates, Mediterranean being cooler. Maybe there was some other factors in there as well. Putting us then that would be 500,000 ish years ago, about five foot four, 122 pounds. Most of the size changes we see represented in humans now came about in the last 3,000 years. So it's it's nutrition made a big difference. But we were ready like our genes were like, yeah, give me more food. I'll just get bigger. Give me give me generations of this, and I will just continue to get bigger. Let's see. So, yeah, before before those those early events, though kind of moved in concert before adding on that that weights as studies authors. But yeah, I think it's yeah, I think it's interesting that it didn't all happen at once, that it wasn't like I'm growing bigger and I'm also gaining weight because that's what you would kind of expect that increase in height would increase mass and that that would also concomitantly increase the weight, right? We had different hunting tactics, different things needs for survival. We were moving to different areas and so things sort of change over there. The exceptions, of course, to this were Homo Naledi and Homo Floriansis, which they don't really know for sure if they were swimming against the tide of body size by going backwards at some point. I think our latest from Homo Floriansis is really kind of ancient Floriansis was the same size as the Hobbit folk that we found. They were still- So, Floriansis was on an island, right? Yeah, but they went back like much further in that area. I don't have it in front of me, but they're native to that area for a really long time and that dwarfism wasn't a sort of quick event because there is no trajectory to that smaller. However, one of the other things is they may both be just an offshoot more closely related to one of our earlier smaller. That answer, right? So it may be that the things that propelled a lot of, and this is, of course, many, there was at one point seven or more hominins on the earth at the same time. So there is, of course, the crossbreeding and all of that sort of braided stream effect that's involved as well. Yeah, a couple got the little smaller or stayed small. The rest of us kept finding ways to get a little bit bigger. Yeah, fast food, you know, fast food and sodas. But yeah, the biggest changes though, that's kind of also the interesting thing. All the, you know, you've gained four inches in a million or two years and then in 3,000 years, we've really exploded in our size. Like we're bigger than we've ever been before. And it's just from- Food availability, right? Yeah, food availability, the invention of farming, you know, hunting, fishing techniques, all that kind of stuff, a steady diet. Steady diet, yeah, as opposed to the intermittent diet that probably came about, yeah, with nomadic people. Fascinating, fascinating, fascinating. Well, let's stop talking about old people as in our ancient ancestors. Let's talk about old people and how we can make them young again. Yes, so resveratrol, right? We've known about this molecule for some time and reverse it all, exactly. It's an antioxidant that is known to have potent effects. I mean, you'd have to really, if you were to actually get it from wine, you'd have to drink many bottles of wine to have it actually influence your cellular metabolism. Those individuals, researchers who have isolated it and put it into pill form or even started using varying dosages of this reverse at all. I'm gonna say it all the time, resveratrol on cells have really discovered that it does influence cellular senescence and aging. And it seems to slow it down and can help to bring cells to a little bit of a younger state. Now, one of the things that resveratrol is known, one of the ways that it's known to work is that it acts on splicing, it's a splicing factor and these splicing factors switch things on and off and they do decrease in cells as you get older. So they also knew that resveratrol that it's not quite the right thing, that it's not quite right. You have to use large concentrations of it and there should have been a better way. And so they developed a bunch of novel small molecules, these researchers who published in BMC cell biology that they call resveratrol analogs. And these analogs they used to determine whether altered splicing factor expression had potential to influence features of replicative senescence. And so they took old skin cells and they treated them with the resveralogs, resveratrol analogs, resveralogs. And they checked, look to see what happened to the cell cycle, look to see what happened to indicators of aging in the old cells and they found really cool stuff. They found increased telomere length. So the short caps at the ends of the chromosomes that get shortened as you age, they were suddenly longer again, long, healthy telomeres. These cells that had stopped dividing, that had stopped their cell cycle that had gone into senescence and were just basically getting ready to die, they re-entered the cell cycle and started proliferating again. They started making new baby skin cells. And so they say this is the first demonstration that moderating these splicing factor levels is associated with the reversal of cellular senescence in human skin cells. And so there are other modulators like CERT-1, CERT-1, which we've reported on before, which is a target that a lot of people are really looking at for cellular aging stuff and anti-aging as an anti-aging target. And this study actually showed that in one situation, in one of the experiments that they ran, that CERT-1 wasn't even really required that these resveralogs did all the work. And so it could be that the resveralogs are kind of triggering the CERT-1 or similar pathways and that the CERT-1 might not be the target that people think it is. Other pathways were involved in the ERC-ERK antagonists and agonists, which is another cellular