 Welcome, everyone, to this week's episode of This Week in Science, our weekly podcast broadcast. Thanks for joining us. We're going to get started in just a second. But as always, I want to remind you that this is a live podcast recording. And, you know, things happen, technical difficulties, ums, odds, and whatever. And you're here for the live thing. The podcast version is edited. So make sure if you want the edited version that you subscribe to the podcast, go ahead and click those like and subscribe buttons and all that kind of stuff. But it's time for us to begin. We ready, friends? Yeah. All right, let's start the show in three, two, this is Twist. This week in Science, episode number 898, recorded on Wednesday, October 26, 2022. It's Twisoine 2022. Hey, everyone, I'm Dr. Kiki. And tonight on the show, we will fill your heads with viruses, Monde, and editing living humans. But first, disclaimer, disclaimer, disclaimer. Everything counts. Every experiment, every drug trial, every data observation, every innovation, it all counts. Even if it doesn't seem like it at the time, even if the hypothesis was a flop or the drug failed to cure, even if the observation turned out to be noise or the innovation, just a modest improvement. Everything in science counts because that's how math works, because the stories in science don't begin nor end with a single paper, researcher, institution or discovery. Science spans across time, across fields of research, all adding to what came before to form a greater ever growing body of knowledge, where every new result leaves us with the same question. What comes next? And the answer to that question is always the same. More science and more, this week in science, coming up next. I've got the kind of mind that can't get enough. I wanna learn discoveries that happen every day of the week. There's only one place to go to find the knowledge I seek. Science to you Kiki and Blair. And a good science to you too, Justin Blair and Dr. Vivek Kumar and everyone out there. Welcome to another episode of This Week in Science. We are back again to talk all about the science that has occurred in the last week or so. We always understand that there's a lot more leading up to it, but we have a great show ahead. I have science news about Monde, viruses, tentacle bots, and we have an interview to discuss biomedical engineering with Dr. Vivek Kumar. Justin, what did you bring for us? I've got a new development by a scientist that may have farmers seeing red. I feel like I'm doing like the six o'clock news every time. Gene editing in humans, in live humans, not the ones that are, you know, not the next generation, but current live humans. What's going on with ancient Brits? A little discovery there. And if there's time, because we've got some stuff, a couple of satellite stories that are very interesting on the global warming front. And Blair, what is in the animal corner? I have electric insects, loud turtles, and chemical camouflage. I'm excited about that animal quarter. Electric insects? What? Okay, we got to get into this. Guys, as we jump into the show, I am needing to remind you that if you have not yet subscribed to this week in science, you can find us all places that podcasts are found. Apple, Google, Spotify, all the other things we broadcast live weekly, 8pm Pacific time on Twitch, YouTube and Facebook. We are Twist Science on Twitch, Instagram and Twitter. And if this is just too much, twist.org is our website and you can find all the things related to every episode right there. But let's jump into the science. So first thing off of my plate is I would love to tell you about Monde. What is Monde? Right? That's the big question. What is Monde? It is modified Newtonian gravity. Modified Newtonian gravity. That doesn't re-add up to Monde. Right. So it is modified Newtonian dynamics and is an alternative to our theories of how the universe works, how gravity works, how everything fits together. And it's contested as to how accurate it is, how much it works. However, some researchers just publishing in the monthly notices of the Royal Astronomical Society have determined that their observations of star clusters are consistent with Monde rather than Newton's regular old, plain old laws of gravity. So the idea being that when star clusters are formed, there's a lot of energy and these clusters, the cluster, the cluster up, but then stars escape and they want to go in different directions. And according to Newton's traditional laws of gravity, there's a couple of ways they could go and they should be evenly balanced. Like if you imagine that there's two doors that these stars in a room could exit those doors of the same size, everybody's going to exit at even probabilities. But that's not what they observed. They observed that there's like a tail and there's an odd clustering in these star clusters that can only be explained by the Monde hypothesis. So of course astrophysicists and physicists are all a flutter in the community going. Aren't they always? Aren't they always? Yeah, so, you know, there's a lot more that needs to be worked out. But these researchers, they use the European Space Agency's GAIA space mission to be able to get the data, to analyze the data. And they have looked at five open clusters and five that are near us and four specifically by this particular group. And yeah, so the question is, is it really a different hypothesis, is it different gravitational physics? Are there a modification based on different parts of space or time or different areas? Does physics change? So it's, I've always find interesting this and it's an old story. Like we have, like I can go all the way back to the ancient Greeks or whatever civilization you'd like to choose who started assigning deities to the movers of things. The north wind, the south wind, yeah, the gods that looked over sheep. One thing that was missing was a god of gravity. It was such a given, you know, you assign powers that move to things that change, but gravity is so consistent, people just sort of overlooked it. Up is up, down is down, that's just how it works. Right. And so as we've gone forward and we've been able to understand and, you know, we have Newtonian physics that explains how gravity will act and predictively. We still don't know the mechanism of gravity. It is still one of those great mysteries. And so, yeah, as we're modifying, we're still just modifying our understanding of gravity through the observation of it taking place. Of apples dropping or star clusters, but we, which will eventually lead us to the mechanism behind gravity. We still don't have it, which is, I think, so fascinating that it is, it was an oblivious thing to us in the beginning and we're still trying to catch up to exactly what's happening with gravity. Dr. Kumar, you look like you had something to say. So, so I am a YouTube and Netflix astrophysicist. All my knowledge comes from YouTube on this. I think my understanding is gravitational waves and gravitons or gravitational particles or whatever quantization is so hard to detect because gravity works at such long distances and is such a weak force that it's almost impossible to measure in most ways. But coming back to Mons, as soon as you started talking about it, it reminded me of dark matter, right? This idea that everything's expanding or collapsing and there's got to be this other force and I don't know, does this have much to do with dark matter? Is this a component of dark matter? I don't know. We don't know. I think that's one of, you know, like Justin's getting at. There are definitely a lot of things we have yet to learn about this wonderful universe that we live in. How does gravity work? So we have all these placeholders for it. We have all these, we understand, you know, Newtonian physics, dark matter. If there's this thing out there, this could explain a lot. But then the lack of detection. And then every once in a while we make an observation that goes, oh, wait, that galaxy isn't behaving according to what the dark matter model was now. This is, we've got a mon thing with the clusters that's not behaving how the other. It keeps showing us that we have missing, a missing component or missing factor there. Yeah. And one of the things that the researchers do point out is that they had to use relatively simple computational methods. And that's quote. And they currently lack the mathematical tools to do more detailed analyses of modified Newtonian dynamics. So there's actually more math that needs to be created. Yeah, they haven't invented the math they need to make their model work yet. That is such an, I mean, it's an honest assessment. But really at this point, that's a really, that's a big statement. We don't have the math that can do this yet. Yeah. Wow. Yeah. Yeah. So that big take home message I think is, you know, yeah, it's stuff to ponder for sure. It's kind of like something's up. We're not 100% sure what it is. We feel like it's probably not what other people think. Yeah. TBD. I don't know. All right, Justin, do you want to tell us a story about something here on Earth possibly? This is a very planetary focused story. So the world right now, as we are somewhat aware, is facing the dual threats of global warming and the effect of agricultural sustainability in that change in climate. So there's this ever growing population here on planet Earth that requires more production from agriculture. So there's some pressure to find solutions that will allow people to continue. And that's it, just to continue. Just, just allowing us to continue. Right. New research out of Hokkaido University might have farmers seeing red in the future while putting them in the black financially. That was my newscastry best attempt there. And allowing, of course, people to continue. Plants like sunlight, they like it a lot, photosynthesis, this process where plants convert sunlight to ATP, the energy carrying molecule found in the cells of all living things. But plants don't use all of the light coming from the sun. Mostly they observe the visible light in red and blue regions, red being mostly, I think, more utilized than the blue, although I think the blue was used maybe early. Sunlight conveniently includes both of these red and blue lights. But it also sends a lot of high energy ultraviolet light in the high energy wavelength region that the plants don't use, don't need, and it can actually be pretty harmful to the plants. So depending on the specific range of the UV light, it can actually even alter the DNA of a plant. Plants without UV light, indoor grown plants with the red and blue light grow just fine. In fact, shading plants from solar UV is one of the key strategies used to suppress growth inhibition and damage to plants, which is why greenhouse materials often have UV blocking properties. Enter Hokkaido University, who has now tested a wavelength converting material to modify UV light coming from the sun into red light. Working with the Institute for Chemical Reaction Design Discovery, they developed a European-based thin film coating, which is, you know, that is actually pretty unusable for most things. I think it's pretty unstable. Somehow they've managed to incorporate it into a thin film coating. They tested this out on Japanese large trees that were cultured under wavelength converting material films in sunlight. Three months into the seedlings were taller than those without the films at the end of the cultivation experiment. The diameter of the stem at soil surface was 1.2-fold larger, and the total biomass of the seedlings was 1.4-fold greater, with significant increments of increased thickness of the roots, branches, stems, and leaves. So these sort of numbers are great for Japanese large tree nurseries. But if this translates into agriculture or other starting plants into biofuel crops, could be a real game changer. It's, you know, anything that increases yield and productivity in that sector has a huge effect on the outcome of food that reaches a table, allowing thus humans to better continue. Yeah, that's really interesting. Just, okay, we're just going to take the most productive part of sunlight and give that to plants. But it seems as though this is the kind of thing that, you know, it's not going to work in the big industrial scale farming where it's outdoors. You know, possibly this is going to be the kind of thing that's going to work in indoor vertical farms or in greenhouses or, you know, places where it's much easier to control that situation. I just, I'm having a hard time, having grown up in the Central Valley of California where there's lots of fields. I'm having a hard time imagining all the fields covered in a material, right? So the other thing about covering a field in material though is you reduce atmospheric water loss from evaporation. And I think the thing that I, every time I drive through the Central Valley and I get so frustrated and I like want to shout at every farm is that they're just spewing water all over the plants. So much of it is getting left into the atmosphere and, you know, drip irrigation is way more water conscious, I guess. But anyway, point being there's a secondary benefit to covering plants, which is you get to retain more moisture too. And a couple of things there too, also having been in the Central Valley, I have seen these small coverings that go down rows because the seedlings are particularly vulnerable to direct sunlight. So the small plants when they're just getting started. Yeah, it looks like trash bags are covering each row of strawberry. Yes, absolutely. And also this research was done in Hokkaido, which is in northern Japan, which is often covered in snow for much of the year. So this is also coming from what you would consider a sort of northern climate. It's also an island, so there's probably plenty of marine layer going on there too. So there's, this is also an option for maybe places that are having agriculture where they can't grow it outdoors all year round. Yeah, less productive areas. But the thing I thought about, because specifically they were doing this on trees, we are going to, as climates change, have to migrate a lot of trees. They're not going to be able to do it on their own. Forests are going to need to move to keep their, their habitat, their range of temperatures that they're used to living in. And so massive efforts to reforest some portions of forest and move them further north or south as the case may be. This would be a really good way to get robust seedlings faster out into the field. Well, and you bring up another point too, which is if you, again, if you think about the Central Valley and climate change and the fact that it's getting hotter, and that can be a stressor on plants, covering them can also be helpful for that. Whereas covering massive farms sounds like a large undertaking might actually be required to keep certain farms going in the next 20, 30, 40 years. And this is also a weird side thing. Like they're converting it to red light so that the plants can use that the ultraviolet, which is just brilliant. But that ultraviolet is also something that often is creating heat. So if you're reducing heat in a greenhouse, you're also running fans less. You're doing less cooling. You're, you know, might be using less electricity in these, in these, which on a large scale farm can be quite a big electricity bill to be keeping this. The big, the big, big question though is, yeah, what can we do as we move forward to really maximize our, our land and our food productivity for a growing population? Because that's got to be an issue. Okay. Just want to jump in real quick. So that first graph that you showed with the wavelengths from the sun. Yes. So the sun is most green. So you know how thinking about what color is the sun. And one of the things I learned recently is it's this off the white sun shines all the colors of the spectrum, as well as infrared and ultraviolet and a whole bunch of other wavelengths. It shines the most in the green wavelengths. That's very cool. But the plants don't use that the most, which is the interesting part. It's like, Well, then of course you have like atmospheric attenuation and a lot of different factors, but in terms of like the spectrum that the sun shines, it's highest in the green, which is what that first graph showed. Yeah. Man, next thing you're going to tell me they're not wearing the sun doesn't wear sunglasses either. Let's go at night. Blair, tell me about these electric insects, please. Okay. Well, I'm going to start by saying researchers don't have a whole lot of information on this topic yet. It's just kind of weird. So researchers discovered that insects can produce as much atmospheric electric charge as a thunderstorm cloud. What? This type of electricity helps shape weather events, aid insects in finding food, and helps to lift spiders up in the air to migrate over large distances. Yes, we've talked about the electrostatic ballooning that spiders do. Yes. So cool. Yeah. But when you go to quantify that electric charge, that is what's really weird about this story. So most living creatures have an electric charge. Thump, thump, thump, thump, right? The researchers have previously found that honeybee hive swarms charge the atmospheric electricity by 100 to 1000 volts per meter. So that increases the electric field force that is normally experienced at ground level. So this research team developed a model that can predict the influence of other species of insects. And it all depends on the density and size of the insect swarm. So locusts, for example, have these huge swarms, sizing about 460 square miles with 80 million locusts and less than a square mile. So their influence is way larger than honeybees. They haven't quantified it yet, but it's huge. And so they think that there are unsuspected links that exist over different spatial scales, ranging from microbes in the soil and plant-pollinator interactions to insect swarms. And indeed, in these locust cases, perhaps even the global electric circuit. So this is a good opportunity to remind us that different realms of science need to talk to each other. Yeah. So electric charge is something that's studied in physics normally, but this is a time when physics and biology need to talk to each other to figure out the impact of this. The first thing I thought of, of course, is if insects are impacting the global electric charge scale and we're going through what some have called an insect apocalypse. I won't say that because that's scary, but some have called it that. You just did. How am I working it? Oh, it's twissouine. It's scary. Insect apocalypse. What will that do to our planet and the electric charge on our planet? I don't know. One side of things, very obvious. Everything with a heartbeat has an electric charge. But then there is that whole conversation about, yeah, there's a swarm of insects that all carry their own electric charge. Is that compounding and doing something to the area around itself? I don't know. Pretty trippy. Oh, gosh. Is it going to turn out that this whole time our electromagnetic shell that protects us from cosmic rays? Oh, right. Produced by the insects. Produced by the insects maintained by that balance, that delegate balance is maintained by the insect population. Without them, the poles will start flipping and the radiation will start bombarding us. I don't think it's that big of an influence. No, I don't think it's that big, but it could be statistically significant, is all this is really saying. Yeah, so the question is, is the electric potential that's changing the gradient, the charges that they're building up that's changing the gradient, is that a factor of the fact that they are flying insects, but these little wings that are moving air molecules around and creating static electricity and building up charge in that sense. Or is it just a factor of they are there? Right. Because like you said, we all have, you know, electrical potentials going through. It's immediate from plants carry electrical potentials through them. It's very, yeah. I'm on the, it's probably the wings and the air movement and a factor of if you get these big swarms together, that are actually impacting the air itself, then maybe that's what's going on. You're talking about quite literally the butterfly effect. That's what you're talking about. Except for the fact that in the study, they did say that Lepidoptera do not actually have a big, big effect on the scope. Sure, sure. If you want to spoil my fun. That's what I do here. With facts, I guess that's the point of this show anyway. But insects impacting our atmosphere. That's wild. Yeah. Who knew we need to start? Yeah, we need to start delving into these things a bit more. So right about now. I want to let you all know that this is this week in science. Thank you so much for joining us for this episode. And if you are enjoying the show, please let others know about this week in science. We'd appreciate your help in spreading the word coming back in right now. I do want to introduce our guest tonight. Our guest on the show is Dr. Vivek Kumar. He's an associate professor in biomedical engineering at the New Jersey Institute of Technology. He began his own faculty position, the Kumar lab with expertise in the areas of tissue engineering, drug development and delivery and specific research interests in the area of inflammation modulation and angiogenesis, especially in understanding the role of small growth factor or cytokine mimics ability to signal biological processes. And I think we've actually talked about some of Dr. Kumar's work related to tooth pulp on the show previously. But welcome to the show, Dr. Kumar. Thank you so much for joining us. Thank you. Thanks for having me. Yeah. It's a pleasure. Happy to chat about, you know, whatever you'd like. Perfect. That just opens the doors to so many things. I don't know if you should have said that. Okay. Just to start off. So biomedical engineering is the, you know, the code word for what you do scientifically. How did you get into this area of science? I think, I think a lot of folks who end up in biomedical engineering at some point have flirted with medicine. As did I in my undergraduate years. But during my undergraduate career, I started working in a research lab as do a lot of pre-med kids. And I realized that the impact I wanted to create was not in seeing sick people and treating them every day or trying to, you know, improve the healthcare system in that sense, but more so develop therapeutics, develop devices, drugs, materials and engineer better cures in that way impacting millions of people potentially. Also, not having to work with sick people every day. Right. Yeah. No, that was a big part of it. So a big part of becoming a doctor is wanting to see sick people every day. And that wasn't something that I generally like to do. I met a doctor who told me exactly this regret of it. The only regret in his life is that, you know, going in, it hadn't occurred to him that this was going to be his every day. So to be fair, now as a professor, I sit on the other side of this and I advise a lot of pre-health students at NGIT where we have a fantastic record of getting students into medical school. Right. And, you know, I think there are a lot of careers that physicians can do nowadays that are outside of medicine, like consulting, public health, enhancing or promoting, you know, even voting in hospitals. Like I saw this guy, Alistair Martin, who has set up these voting booths in hospitals in ERs, right? He's an ER physician who's trying to encourage voting in ERs, registering people who come to ERs. That's fantastic, having multiple layers of impacts. Well, you're sitting here in the waiting room for the next four hours. Why don't you fill out some voter registration? In fact, and