metabolism pathway, but this could be opening up these splicing factors that get affected by resveratrol and its analogs that these could be targets to increase that if we can increase these splicing factors, maybe cellular aging will dig decrease. That said, this is only in skin cells, in a dish, this is not anything else, but maybe it's gonna lead to some nice face creams at some point, if nothing else. While you were telling this story, I ordered 12,000 capsules. Resveratrol? We'll see. We'll see how it works. Yeah, I think I might start mainlining it. Or at least Justin, tell me how it goes, because I probably don't need it yet, but... It's never too early to start. Yeah. Mainlining resveratrol. Yeah, yeah. We were watching those smuckers, everybody over 100 birthdays in the hotel the other day and like, 100, that's nothing. Yeah, researcher, Professor Farragher from the University of Brighton, he says, at a time when our capacity to translate new knowledge about the mechanisms of aging into medicines and lifestyle advice is limited only by a chronic shortage of funds, older people are ill-served by self-indulgent science fiction. They need practical action to restore their health and they need it yesterday. Yeah, that's old people now. We're talking about old people of tomorrow. Yeah, us. Yeah, you had your shot. Look at this now. Oh, no. All right, reverse it's all. Back to you, Justin. What's your next story? Oh, if I have a next story, it must be about septic tank systems. Why? Those things that make me throw the toilet paper away in the trash instead of flushing it. Right, these are commonly used in rural areas where the homes are not connected to a municipal sewer system. The primary treatment removes the solids, the effluent is discharged with a septic drain field where it goes, you know, its own sort of natural treatment. And then magically all of your septic problems are gone. When you have a septic tank, it's kind of the earth filters everything for you. Yeah, it filters it, except maybe it doesn't. Researches from the University of Waterloo went looking for potential effluent contamination of groundwater and river waters. And they had a very hardy human specific tracer that they used to do so. They looked for artificial sweeteners. Oh, I was gonna say pharmaceuticals. Yeah, well, pharmaceuticals can be found as well sometimes but they break down much more so than artificial sweeteners, I guess. The study which appears in the journal Environmental Quality describes how the researchers tested private rural groundwater wells and not the Swah Saga River Watershed, this is Canada, for artificial sweeteners is a way to detect groundwater impacted by human wastewater being released by septic systems in the area. Artificial sweeteners, they're saying are ideal wastewater tracers for humans as they exit the body, essentially unchanged. They're not completely removed by most wastewater treatment processes. Human wastewater contains relatively high concentrations of these artificial sweeteners, meaning nothing else is containing this. That's why we have high levels, whose nature isn't consuming or distributing artificial sweeteners. Nobody wants to. Right. It's just us. Yeah. So this is the quote of John Spolastra, first author of this study, adjunct professor in earth and environmental sciences at Waterloo, although the four artificial sweeteners we measured are all approved for human consumption by Health Canada, it is the other septic contaminants that might also be present in the water that could pose a health risk. As for groundwater entering rivers and lakes, the effects of artificial sweeteners on most aquatic organisms is unknown, but the other contaminants that could be coming with this, E. coli, viruses, pharmaceuticals, personal health care products and elevated levels of nitrate and ammonium. And in conducting the study, they found that more than 30% of samples analyzed from 59 private wells show detectable levels of at least one of four artificial sweeteners indicating that the effluent has made it into the well water. Estimates reveal that between three and 13% of wells could contain at least 1% septic effluent. It has been somewhat filtered by the earth, as you were saying, but still. But still. But still, if there's septic effluent, that means there's probably some amount of sewage that's not being filtered. And maybe that's microbes that are gonna be dangerous to people's health. Maybe that's pharmaceuticals. Or maybe it's just artificial sweeteners. No, no, or just, yeah. Oh, yeah, that's all it is. The team also tested groundwater seeping out of the banks of the Natus Wasasa River and found 32% of their samples tested positive for sweeteners. Again, indicating that some of the groundwater entering the Natus Wasasa River has been affected by septic system effluent. Previous studies by the same group revealed the presence of artificial sweeteners in the Grand River, as well as in treated drinking water sourced from the river. Treated, so the treatment is not removing the sweeteners. What else isn't it removing? Right, and it may be, you know, it may be doing a good job on everything else, we don't know. These sweeteners, they're probably very small molecules, right? Well, and the thing is, it does tell you though that there's a direct connection between- Yes. Between somebody's septic tank and that drinking water, which is not what you want. Yeah, not what I want. Oh my goodness. Oh my goodness, artificial sweeteners. In the water supply, the artificial sweeteners. Daddy, daddy, the effluent is in the well. So if we just don't use artificial sweeteners, we can just pretend we know nothing. That's exactly it. Absolutely, it's the problem with artificial sweeteners getting into the water. It just means that the effluent is getting everywhere. But it's all one small world and we're sharing everything, even our