arguably some of these folks are the people who suffer the most, right, who are least represented in our electorate. And, you know, voting is not the number one priority on their minds. It's getting treatment or figuring out how to pay this bill. But their votes can have those impacts that are needed. To drive that change. Yeah. Okay. So Toothpulp, where did, how did you go from, okay, I'm going to help people. You're like, okay, I'm not going to be a doctor. I'm going to come up with cures and. So, what's going on there? So I started my graduate work at Georgia Tech and at Emory looking at synthetic blood vessels, so creating small blood vessels. And after you finish your PhD, you do more research because just love doing that forever. So I did what's known as a postdoc for four years with a guy at Rice University, Jeffrey Hartrank, where we looked at creating small blood vessels. During that time, I worked with Rena D'Souza. So you guys know Anthony Fauci, right? The NIAID infectious disease guy. So the dental version of that, the head of NIDCR, National Institute of Dental Craniofacial Research, is Rena D'Souza. I trained under her while I was at Rice. And one of the things that we started to look at was using our gels, you know, the stuff that looks like Purell, right? Hydro gels, using our gels to inject into the tooth after you get a root canal. So right now, when you get a root canal, or rather, when you have an infection in the soft tissue, it hurts a whole bunch. They go in, they take out all the infected stuff and they put in little rubber rods and they put cement on top, Portland cement, literally. And you're left with a relatively inert, non-responsive tooth. So if you get infection again, you might lose the whole tooth, you might need to put artificial tooth. So what we said was, what if you can inject a hydrogel, right? A gel that can help blood vessels grow and new tissue grow. So yeah, so essentially what we do in my research lab is engineer hydrogels that help regenerate blood vessels, that regenerate a variety of different tissues. Not just blood vessels, but it was expanded beyond that. But yeah. So we know, we know gels like Purell, like okay, Purell's got a lot of alcohol in it. It's a little gooey gel, it dries out and maybe somebody's put aloe in it or something to keep your skin from drying out. But can you explain how a hydrogel works in this manner? How is this jelly substance doing all this supportive work? So there's a lot of different types of gels. And your Purell gels are, there's a large percentage of Purell gel is alcohol. And the idea is that the alcohol stays on your skin and it kills the bacteria. If you leave it on there for a certain amount of time, what have you. Now what we work with are hydrogels. And as its name suggests, it's 95 to 99 to 99.5% water, hydro water, right? The rest of the material, so like 0.5% to 5%, like a very small amount of it is stuff. Now you can make hydrogels out of synthetic polymers. You can make them out of a variety of different things, but we make them out of peptides. So proteins, short proteins are peptides, right? So our peptides, they self-assemble. They come together on their own. They form little fibers and these fibers entangle and they hydrate. They suck up a whole bunch of water. So these fibers hydrate into a hydrogel. And what's neat about these fibers is that you can syringe, aspirate them and inject them and they form a gel where you put them. So you can pull it up into a syringe, inject it into the tooth and it forms a gel in your tooth. They biodegrade over about two to four weeks as native tissue grows into it. And we've used this in the tooth, in the eye, in the brain. And to be fair, we haven't tested this in humans as yet. We've done mainly rodent, so rat, mouse work, some canine work as well. And so I read that the canine root canals with your hydrogel has been really successful. Right, right, right. So basically before you take a therapeutic or a drug or a technology to market, you have to do human clinical trials. Before human trials, you do animal trials. Before animal trials, you do bench trials. And basically you're de-risking it. You're trying to ensure there is no chance of any adverse effect in humans. So typically before humans, you do a large animal model and that could be in non-human primates, canines, pigs, depending on what is most relevant and mimics the human condition. So in this case, it was a canine model. So we did root canals in dogs, adult beagles, and injected our hydrogels and then looked at the teeth a month later. And what we saw was very nice tissue regeneration into the canal space, into the tooth space. We have a question in the chat. Does the enamel regrow or do you have to seal over the tooth? So we do have to seal. So we don't aim to regenerate enamel. There are a couple of folks who look at the outside of the tooth, the enamel portion. We're more interested in regenerating the soft tissue, the dental pulp. There's a company called Curudon, C-U-R-O-D-O-N-T Curudon. They do some enamelogenesis. They've got a product similar to what we've got, but enamel is the outside, the white porcelain-y part of the tooth. The soft stuff inside that supplies nutrients and nourishes the outside. That's the pulp and we try to regenerate the pulp. So there's also some of these getting very long in the tooth. They're older and they're wiser. It's usually because they have gum disease is basically what it is. Can this be eventually applied to reversing some of the effects of gum disease then? So we've been interested in exploring this material for a number of applications. So we didn't start out looking primarily at dental pulp. We started out looking at vascular disease. I worked for a vascular surgeon. I know a lot about vascular vascularopathies or diseases in the blood vessels and what have you. And we started out looking at peripheral vascular disease or poor circulation in the legs. So right now we have grants and funding to look at this material for poor circulation in the legs, in the heart. It's a very traumatic brain injury like knocks on the head, injecting it into the cranium to preserve some of the function. Interestingly into the eye to treat one of the leading causes of blindness, wet age-related macular degeneration with AMD. It's like the back of the eye just has a bunch of blood vessels grow, but they're like really leaky. So when we injected our angiogenic hydrogel, it stabilized those vessels, which is not your typical treatment. Basically people go for monthly injections when they kill the blood vessels. Anyway, different topic. No, that's awesome. So yeah, the applications then are everywhere within the human body. We're very excited. So far with the largest animal model we've tried is canines in the dental pulp. But we're very excited about moving this to other animal, to other disease models and whatever we can take into the clinic and expanding the platform. So you mentioned that there's a lot of stuff in the hydrogels. So how does it work to support the soft tissue growth? What kind of stuff is in there? Do you have growth factors that have been isolated from human molecular systems? What are you using? And does it depend on where in the body you're applying the hydrogel? So I like simplicity and I also like not reinventing the wheel because I think the millions, hundreds of millions of years of evolution that life has taken and done has done a very good job. So what we do in our lab is that we mimic growth factors. So this is very large growth factor called vascular endothelial growth factor. And through computational modeling we can see how this large growth factor interacts with its receptor. So cells have receptors, growth factor binds to that receptor. Now what we can do is isolate the very specific region that interacts with the receptor, the epitope. We can take that region and then attach it to our peptides. So now our proteins had that signaling domain on every single peptide. When these self-assemble into fibers, we have very high presentation of that domain. Long story short, we make synthetic growth factors that are very small, that are injectable and stay local because they're part of the material. Other than that, it's water. They're more concise. And we try our best not to deliver other growth factors or cells or any other factors because we try to incorporate the signal within the material itself. Does that make sense? Yeah, that does make sense. But it's just a signal that's telling the body, hey, start doing what you haven't been doing. So the second part of this is that these are peptide-based, right? These are protein-based materials. So the cells in the body rapidly infiltrate these gels. They phagocytose, they gobble them up, they degrade them, and they say, well, this looks relatively normal. Let me start depositing collagen, right? So we see a lot of cells infiltrating. They deposit native collagen. We see blood vessels infiltrating. And in the tooth, for example, the cells that infiltrate differentiate towards dental pulp-like cells, right? So depending on where we put these materials, the niche that's surrounding it influences the infiltrating stem cells and what have you. So the tissues themselves take over with the local customs of what we grow here. If you're going to show up here, we can set up your shop, but it's got to be close. We're providing the scaffolding, and we're providing the most, in my opinion, the most important facet of regeneration, which is blood supply, right? You can take organs, you can have all these fancy tissue engineering, all these different crazy ideas. But if you don't have blood supply, that thing's going to die, right? If you don't have a blood vessel, 200 microns from another blood vessel, tissue will die. 200 microns is 0.2 millimeters, right? Like an extremely small amount, right? Like four hairs next to each other. If you don't have two blood vessels that far apart, that tissue will die. Organs will fail, you know, just bad news. So our biggest goal is to engineer microvastleture using injectable gels. In the chat room, JG is asking, can this be used to regrow nerves? So we have, so in a rodent model, in a rat model, we did a craniotomy holding the head and used a fluid jet to create an injury on the cranium, on the brain itself. We then injected the hydrogel onto the brain itself and then closed the craniotomy and then looked at the animals a week later. In that study, we showed that we generated new blood vessels. We could help preserve some of the neurons. We have made a version of this peptide, of this scaffold that is neurogenic, that helps proliferate neurons. We haven't shown that in animals just as yet. So I wouldn't go as far as to say we can regenerate neurons, which is a huge big deal. Let's not go that far, but we can regenerate blood vessels, which is a big part of healing any tissue. But I want to go that far because this sounds like the thing that can finally make me smarter. I feel like I need more neurons than I'm working with. Is there a future where, you know, like athletes, they got all that stuff they can take to build the muscles to determine maybe some other physical health issues? I'd be willing to take on some detrimental side issues to get smarter. Recently, I heard a podcast about how important sleep is. And I'm not one to believe in sleep, but interestingly, almost every cell in your body has some sort of internal clock that responds to light. It has some photoreceptor, right? Obviously, your eyes have rhodopsins or what have you, but different cells respond differently to light, be it daylight, artificial light or what have you. So in that sense, you know, there might be better times for digestion, better times for sleep, better times for learning, which might be dependent on how much you sleep. So I don't know. I got to learn more about sleep. Yes. Of course, the professor doesn't think that people need that much sleep, right? No, sleep is important. But, you know, these, these, these wonderful hydrogels are potentially going to help solve all sorts of issues. So big question, it is around Halloween. Have you ever given any thought to, you know, the kind of instead of just fixing people, maybe the upgrading of people, like, could you develop vampire fangs, for instance, through biomedical engineering? So I'll give you a piece of trivia. So, so rats incisors, rats teeth, a number of the rats teeth, they will grow forever. So even if you knock them out, pull them out, damage them, they'll grow forever. Evolutionarily, rats need their teeth, right? So they regenerate very well. So not the best model when you're trying to evaluate if your materials work, right? Because they regenerate on their own. The other thing I was thinking about today is, you know, to be a mad scientist, you got to be a really good scientist. And then you have to become crazy, right? Because if you want to reanimate a Frankenstein or something like that, you need to be extremely good at science and then want to do crazy stuff. So, but to answer your question, I don't know. This is just your step one. Well, I mean, this is, it's a long process. You're on your journey though. I think, you know, the field is moving so rapidly in so many different directions. My contribution to it, I think is we will give you materials that will help you vascularize, that will help provide a blood supply, nutrient exchange, oxygen supply to what you're doing. Be that transplanted organs, be that bone implants, be that, you know, heart disease, right? We have an ongoing trial where we're doing heart attacks and mice, injecting these hydrogels into the heart directly and seeing whether we can regenerate blood vessels and therefore improve cardiac outcomes or cardiac output. So to answer your question key, I decided to look at how vampire bat teeth are different from our teeth to see if we could actually engineer this right now. Good direction. So the, the upper incisors and canines of vampire bats are large, flat, blade like and razor sharp. They do not have enamel, which allows for them to stay especially sharp and not wear down from use. A lot of people think that vampire bats have have like holes in their teeth and drink through their teeth, but they just bite to make cuts and then lap up blood with their tongues. But so could we, could we make some enamel-less teeth that are extra sharp? I don't see why not. There you go. Yeah. Yeah. Wow. I think the interesting point here that you've brought up is the angiogenesis, right? So how can we support the angiogenesis that's necessary for so many things? In terms of, you know, creating organs for, you know, organ donation, right? We don't have a good organ donation supply. We want to create organs potentially and angiogenesis has been a huge part of this. Where are we in our ability to get those really important small vessels where they need to be in a large organ? Like have we, have we made that progress? So we do a little bit of work in this, but if you think about a complex three-dimensional organ, you need to 3D print. Let's be honest, you need to have some kind of sophisticated 3D architecture making program and 3D printing kind of answers that. Now the problem with 3D printing is that your resolution for your nozzle is needle-based, right? So you look, and also Taylor Coette Cone, but let's not go there, is needle-based. And let's, and that's on the order of about maybe 50 microns at best. Right? If the best capillary or tube you can make is 50 microns, that's still not good enough to make a blood vessel with a capillary, which is on the order of 10 microns, 5 to 10 microns in diameter. Right? So you can't really 3D print every size of vessel architecture. That being said, even if you were able to 3D print or make it through some other fabrication scheme, sacrificial molding, XYZ. In my opinion, the biggest concern is not so much making something that looks cool and publishing a nice paper, but ensuring that once you're implanted, first of all, you don't have rejection. Well, no, first of all, you don't have clotting, right? Almost every collagen is highly thrombotic. The minute you blood touches collagen, which is like the basis for every tissue or organ in the body, as soon as blood touches collagen, it clots. It's just how it works. If blood touches endothelial cells, it doesn't clot. The collagen immediately clots. Right? So many challenges just with transplant, let alone blood vessels, let alone perfusion, that I think we must first face. Yeah. We have angiogenesis covered. How long does this take to start to grow up? Because one of the things where is an immediate concern for where you would need to add vasculature? Sure. The first thing I thought of was if somebody's got gangrene. That's exactly the example I wanted to give you, right? So let's imagine I've got an ulcerative wound here, right? And if I've got diabetes, which let's be honest, I'm halfway there. If I've got diabetes, then I have vasculopathies and neuropathies, meaning I don't feel that I have an injury here and my blood vessels don't supply it very well. So this region is not healing very well, which means if I get an infection, it might spread to the bone, gangrene, amputation, all that stuff. But before we get there, to heal this wound, what I can do is remove all the dead scar tissue, debride it, right? Infection, debride it, fill it with a gel. Now, you could fill it, you could create a blood clot and that's a fibrin gel, right? Your body has fibrinogen circulating in your system. And when you have a cut, that fibrinogen gets polymerized into fibrin and that's your scab. It's a white polymer, but it contains red blood cells, which is why your scab looks reddish brown, right? Because it has trapped red blood cells in a white scab. That scab degrades over about four to seven days and is somewhat water soluble, right? So you shower, you can kind of wear it off. Here's the thing, ours degrades in three to four weeks. So the way I like to tell people, the way I like to explain our scaffolds is like, I wouldn't call it a synthetic fibrin, but it degrades similar to fibrin over a three to four week period. So you provide slightly longer for the tissue to grow. So coming back to that wound example, if you had just a blood clot within seven days, you might not have good healing, especially if you're diabetic, right? However, if you have a hydrogel that persists, that sticks around for three to four weeks, that allows good tissue infiltration and angiogenesis, then you might have better outcomes. That being said, we just published a study where we showed that these hydrogels can accelerate angiogenesis in diabetic wound healing in rats earlier this year. So, okay. So this is all really exciting and there's a bunch of potential medical applications. And so how far away are we from me going to the hospital for something and going, give me that hydrogel? How many hours do we have to talk about this? So the benefit, when I started my academic job, I was wearing my academic hat. I had this vision and this hope of bringing these products or these technologies I make to humans. Five years, six years in, I have ten year now. I have multiple startups and I'm realizing that this is a huge pain because there are so many factors that influence translation. Just because people are excited, just because there is a good appetite, there is a good market and what have you, you need so many other things to line up. For example, to bring a drug, because we activate receptors, we're classified as a drug. To bring a drug to market, the average drug, you need to do phase one, phase two, phase three clinical trials. You're looking at at least a hundred million dollars. Most startups don't have that and to raise that from BC is hard unless you have a lot of track record. So you need to collaborate with, you need to do a strategic partnership with pharma. So that has happened in phase one clinical trials because pharma doesn't want to invest in everyone at the idea stage. So you can't just go in with everyone who has animal data. So between where I am now, which is large animal efficacy and phase one human trials where I can get pharma interested, is about two million dollars in what we call the Valley of Death. The Valley of Death for biotech startups is your typical toxicity, manufacturing studies. The studies which don't create much value in terms of investors, but every drug has to do before you go to human trials. Before you go to human trials, you have to do talks and manufacturing, which the FDA requires, but costs a whole bunch of money. And who wants to invest in that over? And if you don't know, if it's actually like that, so risky in terms of investment. I want to invest in it. I don't have any money. So we have a lot of people who email me and say, Hey, when can I get this in the clinic? Right? Like, when can I do this? And, you know, sometimes like we've published papers on neurogenic hydrogels or even hydrogels that decrease injury from after traumatic brain injury. And there are folks who have had traumatic brain injury who reach out and say, Hey, you know, is this available? Can I go to the hospital and get it? And it's, you know, it's almost heartbreaking to say, look, we have a lot of development to do. But we're very excited about this, you know, stay in touch. And yeah. Yeah, for the price of a house in California or a town in Florida, it seems like you would, you know, for all of the impact that it could potentially have to so many people in so many different areas that you would think that this would be, this would be an enticing investment for an investor or for federal funding. So that's our, that's our other approach. So the approach that we're taking, which is somewhat tried and true and trusted is to go through federal funding. So it's a slower process. There's grant reviews, what have you. We just received a large NIH grant for our research lab to understand some of the mechanisms behind this as well. And we're interested in some translational funding as well. This is also exciting. And it just, what you're doing sounds very promising. You know, getting the funding behind what you're doing is a big part of the steps. So congratulations on that part of it. And my fingers are crossed for Blair so that she can go into the clinic and say, give me that. Well, I just, I know I'm going to need root canals eventually. I really want the gel. I want that. Is that, is it possible in my lifetime? It is, right? That's my hope. I mean, yeah, my hope is within the next five to seven years that we can hopefully have something. But to be fair, like, this is the dream, right? The dream of every biomedical engineer, in my opinion, is to make something that touches a human. And then to see that flourish, right, would be really cool. And this is, this is sort of on that note. When did you realize you had something like that? Like, what part, like, where were you in your career? You were like, this is the thing I'm going to chase down and got to a point where you're like, I think it will also work. Ask me that five years from now because I tell the students I mentor, you know, genius. I don't believe in genius. I don't believe in Intel. I believe in hard work. I think end of the day, like, if and when this makes it to human trials, it will make sense because everything that has led up to that had to have happened, right? Like we had to have done small animal rodent work. We had to have done in vitro studies, publish that small animal rodent work, publish that canine work, publish that. And tomorrow we're going to have to raise some, we're going to have to raise a lot of funds. We're going to have, you know, these press releases, what have you. All of this will fall in place and then we'll do human trials. And at that point I would