septic tank discharge. But sharing might be in our genes, in our ancestry. It might- How is that possible? It might not just be something that arrived, de novo in humanity, that this ability to trust and share and help people might not just be something that humans have a capacity for. Research has shown that chimpanzees, when given the opportunity to help other individuals, strangers. If it's strangers, chimpanzees are really not likely to help a stranger out. People though, will help a stranger out from time to time in the right situation. But we're able to do it. We do it, right? Chimpanzees really don't. They'll help individuals they know, but they don't help strangers very much. But a new study looking out of Duke University, looking at bonobos at Lola Yab, Lola Yab bonobos sanctuary in the Democratic Republic of Congo, they found that bonobos will actually help a stranger get food, even when they're not gonna get anything in return at that point in time. If there's no immediate reward, they will still help the stranger get food. Yeah, and so the researchers had set up a kind of interesting arrangement for their experiment. In which they had one subject in a cage unable to reach food that was hanging from the top of the larger cage structure. Now, the bonobo, there was one bonobo outside of the cage and the bonobo could go and release a stick that would drop the food to within arms distance of the recipient. And so in the control situation, the recipient would never be able to get the food, just kind of mean to the recipient. But they had a couple of cage setups where the bars in one arrangement allowed the recipient, the one who was looking at the food and couldn't reach it, they could reach their arm through the bars to kind of indicate that they were reaching there and that they wanted the food. And then in another situation, the bars were too close together and they couldn't reach, they just sat there and stared at it. And so they were looking at the difference in how often the bonobo, the generous bonobo would help out the bonobo who couldn't get any food. The stranger, would they not help? Would they only help during the situation where reaching was allowed? Well, it turns out that they helped a lot and it didn't matter whether the stranger could reach for the food or not, the bonobos on there of their own accord decided to leave a toy that they were playing with, climb up the cage and very often release the food for the stranger. More often in the reaching condition than in the blocked condition, but still, they did it, they released it. And so once again, this innately human thing that separates us from the animals. Doesn't, that it maybe, I mean, this is our closest relative, the bonobo, and maybe this is something, this trust and sharing that we have, maybe it is something that came from the bonobos. They do think that they discuss in the paper the possibility that bonobos are not aggressive in general. They do have some stressful situations when they interact with strain with other groups of bonobos, but then everybody starts grooming or having sex and the females are in charge. And then everybody gets along and it's all fine. So there are like some tense moments but everything gets worked out without aggression. But this is beyond that. They think that as bonobos entered an area of the world, a habitat that where food was plentiful, they became vegetarians and not meat eaters. So they weren't hunting for their food and not having to produce these hunting packs. And that the situation over thousands of years that maybe they evolved to be more trustworthy and to help out strangers more often. And that maybe that led to, maybe somehow that we got it also, maybe got passed out. Yeah, so maybe you don't pull over to help the person on the side of the road because it's dark and they could be trying to murder you. But when you feel like it's a populated area and an old woman is asking for help across the street, you're like, that old woman probably isn't gonna beat me up. Let me help her across the street. I can help her across the street. I mean, there's being smart and there's being like, I'm gonna go, yeah, this is a bad situation. So here's my only question about this because as much as I loves me a bonobo and- I have more for this story. We're not done yet, but- But just tell me this part. Is there in that first example, did they do that same experiment with no other strange bonobo in a cage? Because what if they just liked pulling a stick because it's the only thing they could reach and they were bored with what was in the cage? Like, there's an element of, there's nothing else to do, you're in a cage. They get that through the one toy in there and it played with it for a minute. But if it goes over and pulls that stick to see what happens, even when there's not, you know, another bonobo in a far off cage, then it would just mean that, you know, we share an interest in novel objects and not so much altruistic. Well, one could argue because they did it more when they were reaching for it that that had something to do with it that they were trying to help. Oh, wait, I guess there's more. Yeah, I don't know if anyone's yawning out there right now. I was just yawning a little. Sometimes when we yawn, it's a contagious response that we have no control over. And it's been shown that chimpanzees don't yawn in response to stranger faces, they don't recognize. So they put bonobos in front of screens with videos of other bonobos from the United States yawning or not yawning and just having a blank face. And they found that the bonobos contagiously yawned in response to videos of stranger bonobos yawning. Yeah, so this is, and so you ask the question of, all right, maybe they were bored and they're doing this thing. What this second part of the study underlines is that the xenophilia, they call it the liking of strangeness