say, yeah, it kind of makes sense. We have to do all of this. So I don't know that this is sliced bread. I think it is. And I think, you know, when folks were working on mRNA therapeutics, when folks were working on whatever else, right? Like a lipid nanoparticles or what have you. The highest and best use of it where it becomes the most impactful and saves the most lives you haven't even thought of yet. Maybe. Somebody else is going to come along go, I've got an application for this that's going to expand human living for another five decades. We might need a COVID that has helped take many companies from where they were to much greater heights, depending on the need. But that being said, I think Johnson and Johnson recently announced that they are interested in peripheral artery disease, which was one of our initial indications. We've made a lot of head headway with dental device companies. A lot of dental companies are device companies, which are much which have a different reimbursement scheme different trial plan. But we've made some inroads there and trying to get them more interested in a drug and things like that. Is there anything else that you want to let our audience know about that you're working on? So I think so these are examples, right? These are examples of cool things that we could potentially do. But what I'm most excited about is what my some of my students in the lab are doing today, which is taking taking structures, taking protein structures and designing new drugs to target them. So let me take a step back. So we have a whole bunch of gay gamers who love playing, you know, your war pass and all these different games. And because of that, the market because of the gaming market, we had so much better graphical processing unit power GPUs graphics cards, right? Yeah. And turns out to run a lot of these computer simulations to doc proteins or peptides or receptors and all that stuff. Those simulations run so much better on GPUs than CPUs, right? So forget these, forget these, you know, large computer clusters, big data clusters or whatever they have bunch of CPU power. We bought these awesome gaming graphics cards and we run process. We run our simulations on that. And we use super, you know, supercomputers and clusters where we run, you know, our computer computational simulations. Anyway, I can get something like fold it on an Xbox. And so alpha, right, alpha fold to all these docking softwares. So we take known structures. We truncate them or we modify them. We mutate them all in silico on computers. Right. And then we synthesize them in the lab and our forte is self assembling peptides. So we attach another domain to it. But essentially long story short. The PhD students that I've just hired now, my hope for them is to come up with an idea and develop a drug all the way to hopefully small or large animal trials within a PhD, which I think is pretty awesome. You know, that that wasn't possible historically like it like now because of the five years ago, it wasn't possible. No, this is amazing. Five years ago, it wasn't possible for the masses. 10 years ago, it wasn't possible at all. Right. Like five years ago, you know, you'd have to be at the right place, know everything. But nowadays, I have high school students who are who have come to me with ideas on how to treat SARS-CoV-2. Right. Because they ran code and not bad ideas, you know, and never get peer reviewed. Yeah. What are the skills now? So the PhDs that you've hired. I mean, this is, you know, bioengineering. So if you're going into, you know, you've got engineering, you've got biology background, medical background. I mean, and now computer science also. So biomedical engineering when it started started with a bunch of mechanical engineers, chemical engineers, electrical engineers and physicians who were trying to figure out how to solve problems. Right. And because of that, if you look at a lot of different BME departments around the country, around the world, they have different focuses, focuses on specific aspects. Right. Like by materials, by instrumentation, by mechanics, that's what we do. Other folks might have more immuno engineering or rehabilitation or some other aspect. But for what we do, you know, yeah, sorry. Yeah, there's a little confused. There's a cardiologist that I met who started out as a medical engineer and took a medical class on the side just to round out his educational a bit, learned about the heart and was like, everything I learned about pumps applies to this and switched careers. And I was like, does heart surgery stuff or whatever. But it was so applicable to the human machine that he just went in that direction. And I think the point was basically by my engineering in general is highly interdisciplinary. And as we go forward, I think there's this huge focus on data science and how we can use big data to solve problems. Right. Because if you I was just thinking about this today, like, if you can get if you can optimize shipping for Amazon, if you can optimize one small process to save 10 cents per package, one cent per package. That's a huge deal. Right. And that's a data science problem. Right, which is why those people get paid so much nowadays. And but if you can apply those kinds of things to human health. Exactly. Exactly. I think those are big changes that that that we should that I would encourage the next generation to look at. Yeah. Thank you so much for joining us and telling us about your work. This is just just fascinating stuff that you're working on. And yeah, good luck on bringing it to market because that's that. Thank you. Can I plug my my lab? That's what I was just going to ask you to do. Yes, please. It's my last. So it's Kumar. Lab dot njit.edu New Jersey Institute of Technology. Kumar lab dot njit.edu. Fantastic. There's links to the other stuff I do there as well. So we'll be watching our audience will too. That is an amazing array of potentials and possibilities. Let's let's get the let's get the funding. Let's get this trial started. Come on, people got to work hard at it. That's that's that's yeah. Yes, let's yeah, keep working hard everybody. And yes, we will have the links to all of these things on our website after we've posted the show. And again, thank you so much, Dr. Kumar. It's been great. Great speaking with you. Thank you for the opportunity. You're welcome. All right, everybody. This is this week in science. Thank you so much for joining us once again for another episode. Of this week in science. If you are really enjoying the show, you know, you can support us because listener support is how we keep the show going. So head over to twist.org. Click on our Patreon link and choose your level of support. Anyone donating at $10 or more per month. We will thank by name at the end of the show. I hope I get to read your name. We really can't do this without you. Thank you for your support. Okay, time to come back now with more this week in science. And it is time for that wonderful part of the show that we love. Blair's Animal Corner with Blair. What you got, Blair? Oh my goodness. I have chemical camouflage. Did you know that exists? Chemical camouflage. I don't know if we've talked about it on the show before, but it's exactly what it sounds like, right? So instead of visual camouflage by blending into your environment or confusing a predator, this is chemical camouflage, confusing a predator via smell. And so this is a study looking at artificial chemical camouflage to save endangered birds. This is specifically to protect them in Finland from red foxes and raccoon dogs. Raccoon dogs are actually native to Asia, but they are invasives in Finland. And they are exactly what they sound like. They look like a mix between a raccoon and a dog, and they are a real thing, so Google it. Anyway, researchers recently tested two different methods for reducing nest predation from these predators. And normally, if you had a predator that was predating a bunch of endangered species, you might hunt them or capture them or try to exclude them from a space where those animals are that they're eating. But in a case where they're everywhere, in the case of red foxes, they're actually native, but their apex predators are gone, so their population has exploded. They're not the top dog, but they are now, so there's way too many of them. They don't have population control. So between too many red foxes and this invasive raccoon dog, the native birds are really feeling the pressure from predators, and so this research wanted to look at two different ways to try to reduce predation without having to hunt or trap these individuals because it is such a widespread issue. It's just not viable at all as a solution. You don't want to influence the populations negatively in the process of doing the research. And it also just, you couldn't do it enough to actually make a dent on the impact to the seabirds. That's how pervasive these predators are. So what they did is they tested two different methods, as I said. The first was to spread waterfowl odor all over the wetlands. So this was chemical camouflage because suddenly everything smelled like birds. So there's no way to sniff out where the predators are. So it was really just confusing. It's like, where's the pizza? In the bathroom? No, that's not right. In the bedroom? No, it can't be in the bedroom. It's got to be in the kitchen, right? No, it's not in the kitchen. It was under the couch the whole time. You'd never know, though, because the whole house smelled like pizza, right? So that was one way to check it. And then the other one was using eggs containing an adversive agent that causes nausea. So they were like, ah, go ahead and eat these eggs, but it'll give you a stomach ache. And then you're going to want to eat eggs ever again. It'll be like that time that you had that one food and then you're right. And you never want to have it again because you have like an aversion to it now. So these are their two tests. And overall, both worked pretty well on the red foxes. Neither really worked on the raccoon dogs, the invasive species. The chemical camouflage worked really well. It decreased the predation of artificial waterfowl by the red foxes. And it was really a significant amount. They also had control sites to test kind of... The researchers would walk around, visit those sites, touch the nests, and then leave and not do anything. And so with all this kind of design, they said chemical camouflage were pretty confident that helps with red foxes. And that also reveals a little bit about the strategies of those predators. Exactly. So it means that red foxes rely on their smell to find bird nests. They think that maybe raccoon dogs just stumble across nests and eat them. So that's why they're not like doing it. There's a nest. I'm going to eat it. Yeah. And so they had good results with red foxes, with the eggs, with the upset stomach ingredients. But it wasn't quite as significant. It wasn't large numbers like the chemical camouflage was. So essentially this is... I have to interject this for a second. I'm sorry. I just had to Google raccoon dog because I wasn't sure what we were talking about. I didn't know that existed. Yeah, yeah, yeah. We were talking about that at the beginning of the story. So yeah, they're from Asia. They're an invasive species in Finland. Yeah, and they just look like a mix between a raccoon and a dog. Yeah. But so these methods could potentially help with vulnerable and endangered waterfowl species. But of course this is one of those preliminary species where ultimately more research is required. So these were all done on artificial nests. So the next step is to go ahead and try these methods with real bird's nests to see what happens functionally in the wild. And from there, they might be able to make some good suggestions for managing these species. But I brought it up because chemical camouflage, I feel like I don't hear about that in conservation biology very often. Right. But these were fake nests though. How did they know that they got everything right for the nests? Great question, right? So there could be a million variables into what makes a nest a nest and they could have missed something which made the chemical camouflage work because they were missing this little bit of genuine article that otherwise red foxes would recognize, right? So that's exactly what they have to move on to the next series and the study where they test it with real birds. So there's a thing that I'm thinking of in the game theory of how this all works, which you ever hear of, you know those little electric bug zappers? That, I don't know where you would buy a thing like that, but you get it, you hang it up and it attracts the bugs and they get electrocuted when they run into this little electrified thing that you hang up somewhere. But I've heard that if you really want to get rid of insects at your house, give it to your neighbor across the street, down the street because it actually attracts more insects to the general area than it is electrifying. So like, is there potential here? Yes, this is where I thought you were going. Yep. Doing the camouflage across an area. So now the predators who are there can't really find the localized prey. So they're going to move on? No, or is it attracting more predators from other areas because the camouflage makes everybody think that's the place to go and then you just end up with more predators and then the numbers start to track the other way. Great for those areas then that aren't being camouflaged because all the predators are like... So that's what you've got to do is you've got to spray all of Finland. The whole country. Make the whole thing smell like bird. I mean it's... Bird everywhere. Once you start trying to play chess with nature you find it's a lot better than you think at the game. It's thinking... It's got a few million, billion years ahead of it. Yeah, it's been working. But I wonder if then you are better affecting eventually better affecting the neighboring un-camouflaged area and if you're actually reducing your effect of the camouflage by increasing the number of predators attracted to an area. I guess it depends on how broad of a... More research is needed. But what if we were really loud about things instead of being quiet Blair? I love this story. This story is all about a researcher who said I wonder if my turtle makes noise. The pet turtle Homer. It was time to put a hydrophone and other microphones up to Homer to see if he had anything to say. This is evolutionary biologist Gabriel Horjiewicz Cohen. There's a J there. I'm not sure if it's a J. Gabriel, he recently had this idea of recording species that we've previously considered mute while he was researching turtles in Brazil's Amazon rainforest. And so when he came home it was time to listen to Homer. He started recording other turtle species in addition. He used a hydrophone or normal microphones. I almost said telephone. That worked too, I suppose. And every species he recorded made sounds. This study is through Zurich University in Switzerland. And he found 50 species of turtles, lungfish, Sicilians, and the subject of the animal quarter last week, all made vocal sounds like clicks and chirps or tonal noises. They might be very quiet. They might only happen a few times a day, but they were all making these noises. So first of all, first of all, step one of this study, all these animals are making sounds that we assumed couldn't make sounds. And of course I was reminded and I couldn't find the episode but I swear in the first year or two I was on this show, I had a story about giraffes making sounds and I said, Mark my words. There are lots of animals making sounds that we assume don't make sounds. Right. So I feel very vindicated. So there are lots of animals making sounds. We have a terrible sense of hearing and we're here like, I don't hear anything. Come on. So lots of animals are making sounds. Now the secondary part of this study is what is bonkers. So they combine their findings with data on evolutionary history of acoustic communication for 1,800 other species to do a type of analysis called ancestral state reconstruction. This calculates the probability of a shared link back through time. So essentially you can through statistical analysis you can find a common ancestor for a trait. So you can, based on what animals have a trait now kind of permutate backwards to find the common ancestor and to say this trait has been around for X million years on this planet. So previously it was thought that tetrapods for limbed animals and lungfish all had evolved their vocal communications separately. It was evolutionary convergence where they all kind of developed it at the same time. Probably there's a lot of expectation about going on to land and like sound traveling different or I don't know. But anyway, so the expectation was that it happened over and over and over. This thing evolved over and over in the animal kingdom. First of all, that is not the easiest answer to this question. So if you're thinking about what's most likely to be the case that seems very unlikely for this many animals. And in fact, in this analysis they found that all vocal communication likely came from the same place. They found what they thought is a common ancestor of sound production for communication around 407 million years ago in the Paleozoic era. So there's this really good idea. Now again, this is all very new information, a newly extrapolated model. And so of course there's some critics out there. And so one of the main critiques of this study is that they may not have done as good of a job as they could of distinguishing between just making sounds and using sounds for communication. Are they popping because they're burping? Are they popping because they're clearing their throat? Are they clicking because they're echolocating? Or are they using communication via sound? And so you really need to drill down and figure out if that's actually what's happening. And I think isn't that kind of a low bar to have to cross? Because even if you're not making a vocalization to tell your neighbor to visit you or to get further away from you if you make a distressing sound your neighbor's going to hear that and recognize that that's a distressed sound or a happy sound like communication doesn't have to be nearly as intentionally communicative as we think it is it's just picking up cues from something else's vocalization or sound that they make it's sufficient for a communication of some form to have taken place. Yeah, no I completely agree and I'm on the side of the main researcher here on Gabriel Horwich Cohen that most animal sounds in the animal kingdom I feel like fit into I'm going to say three categories it's help I'm scared it's I want to make babies right now or it's I'm here and this is my space and most animal communications mean those things so if that's what they mean then they're communicating something to your point Justin so I totally agree with you I think that it is a low bar I think it's likely most animals make noise and it's likely that most of it is trying to communicate something in fact they tried to kind of whittle down and figure out if this was communication or not by comparing video and audio recordings of different species to find matches for behavior different individuals over time they also put them in different groups to see if they had similar noises or different noises depending on who was around them and they really feel like it it hit the criteria for communication but they also acknowledge that some species are really hard to study because they don't vocalize very often and they're shy and so much more study is needed but based on this preliminary look at these animals that are making sounds that we can record and the extrapolation in the evolutionary record it's been around for a long time millions of years within this one group imagine this is vocalization of course it's got to be much older but this is like vertebrates this is vertebrates because if longfisher included along with turtles that is that's everything with a skeleton for sure does it go past that vertebrate sounds that we're not capturing that are similar that have a common ancestor and if you think about if you just look at vertebrates and you think about the hyoid structures and the inner ear and all these things that exist and the the structures that we have had for all of evolutionary history that help us listen it would make sense that if hearing existed that there would be some sort of vocalization I mean even just sensing vibrations sensing vibrations you can get a sense it's sensory what's in my environment what's happening in my environment how am I going to respond to things so before an ear is even developed there's a sensor that's paying attention to those vibrations exactly but this is an interesting study showing these evolutionary links going way way back yeah so listen to your turtles everyone yeah you think turtles are quiet they're actually saying a lot in there judging you hey Justin okay so you've got stories I know you missed a couple of stories at the top of the show but let's get to it what do you want to talk about so one of the greatest potentials of genetic modification is combating diseases caused by abnormal missing or silenced genes one of the greatest obstacles of course is how to do it we can genetically modify mice we can knock out a gene introduce a gene but this engineering is not done in an already living mouse the changes are introduced to embryotic stem cells which then later become the mouse the genetically modified mouse so anyway when we think about genetically modifying humans with genetic diseases we don't really have a way of doing that once the cells are up and running it's too big of a system to have an effect on University College London researchers have found a workaround published in Science Transitional Medicine the researchers took on a rare condition known as CTLA-4 insufficiency so these folks carry mutations in the gene that cause T cells to attack their own tissues and organs including their own blood cells the condition also compromises the immune system's memory so instead of getting a cold and building immunity to it you can catch the same cold over and over and over again it goes down to a single gene actually it's two of the same gene that produce an important protein if one of the genes is faulty if it's misspelled call it there's not enough of the protein produced by the T cells and the condition there takes place so they took human patients this is sort of great launching off of what Dr. Kumar was talking about they took human patient T cells and they did some cutting and pasting via CRISPR-Cas gene editing technique and the researchers were able to basically rewrite the faulty portion of the gene restoring the ability to produce CTLA-4 proteins back to the normal levels so they didn't put these cells back into the human patients because that's a human trial and they're not there yet it's a clinical trial that comes much later but they did manage to try this out on mice CTLA-4 insufficiency was edited into mice and gene editing of the mice from the mouse T cells from the mouse were extracted, modified and reintroduced so currently the strategy for CTLA-4 insufficiency is a bone marrow transplant to replace stem cells responsible for producing the T cells but this is very intensive chemotherapy grafting issues, rejection issues many weeks can be spent in the hospital by doing this version where they're taking out cells manipulating them, editing them and then sending them back into the body afterwards you can go in get an extraction, come back later get an injection and off you go this is amazing so this is one rare gene insufficiency syndrome kind of a condition or protein