that bonobos evidence is, there's part of it that is unconscious. That there is a, not a fear of strange faces and that there is a recognition of stranger faces and that they respond to them in a similar way as they would to a friend or a friendly face. That's cool. I yawn at reading the word yawn. But we also, That makes me empathetic George. We reported on the show about how with humans, supposedly you are more likely to yawn contagiously. Yeah, yeah, yeah, I can't even talk about it. In relation to people that you care more about, you have more emotional tie to, the yawns are more contagious from those individuals. Yes, yeah, from individuals that you care for, exactly. So once again, humans kind of in the middle willing to help strangers, but only if it's safe. Yawning contagiously to everyone, but more so to people they're familiar with. So there's this weird kind of mixture of these two extremes. I can't read Dr. Seuss's yawn book. Dr. Seuss's yawn, no, sleep book because it starts with page after page of his little pictures yawning and it's I just start yawning. Oh, wow. Read the book. Read the book, keep reading the book. Read it. And then this is the other one's yawning too. Oh, God, oh, God. When I say strangers, I mean, these were bonobos that the bonobos they were testing had never met before. So not that they were weird, strange. They're all wearing fedoras and black trench coats. Yeah, so yawning being used as a measure of positive social preference and implicit measure of positive social preference in bonobos and that added to the fact that they spontaneously helped unfamiliar bonobos out of their food situation adds to this idea that this human potential for xenophilia is either evolutionarily shared or it could be convergent evolution with bonobos and not unique. Just one more piece of evidence that we are not unique. But that hominids, maybe, rather. Well, but what we've done stories about rats helping out other rats and stuff like that, I would argue probably not. But were they strangers? Maybe, some of them. I think some of them, no. You'll have to listen to previous episodes. Yeah, go back and listen to that. We can't remember about them. No, I can remember. I'm just not gonna do an entire story right now that's not from this week. All right, let's finish up this show. I've got a couple of quick stories. Oh my goodness. It was discovered that a parasitic fungus, I'm one of these, you know, what we've called mind control parasites that gets into the insect and makes the insect do weird behaviors. This particular fungus causes the insect, usually ants, to immobilize themselves by using their mandibles to grab onto a surface somewhere. And then the fungus can make use of its entire body, use it as fodder for its future growth. And so researchers thought that it was mind control, right? This is all, all of them, get in there. It's parasitic mind control. No, this is worse. No, no. I mean, at least with parasitic mind control, you know, it's like dementia. Your mind is gone at a certain point and you don't know what's happening anymore, right? In this situation, they did use electron microscopy and 3D reconstructions of host and parasite tissues to reveal that the fungus invades muscle fibers throughout the ants body, leaving the brain intact and that the fungal cells connect to form extensive networks. And these connections are likened to structures that aid in transporting nutrients and organelles in several plant-associated fungi. And so what's happening is that the behavior is not brain down this behavioral control. It's just physically controlling the muscles and forcing the muscles to do what it wants it to do. So it's like a body snatcher, but it doesn't just take, but it leaves your brain there. Like, I'm so sorry, I'm doing all of these monster-y things because this has invaded my body, but I really have nothing to do with it now. Yeah, so it's a, I mean, I really, from now on, really want to think of ants as not being conscious and or aware in any sense or form because if I do, now I'm going to be thinking about them looking at their mandibles clasping on to the surface of this leaf or tree and going, why, why? I'm just knowing that they're going to die. Yeah, this is, there are worse ways to die and that's one of them. Yeah, yeah. Yep. In fun news though, you can help name a world, get in on the contest that the New Horizons team is holding right now, their next destination, the next destination of the New Horizons mission, it's gone past Pluto and it's heading out into the outer solar system, out into the frontiers of the Kuiper Belt. It's headed to an object called 486958 to 2014 Mu69. It's also called Mu69 for short right now, but they're holding a contest for you to vote, enter your name ideas, suggest nicknames, vote for your favorites and in early January, the winner will be released. New Horizons is set to rendezvous with Mu69 or unnamed weird number name. In New Year's Day, January 2019. Well, Bleak in the chatroom calls worldy McWorld face. That's a good one, go, go send it out there. I would say not that. And you can go to frontierworlds.org. Frontierworlds.org is the website where you can find information about this contest and do all the neat things, nominate and vote. Indeed, indeed, indeed. Blair, what you got? Oh, I have some sheep that can recognize human faces. A recent study from University of Cambridge trained sheep to recognize a celebrity's face. The sheep correctly chose to learn a celebrity face eight times out of 10 in contrast to a random face. Then they had to show them the faces at an angle because really they were trying to see face recognition and face recognition via a photograph. So then they popped in the same celebrities that their faces at an angle. The sheep's performance dropped at only by about 15% comparable to what the humans do when they perform the task. And then the final wrinkle, they actually threw in pictures of the sheep's handler versus a random person's face. And when the portrait photograph of the handler was interspersed randomly in place of a celebrity, the sheep chose the handler's photograph over the unfamiliar face seven out of 10 times. So, oh, this is the best part too. Upon seeing the photographic image of the handler for the first time, the sheep had never seen an image of this person before, they did a double take. The sheep checked for the unfamiliar, first the unfamiliar face, then the handler's image, then the unfamiliar face again, and then chose the handler. So what you see here is advanced face recognition abilities comparable with those of humans and monkeys and that they were really able to understand pictures better than other mammals, other than humans and monkeys that we've tested before. So not only face recognition of humans but face recognition of humans via a photograph. And now what they need to do is go back on that study and redo it but reverse the roles and see if humans can recognize celebrity sheep. Yeah. Yeah, I feel like we would not do so well. I don't think we would do as well with the sheep as they did with these human fit. I'd love to know also if they've done this with photos of sheep, have they had sheep recognize the faces of familiar? I mean, this is my mom, I'm gonna choose my mom over, I mean, that's a great question. I did not see anything about that, I only saw human faces but yeah, what a great question. I mean, to us all sheep look the same. Yeah, well and the basis for this study is actually pretty interesting. It's for research on Huntington's disease because the way site and the brain kind of work together in the sheep are comparable enough that they're very commonly used for Huntington disease research. And one of the things that happens in Huntington disease is that they actually have problems recognizing facial motion in the later stages. So face recognition is a big part of studying this troublesome disease. So the more the sheep can recognize faces, the better they can be used in research because they could actually give sheep what is essentially Huntington's disease in their brain and then test on them and fix it. Yeah, so it's actually really exciting from the human element what this means and how we can use that to make people healthy potentially. Yeah, fantastic. So it's fun, but it's also helpful. Yeah, yeah, it's good to know the helpful aspect of it for sure. All right, Justin, do you have one more? Oh, yeah, this is just sort of interesting. This is humans. We have cones and rods in our eyes. And during the day, we're relying on the cones. At night, we're relying on the rods. Some of us just have rods. And then the twilight. And the twilight's a combination. Deep sea fish, those living many, many depth, hundreds of meters under the water, have only rods. They don't have cones at all. There's this particular fish though, they were studying that seems to be active at dusk and dawn close to the water's surface. And they had assumed that the retinas were composed entirely of rods. But when they took the closer look, they found something they hadn't thought was a thing. They found rod-like cones. They were basically rod cones. They found something different. Like a tapered rod? It was neither rod nor cone. It's a new way. And so basically what they're saying is that we may have, there may be other paths to vision or other vision equipment out there. There may be more than just rods and cones. And then maybe the fish world, maybe other places that we've overlooked the idea. Just need to look closer, the scientists are suggesting. More comprehensive studies in caution are needed when categorizing photoreceptor cells into cones and rods, study says. So there's more variation than what we have seen in just our own eyes. Yeah, keep looking for variation, especially in fish in the deep dark ocean. It makes sense that there would be some kind of adaptation to potentially help them because bioluminescence in the deep ocean very often does come in colors. So to be able to not just see basically in black and white would be a potential benefit, you know. And interesting too, these are rod-like cones. Rod-like cones. So maybe cones that adapted to darkness. To darkness, yeah. I don't know. Fascinating. Fascinating. Thanks, Deepsea Fish. Who wouldn't know about this without you? You guys, this is it for this week. This is our second show of the week and we have done it. We've come to the end. Yeah, made it all the way to the end. Thank you everyone who's watching. Everyone who is listening right now. Thank you for being here with us. Thanks everyone in our chat room. Hey there. You're over on YouTube or Facebook. Hi there. I see you. Thanks for watching. And thank you to Fada and Identity Four and Brandon for helping us make this show possible in the way that we do to you on a week by week basis. Thank you so much. I would like to also take this moment right now to also thank our Patreon sponsors. We have a few of them. So thank you too. A honey moss, Aaron Luthan, Adam Mishkon, Alec Doty, Alex Wilson, Andy Groh, Arlene Moss, Artyom, Ben Rothig, Bill Cursey, Bob Calder, Braxton Howard, Brendan Minnish, Brian Hedrick, Brian Condren, Brian Hone, Bruce Cordell, Byron Lee, Charlene Henry, Christopher Dreyer, Christopher Wrapp, and Colombo Ahmed, Craig Porter, Dale Bryant, Dana Pearson, Dale Daniel Garcia, Darwin Hannon, Daryl, Dave Neighbor, Dave Wilkinson, David Frydall, David Simerly, David Wiley, Donald Trump, the dubious, Dougal Campbell, E.O. Deadwood Dyer, Emma Grenier, Eric Knapp, Eric Wolf, Felix Alvarez flying out, Gary S. Gerald Sorrells, G. 