insufficiency due to a single gene that's missing or not working or miswritten so the research team says that they may have actually may be a proof of principle for their approach that can be adapted to tackle other conditions so when you have specific tissues specific tissues or something like T cells is a great example that can be adjusted edited and then reintroduced as opposed to having to edit the entire human genome right you go into a specific cell type and we know that this T cell therapy is already being used so this isn't entirely new so the versions of that I've seen in the T cell therapy though a lot of the times what they're doing is they're creating a T cell that goes back and just trains the other T cells yeah okay but this is correcting them yeah and this is actually editing those T cells to be genetically to produce a protein themselves differently than they were doing and then reintroducing them so it's truly genetic engineering of human cells so far it's only been demonstrated to be efficient effective on mice but again as we've been talking about you do the you do your lab tests with the taking the cells out and seeing if you can modify them then you do the some day hey maybe it's only in the final but that's for just one condition right so there's so many conditions that if this works they're also saying it's less time in the hospital less expensive actually to do than the grafting therapies there may be a lot of diseases that find an easier, cheaper and then more accessible cure awesome and then at some point we'll just edit before you're born maybe maybe not yeah we'll get there and you want to talk about yeah and then I guess the last story I'll bring tonight is another story from University College London this week takes a look at ancient humans in Britain and in fact the oldest modern human DNA has been obtained from the British is published in Nature ecology and evolution new study that at least there were two distinct groups distinct origins, distinct cultures that inhabited the isles relatively the same time 13,500 to 15,000 years ago so they looked at remains from an individual found in a cave in Somerset which is in the south of England and remains from an individual found in a cave in North Wales which would also be in southern England except it's in Wales researchers found that the DNA from the Somerset individual died about 15,000 years ago indicates that her ancestors were part of an initial migration into Northwest Europe around 16,000 years ago the individual from the I guess Kendrick's cave in Wales is from 13,500 ancestry from a southern hunter-gatherer group whose ancestral origins are thought to be all the way over into the near east which is sort of the Middle East and then migrated to Britain around 14,000 years ago the authors note that these migrations occurred after the last Ice Age when approximately two-thirds of Britain was still covered with glaciers it's the climate war and glaciers melted and the biological environmental changes took place and humans began moving back into northern Europe and they could also just walk to England there's this doggirland this whole area between England and Denmark that was inhabited because the North Sea wasn't there because of the Ice Age and there's actually probably all sorts of wonderful marine archaeology that still needs to take place there so this is the old stone age as well as being genetically diverse these two groups they found that they were culturally distinct chemical analysis of the bones showed that the individuals from Wales ate a lot of marine and freshwater foods including large marine mammals while the humans that summer set showed no evidence of eating marine or freshwater foods they primarily ate land mammals deer, wild cattle, horses so two different cultures, two very different survival strategies the researchers also discovered some cultural differences about the mortuary practices of the two groups animal bones found at the Wales site were decorated art pieces there were no animal bones found there that showed any evidence of being used for food, food prep or rendering of animals so they think this indicates the cave was a dedicated burial site in contrast the animal and human bones found in the summer set cave showed significant human modification including human skulls modified into cups for drinking which the researchers believed to be evidence of ritualistic cannibalism very different very different cultures very different these also aren't the current British ancestors there was large scale migration around 4,500 years ago large population shift again under 400 years of Roman rule Anglo-Saxon, Viking, Norman invasion changed things a lot so little or no trace of these ancient people existing there now even though these two findings are 1500 years apart they found other evidence that shows that they could have been as close as 600 years and that means that there's a potential that these two groups inhabited at the same time and overlapped at some point over those centuries there could be some overlap there although within these groups they are very distinct and they showed no overlap apparently the conditions are terrible in England for this archaeology they don't have very many fossils to look at from this time because it's too wet over there very very damp both of these finds are caves caves are great places if you want to be preserved go to a cave go dying a cave a very dark not damp cave if you're in the desert you've got to build a whole pyramid to make your own cave whatever but if the place has got a lot of caves just go in there when it's time to die or get buried in a hermetically sealed coffin as so many people do so future archaeologists in like a couple thousand years are going to have a field day too many a field day all archaeologists have field days yeah that's true funny funny this is this week in science I have a few stories to finish out our show this evening we love viruses it's our twist of wean episode so let's talk about viruses that have been discovered in the melting Tibetan glaciers oh dear yeah researchers have just published their study identifying an archive of dozens of unique 15,000 year old viruses from the Gulia ice cap of the Tibetan plateau the glaciers apparently according to the researchers formed gradually along with dust and gases and so as a result lots of viruses ended up in there as well and past studies have shown that microbial communities change with dust levels and ion concentrations and all that kind of stuff so they can also get some kind of information about the atmosphere 15,000 years ago when these glaciers were being formed from these viruses which is very interesting but on top of that the researchers are saying that these viruses probably thrived in very extreme environments so these viruses have genes that somehow allowed them to infect cells in very cold environments they so these are like the archaea bacteria of the virus world the team did find that a lot of these viruses were just completely unique they don't exist anymore we don't have any examples of them currently 28 of the 33 viruses they had identified had never been seen before and so while there might be a concern about ancient viruses returning to the earth it's more that researchers are potentially going to gain insight from studying these viruses learning how they lived in these environments in microbial communities were like during the ice ages 15,000 years the ice age 15,000 years ago that resulted in the formation of these glaciers so we can worry about the you know scary halloween side of it but let's look on the positive side so there's more viruses than there are anything else like we also have to just by the sheer numbers game the ones that we've run into that are pathogens exceedingly rare exceedingly rare yes but let's talk about how pathogenic viruses can possibly go even worse you know we talk about horizontal genetic transfer among bacteria all the time we know that viruses interact with bacteria we know that last week there was news of these borg bacteria that researchers have been looking at that have been taking on the genetic components of methane eating bacteria to allow them to be the borg assimilating assimilating yes yes well I had a new paper in nature microbiology researchers at the University of Glasgow were like oh you know it's cold and flu season and people often get double infected with respiratory sensational virus RSV and the flu at the same time and that must be bad but I wonder what happens and so they decided to take a bunch of lung cells put them in a petri dish and then add RSV virus RSV and flu at the same time and instead of just seeing these viruses separately infect the lung tissue what they found is that the virus is hybridized they connected to each other good good good yes and what they found is that it was kind of like a palm tree the RSV virus forming the trunk and influenza the flu forming the leafy part at the top it's the worst tree we have ever heard of so actually it's done in agriculture all the time and I can't remember it's some kind of apple tree that they always start a different kind of tree at the base and then graft on the apple tree at the top so you look across agland and you'll see these trees that have this sort of darker trunk and then there's a line where it's like a lighter trunk going up the rest of the way and that's just a grafting hybridization you have better root system that way the canopy above yeah so the question I don't want this happening we don't want this happening in viruses but you know this is we're in a micro world right so this kind of stuff has probably been happening for a very very long time but we haven't really you know been like oh look huh and now this is obviously an experiment in a petri dish we don't actually know what's happening in human bodies in human cells and so the theories of experiments are what is actually going on because respiratory sensational virus infects different tissues than flu virus does even though they both have some of the same effects that they end up in different places and so the concern is with the hybridizing that they may both be able to have a larger cross the board in the throat the lungs and naval cavities sinus and that kind of stuff so yeah so more research to be done but yay viruses hybridizing scary palm trees scary palm trees yeah scary palm trees woot woot and then tentacles where I know you love interesting weird robots yeah I'm listening yeah so researchers at Harvard school of engineering and applied sciences decided that hey tentacles let's make robots with tentacles instead of robots with hands and so they took inspiration from say like curly hair and they were like yeah and that really like as I was trying to comb my hair earlier today and there were bits of schmutz curls I was like this was to comb curly hair kiki oh I know I know but sometimes you know you start getting the big tangles and you gotta do something about it but yes these researchers have decided to take biological inspiration from the tentacle world and enable robots to be able to grasp very delicate objects and so they now have a tentacle robotic gripper but the thing is it doesn't it's like it doesn't look like those gripper the weird hands that go down and grab toys it's like a scary spaghetti noodle gripper oh that's very strange and scary spaghetti noodle is the best description for sure so they're pneumatic rubber tentacles filaments they're like spaghetti noodles that then twist up like curly hair and grab stuff if only I could pneumatically straighten out my hair so yeah so what it looks like is it looks like this robotic arm I will try to describe what we're seeing with a bunch of hanging wet spaghetti noodles it moves over an object to grab and you think right away no way this is like worse than the claw hand in the thing where you try to get the little stuffed