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Thank you everyone for all of your support on Patreon. And if you're interested in supporting us on Patreon, you can find information at patreon.com slash this week in science, or just by clicking the Patreon button at twist.org. A next week show, once again, we're gonna broadcast live online at 8 p.m. Pacific time, twist.org slash live. You can watch online, join our chat room. If you wanna jump in there, there's a bunch of fun in there, but don't worry if you can't make it. It's all right. All of our episodes are archived on YouTube and Facebook, and you can always find them at twist.org. Thank you for enjoying the show. Twist is also available as a podcast. Just Google this week in science and your iTunes directory, or if you have a mobile type device, you can look up Twist, the number four droid app in the Android marketplace, or simply this week in science and anything Apple Marketplace-y. For more information on anything you've heard here today, show notes will be available on our website. That website is, of course, www.twist.org. That's T-W-I-S dot O-R-G, where you can also make comments and start conversations with the hosts and other listeners. Or you can contact us directly, email Kirsten at kirsten at thisweekin science.com or Justin at twistminion at gmail.com or Blair at BlairBazz at twist.org. Just be sure to put twist, T-W-I-S, somewhere in your subject line. Otherwise, your email may very well be spam-filtered into oblivion. You can also hit us up on the Twitter, where we are at twist science, at Dr. Kiki, at Jackson Fly, and at Blair's Menagerie. 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 tonight, please let us know. We'll be back here next week. And we hope you'll join us again for more great science news. And if you've learned anything from the show, remember. It's all in your head. This week in science. This week in science. This week in science. This week in science, it's 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 their robots with a simple device. I'll reverse global warming with a wave of my hand. And all it'll cost you is a couple of grand. This week science is coming your way. So everybody listen to what I say. I use the scientific method for all that it's worth. And I'll broadcast my opinion all over. It's this week in science. This week in science. This week in science. Science, science. This week in science. This week in science. This week in science. 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. If you listen to the science, you make us that understand. That we're not trying to threaten your philosophy. 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We're gonna have an after show, but not really long because Blair's nose is stuffed up and I can hear it. Yeah. Oh, oh, kiddies, you found kiddies that you'd saved kiddies, bleak little kittens to see the pictures of the kittens. Those aren't kittens. Those are cranky looking cats. Feed me. Meow. Look at those cats. They're cute fuzzy cats. Oh my, they all are giving the devil stare. I know, aren't they? That's cute kitty. Kitties. My cats. They're my cutie girl. She's the one who doesn't like to be held as much. Why does every episode have to end with a cat now? Because they claw underneath the door because the door is closed and their little paws like attack under the door and they make noise at me and they say, let me in. Let me in. So my daughter and I were playing. And they follow me places. My four-year-old was playing a game where she would knock and she go, there's a vampire at the door and then we go hide. And then a little bit later, there's a werewolf at the door and we go hide. And then I did one. I went, there's a cat at the door. And then I went, she's like, why are you hiding? I'm afraid of cats. What do you want? Did you see, I sent you, I forwarded an email today from this owner. Yes. Fantastic. Yeah, it's pretty funny. Yeah. The song about various parasites talks about Gandhi. I was right in there. Yeah, it was terrific. Vada wants to know more about the trip. Oh yeah. So it was an immersive environment in which we were surrounded by entomologists. And it's just so fantastic to walk through a crowd and hear things like, wow, yeah, well, good luck with your fleas. That sounds fantastic. Yeah, or, oh, yeah, I love your bedbugs. Those are the greatest bedbugs. Like, have fun with those mosquitoes. My gosh, that's going to be exciting to have. Yeah, do some good work with those mosquitoes. That's great. It's really fascinating. We had a group of you social organisms that was about 60 individuals, large. And on some other level, there was this sort of amazing thing of being around, immersed in a culture that's dedicated to studying thousands of other species, but classes of species, and they're all, but not themselves. Like, they're all like, wait, you're all humans who are dedicated to studying species other than yourselves. I thought that was also somehow interesting. Yeah. I think there's a room for ants somewhere. I also love the terminology. Entomology is weird because so much of your study involves killing your study subject. Exactly. It makes it very different from studying giraffes. Yeah, but wasn't it that somebody who did, was it Bonnie, who came over to the table for our meetup for a quick minute? I think she said something about, she's like, yeah, we're all entomologists. And nobody here is outgoing. Everybody's just way overstimulated. Basically, her comment was that everybody works with insects because they're not good with people. Yeah. And there is, there was a trading floor too. There was a trading floor and there was, you know, like the prices. Wow, these are like, I think is Dr. Jem still in the, yeah, the Jem doctor is out there. These, like a gem trading or a stone trading or a floor or if you're into baseball cards or whatever, you know, comic books, trading floor, like they had this one on the main floor of all of it, you could buy like insects that were like, you know, had the little pin put through them. And they ranged from like, pinned, all these pinned butterflies and moths and insects, they ranged anywhere from like $15 up to like $700, $800. And so we're like, amazing. Like that was, that was just sort of fun because there's butterflies the size of, you know, a human head. Like there was like some really amazing specimens in there, things that I didn't know existed or never seen or never Googled or what happened with it. But even when you Google something, you can't tell that it's a butterfly the size of your head. Okay, yeah. Well, so I was talking to my roommate who picked me up from the airport yesterday and I showed her the little calendar that we got with the fun pictures. And I noticed that there was a damsel fly in there. And then I remembered that our first interview said, most people that say they have dragonfly tattoos, they're actually damsel fly tattoos. I love that. Oh, and so we looked up the ways to tell the difference between a damsel fly and a dragon fly. And we were able, then there was like a quiz and we were totally able to tell. And it's pretty interesting. I mean, the ones that I remember are that the damsel fly have a very long, thin, like stick-like back of their body. And the dragonflies are kind of stumpier and wider. And then their wings, the damsel flies like come into a point and the dragonflies kind of bow out before they come in. And then damsel flies rest with their wings up behind them like this and dragonflies rest with their wings out like that. Well, a tattoo, it's like, yeah, a tattoo though would be getting a dragonfly resting with the wings out. Right, unless the wing shape, it sounds like the wing shape and the body shape are generally, usually damsel fly shaped. That's funny. Yeah, Kara should do a... I'm gonna go around and I'm gonna check people. I'm gonna, maybe we should start doing this, checking people's tattoos. I know, this is something like, I've seen some that were animals that were definitely wrong too. And I was like, oh, your spider doesn't have enough legs or like, your octopus doesn't have enough legs or just other things that I'm like, that's wrong. But I don't wanna tell them, of course. Okay, so here we go. So let me see if I can screen share. So I'm already seeing a whole bunch of damsel flies. I just Google search dragonfly tattoo. So can you see my cursor? Yes. Okay, so this is definitely a damsel fly because of the long slender body. And body. And the fact that the wings go into a point they don't bow out, they don't bow out at the outskirts either. So then like... And then when there is like a hybrid, because look, it's got the long thin body, but it has the bowing. The third one. Oh, this one? Yeah. So those are more like dragonfly wings, but that's definitely a damsel fly abdomen. Maybe. So this looks like a dragonfly. Let me show you this picture here that I... Wait, can you compete, competitively be screen sharing? Yeah. So this image here, they're saying that this is a dragonfly. Right. And that even though it has a slender abdomen, the thorax is thicker. Uh-huh. Oh, and the other thing was the eyes. The eyes on a dragonfly, which is it? One of them, the eyes meet at the middle and one of them, they don't. Yeah, so this is the eyes are broadly rounded and lie mostly flat against the head. Yeah. Yeah. So this is a damsel fly. Yeah. So like a lot of these I can see. Like this is more like a dragonfly for sure. Oops, sorry, I'm trying to do you and I need to stop my own sharing. This is a damsel fly though. That's so interesting. I got my dragonfly tattoo. You just tried it and it didn't. There's a damsel fly? No, that's a dragonfly too. But that's definitely, this is definitely a damsel fly. Yep. Yeah, that one would be. Wow, that's fascinating. I'm gonna be looking at them differently from now on. There's a damsel fly? Yeah, they have more buggy eyes. Yeah. The dragonflies, yeah. How funny. I love that. That's gonna make looking at people's tattoos so much more interesting. That's a damsel fly on your hand? Yeah. Oh my God. I got a dragonfly. No, you didn't. I don't think that was a real tattoo. Who knows? Maybe it was a temp tattoo. We can hope. Oh my gosh, I am so gonna. Look at this one. That looks like a flower. That's not even. Yeah, that's more conceptual. That's a conceptual dragonfly that's actually a damsel fly, but conceptual. So this is definitely a damsel fly too because of the way it's standing and the eyes. Yeah. How funny. What happens if you Google damsel fly tattoo? That's a good question. Yeah. We get a bunch of dragonflies show up? No, those are actual damsel flies for sure. Oh, there's a couple dragonflies, but mostly it's damsel flies. Interesting. I bet also some of them, they just went like dragonfly, damsel fly as keywords. I bet most people were like, I really want a dragonfly and just didn't even look because they don't really know the difference anyway. Yeah, I don't think Brown Tense's purpose is many people cared. No, thanks, Fada. I don't need a dragonfly tattoo. I'm all good. I think I'm going to get one now. Now I'm inspired. Yeah, you totally should. I'm going to be like, oh, nice damsel fly. That's a dragonfly. No, this is a dragonfly right there. You should get a tattoo of a clumsy mammoth falling in ice. That would be funny. Well, though, it is important. We won't have any lightly frozen over water areas in our... Dr. Justin's not a real Dr. Mammoth. Yeah, our meetup was very small, Fada. Dave Freidahl came. We got to hang out with Dave and then a woman named Bonnie showed up. There were a couple of people who had said they were going to come by, but then we didn't see them. So it was a busy conference. People were very busy. And when we went looking for that rooftop bar later, we found that all of the universities were having their mixers at that exact time, which I think was the other problem. They were like, go to a bar and