animal out of the it's even worse it's just hanging loose noodley things that's not gonna do anything and then they actuate and they all stiffen and roll up they like stiffen up and they curl up and they just absolutely grab this thing and a whole bunch of it and they're really good at grabbing stuff and it's really kind of freaky looky the really impressive part is the fact that when it releases they all go back to unentangled I wonder how many times it took them to get that they're not tangling up together yeah they don't have any split ends I don't know maybe that or maybe they took that video like that was like the 30th take because I feel like I feel like that would work once and then it would just be too tangly but obviously it's working that was very cool I want to share Kiki the article that you included has an up close picture of the little tentacles yeah let me open that up so it really looks kind of like when you take Play-Doh in between your two hands and roll your hands together to make like a noodle kind of or a log of some sort but it looks yeah it looks like wet and sticky and squishy in a way that from far away it really didn't look like that it looked like wet spaghetti but when you look at it like this it kind of makes more sense that it reacts the way that it does but it still is wild looking I mean is it just like just pneumatic tubes though is that really just it's pneumatic tubes that tangle up and curl up at different points and so when you they curl up yeah yeah is it differences in thicknesses or is it differences in fulfillment organization it kind of looks like just with the picture you showed they're not very uniform looking tubes they're hollow rubber tubes one side of the tube has thicker rubber than the other so that enables the that's a very simple design in a lot of ways really effective creepy tentacle robots coming soon to a warehouse near you I love it and then my final story as we end the show is just kind of an interesting one when you think about as we come up to Halloween and people start putting on their costumes and pretending to be different characters researchers at University College London a bunch of studies out from them this week they published in the Journal of Cognitive Neuroscience and did a very limited study without control groups of a small number of actors but used wearable brain imaging technologies while they were acting as characters to see how their brains responded to them being addressed by their real self and not the character that they were playing and so during the performances the actors heard their own name and they found that an area of the brain called the left anterior prefrontal cortex was suppressed and this is part of the brain that we think is related to self-awareness and the question is like what's happening here is is this a as you play a role have you trained your brain to just like oh don't ignore that ignore that we're not going to do that right researchers are very interested in how the potential theater training could also influence individual autistic individuals who have social deficiencies and have issues with particular social dynamics and how self-awareness actually works in the brain so they're looking at theater and the taking on a new persona which you can learn many methods to do that in theater as a possible new way to understand social dynamics and how people work together and how the brain allows it yeah and they also found in pairs of actors who were doing a scene together they found that they had similar activity in the right inferior frontal gyrus and the right frontal polar cortex and those are areas of the brain involved in social interaction and action planning they didn't see anything involved in like heartbeat or breathing data but specifically the brains of these actors they were expressing self-awareness while at the same time increasing the social planning and activity which again very interesting go play your parts it's especially interesting because in a lot of cases I feel like in most cases actors have learned lines and so if you just learned your lines and you are just repeating your lines back it doesn't really matter what you respond to or what you call people because if you're just doing your lines back and forth that shouldn't take that part of your brain at all so this is like an interesting piece of that where it's not just that they learned their lines it's that they have internalized that they are this other character with a different name you hear about it a lot from method actors that they once they've immersed into a role that they're playing they have a really hard time turning it off they kind of stay in that mode the entire time that they might be on the set of a movie, they might be at home they only want to be called that name yeah there's a lot of examples of this anyway but it makes me wonder then if there isn't also for post traumatic stress disorders could you get better living through method acting if you can separate your own self-awareness of what you're experiencing by playing it it'd be very interesting to see theater and science come together to try to super fun right arts do need to be arts do need to be part of this yeah so for the rest of today I only want you to call me Oscar alright grouchy, whatever have we come to the end of the show did we do it? everyone thank you so much for joining us for another episode of this week in science it's just been wonderful to spend this time with you to have you spend this time with us and want to thank once again Dr Vivek Kumar for joining us and for the great interview wonderful conversation about his work in biomedical engineering learned a lot from he was very well spoken really enjoyed speaking with him that was great time for shout outs thank you to Fada thank you so much for help with show notes and show descriptions and social media and for recording the show every week thank you so much to Gord and Aran Lor and others who help keep our chat room a happy shiny place to exist and also Rachel thank you so much for editing our program and to our patreon sponsors thank you too Teresa Smith, James Schaefer, Richard Badge Kent Northcote, Rick Levin, Pierre Verlesarb Ralphie Figueroa, John Ratnaswamy Karen Tauzy, Woody M.S. 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With a simple device I'll reverse global warming with a wave of my hand and all is coming your way So everybody listen to what I say I use the scientific method for all that is worth and I'll broadcast my app. This Week in Science This Week in Science Science This Week in Science This Week in Science Science Science Science Science Science Science Science Science I've got one disclaimer and it shouldn't be news That what I say may not represent after sure Blair's gone batty No Jeez a gone Oscar the Grouch And I think she's showing us Legos. A batty Lego Very cute And then here's the cover so um do what's going behind him. But ultimately, here's my chocolate horn frog for the cover. So, hopefully we'll be able to get pre-sales up really soon. I should have a cover image for you and a price by this weekend. Okay, awesome. Yes. And I only have a few more left. I'm almost done. Oh my goodness. The calendar is coming everyone. The calendar is coming. Down to the wire always. It's hard to be creative on a schedule. I have to do it now. Make this many arts in this amount of time. Yes, Anthony. Yes, we are doing the calendar. And that's what Blair is working on right now, finishing her special designs for this year. It's coming. It is coming. Lego based everyone. Every year, Blair does something new artistically. And so this is the Lego year. Hey, Dana Pearson. Thank you. Yeah, hit the like. Science freaks. Hitting the like button is very helpful. Oh, I was going to do this, but I wasn't sure if it was going to mess up our YouTube permission. So I waited until the show was over. What are you wanting to do? Hold on. We're still on the air. I know, but there's, you'll tell me and I'll turn it off right away. Okay. Here we go. Come on. Everything takes so long. There we go. Are you sharing it? I changed my background. Oh, you did. There you go. I'm on Sesame Street. You're on Sesame Street. Okay. I was like, I don't know. Our background's copy written. I don't know. I don't know. I don't know. I can't say. I don't know. I downloaded it. It was shared on Sesame Street's Facebook page for people to use. That seems fairly open public domain. Thank you, Sesame Street. I wanted to wait just in case. Yeah. Anyone who was wondering why Blair and I were in a costume and Justin isn't it? Justin is Justin and Blair is Oscar the Grouch. Scream. Scream. And I'm Spider Gwen. There you go. Are you wearing ballet shoes? You'll never know. I'm method acting as a normal human being who interacts with other human beings on a planet. What's your character's name? I call him Justin. Got it. How'd you prepare for this role? I studied human television from space on my way here. It's all we had. Just constant broadcast television and radio. Justin is cosplaying as Warmbo's friend. I like Warmbo. Warmbo seems like a good guy. I think I would get along with Warmbo just fine. Warmbo? Warmbo is a puppet character on a different podcast who I think is underappreciated on that show. I think we'd have better chemistry with Warmbo here, but I could regret that quickly. Although in some ways I feel like I am the Warmbo of the show too, so it might be. I'm so confused. What is Warmbo? Cody's Shoddy. It's from the news daddy. The news daddy? Well, no. Okay, worry about it. So yeah, some more news I think is one of the shows. Oh yeah, some more news. TV jokes. Yeah, I like it. It's one of my favorites. Justin is Orson Welles. This is like, I can't even find it via Google. How is this a real thing? It's just look at it. Look it up in the YouTubes. It's in the YouTubes. Yeah, go look in the YouTubes. Some more news. But there's no, like it doesn't seem like Warmbo has a Wikipedia page. What? Warmbo? Warmbo doesn't have a Wikipedia page? See, Warmbo is being underrepresented on this other show. But I do recommend it. I think it is my, it is definitely, it's a show that reminds me of, it's news done from the point of view of an extremely exasperated host, News Anchor. Which is most of us now. Yeah, which is very reminiscent of sometimes what it's like to do, to talk about things like climate change on this show. We're like, why is this still not, how is it not being, oh yeah, it's because money. It's hilarious and it's a fun show. For adultish audiences, I don't know, I would send my young children there to watch it. Yeah, would you send your children to watch it? Yeah, I would, but I, do we trust Justin's parenting advice? I would, but my kids are also pretty, pretty tough. Your kids, yes. Yeah. They're your children. The, the, the, by the way, I will also give that show props for a episodic time travel shows that they did, which were spot on brilliant. Awesome. They were just fantastic. Yeah. Anyway. Good night, Fada. Yes. Go watch, go stay up late and watch your shows. Blair, yeah, Blair, don't give them a hard time about it. That's funny. I'll continue to give you a hard time about it. You can watch it tomorrow instead of staying up till midnight, is all of it? Yeah. Well, speaking of going, I am tired. Oh no. Okay. Yeah, I'm tired. I'm tired today. Well, if you're tired, that means it's time to say good night, Blair. Good night, Blair. Say good night, Justin. Say good morning, Justin. Good morning, Justin. Good night, Kiki. Good night, everyone. Thank you once again for joining us for another episode of This Week in Science. We hope that you will come back again next week. I'll be out of this hood that won't stay on my head that I'm fiddling with. Yes. It's time for morning. It's time for night. Stay safe, stay healthy, and stay curious, and we will see you again next week. Thank you so much once again.