pay for beer or go and get the free beer at the university mixer. Yeah, yeah. And mix with other people. Ben Rothegg, yes, tattoos of normal skin complexion. There we go. Yeah, it was fun. Dave Freidahl has stories of me jumping in elevators of the usual drama between Blair and Justin. Mwah! Mwah! Mwah! I could summarize that. Let's not revisit it. We don't have to revisit it, but I can summarize it real quick. Oh, boy. It goes like this. Hey, Justin, can you not? I was raised by lesbians. You're a misogynist. No, I was raised by lesbians. You're a misogynist. No, I was raised by lesbians. And that's kind of the whole conversation. Yeah, don't talk over me. That's kind of it in that show. Yes, yes, Ben, drama. There was drama. It was intense. No idea. We did have fun. We had a great time. Denver got cold while we were there. It snowed on our last night. There was a little scattering of snow around in the morning when we got up. And then we left. Oh, but get this, you guys. So the travel agent that booked our flights coordinated all of us so well. And it was like, all right, we're all basically leaving at the same time. It was like, go get on your planes. Justin got on his plane. I got on my plane. I sat on my plane and we sat on the plane for a little while. And then suddenly, shh. All right, everybody. We've got a mechanical problem with the plane. Everybody needs to get up and take all their stuff with them over to gate B24. They found us another plane. So that's pretty good. But we're gonna have to move. No, you were already boarded. Yeah, I was waving at that plane because I knew that was your gate. I could see the gate number from the outside. So I was like waving. I'm like, I don't know where she is, but I'm just waving at the plane as I taxi back. But I didn't see your, because yeah, wow. Yeah, I'm like, okay. As long as we have a working plane and we can get home, that's all, it was fine. I was only delayed like an hour, but. Yeah, we sat for almost a whole hour, which I don't understand. Yeah, because we were supposed to be leaving at, what was it, like 1150. And I didn't get home till two o'clock California time. So that's four hours for a two hour, 15 minute flight. And I was like, why, why is this taking so long? It's cause they had scheduled us to sit on the tarmac for like 45 minutes. Oh my goodness. Which I'll never understand. I guess it's because, you know, they know it's gonna take a while to board, but then they also know that they might get an earlier time on the departure lane, but they might have to wait, would be my guess. I don't know. But so that's, that's what doesn't make sense is that the flight only takes two hours and 15 minutes. But, and so, but we got in or still technically ahead of schedule, like before our planned like arrival time, but we sat around for 45 minutes before we took off. So that's interesting because United has been dinged a ton for delays. So maybe they're starting to like plan delays into their flight times. Yeah, they're just padding all of their flight times. Just pad it with a little bit. Yeah. Ooh, an electrical storm. That sounds great. Good night, Fada. There was a lot of turbulence. Did you guys have a lot of turbulence? A little bit, yeah. I feel like it's just quite a bit. Part of going to Denver. You have to go over the Rocky Mountains. There's bound to be turbulence. Which, yeah, when I was a kid, I used to be terrified of turbulence. And now it honestly just puts me to sleep. It happened to me again on the way home. I was telling Justin Kiki about this when we were in Denver. But again, on the way home, we started hitting turbulence. And he's kind of like fell asleep. That's awesome. I was just being jostled to sleep like a baby in the back seat of a car. Which my parents used to carry me around while they vacuumed. And that would put me to sleep. I think of the vibration. So there it is. A little turbulence. Just like the vacuum of old. Just like the vacuum. That's right, that's right. So you might have an interview next week. I have to confirm it still. There's a book called, what's it called, Soonish, I think, but it's Zach and Kelly Wienersmith. Yeah, Wienersmith. Zach and Kelly Wienersmith. Zach is a geek cartoonist and his wife Kelly is a scientist. And they've written a book about future technologies and what's coming. So yeah, we might not, we probably won't get Zach on the show, but his wife Kelly will probably join us. Neat. Would you be fun? Yeah, she's a scientist anyway. She's the one we want to talk with. Zach is, so his comic, Zach's comic is Saturday morning breakfast cereal. You've seen it. It's pretty funny. It's a good comic. Yes. So we might, I just have to confirm the interview but it's still happening. That's what we might have next week. That we might, yeah. Cool. All right, I got to roll. Okay. So I'm gonna say it now. Good night. But you broke up. You broke up. You said good night. And then you broke nothing. Yeah. Good night, Blair. Good night, Blair. Say good night, Justin. Good night, Justin. Good night, Kiki. Good night, Kiki. Good night, everyone. Thank you for joining us. We're gonna hope that Blair's cold goes away as she gets some sleep tonight. And no great green globs of greasy, grimy. Never mind. Gluffy, glup. Gluffy, glup. Come out of her nose anymore. Yeah. Everyone's yawning. That means it's time. Everyone who's on the East Coast, hey, Dick, tell you're late. We're just leaving, but thanks for joining us. I hope everyone has a wonderful night's sleep. I will be getting the live podcast out probably tomorrow and work on the audio and video re-upload for the video on YouTube. So it's a clean version if you wanna watch it from the live show and then get the right, we had this podcast out by Friday. We're gonna do it. Doubleheader this week. Maybe I'll put things on Patreon first. All right, thanks, everyone. We'll see you next week.