 for the internet. Sometimes you have to wait for the internet to help you out. Hello, everyone. This is This Week in Science. This is the live recording of the TWIST podcast. If you're joining us live, we're so glad that you're here. Just remember, if you're watching this in video, that means this is the completely uncut, unedited version of TWIST. If you like the nicely edited, a little bit shorter version, then make sure you sign up for that podcast of ours, because that's, you know, that'll be out after the show. Okay, are we ready, everyone? Yeah, there's a bunch of mm-hmms and knowing, knowing nods, okay. All right, everyone, going live in a three, two, this is TWIST. This Week in Science, episode number 793, recorded on Wednesday, September 30th, 2020. Better know a virus. Hi, everyone, I'm Dr. Kiki, and tonight on This Week in Science, we will fill your head with Neanderthals, consciousness and disemboweling, but first. Disclaimer, disclaimer, disclaimer. The following program contains civil discourse. That's the thing where one person speaks while others listen, and then that first person stops talking and listens as somebody else talks. There may be occasions where more than one person is talking at once, largely due to enthusiasm for these subject matters being discussed, but we will try to keep that to a minimum. A informal, loosely formatted and completely unmoderated conversation is expected, and while no ground rules have been agreed upon, at no point will you hear anyone attack anyone else's character or belittle their intelligence or besmirch someone else's family members because even without rules and moderators, people can be well-behaved and interact in a civil matter like adults or children even. I'm pretty good at that too. We choose to be civil. We choose to be civil with one another on this podcast and not say the bad things, not because it is easy, but because it is hard to listen to people talk when they aren't being civil. So all you really need to do, it's really actually easy to be civil. All you need to do is listen to This Week in Science coming up next. I've got the kind of mind that can't get enough. I wanna let it happen every day of the week. There's only one place to go to find the knowledge I seek. I wanna know what's happening, what's happening. Good science to you, Kiki and Blair. And a good science to you too, Justin Blair and everyone out there. Welcome to another episode of This Week in Science. We're back and yeah, let's be nice to each other and talk about science. I mean, I do have to say it's one of the reasons I love coming back to this show week after week, getting to talk about science and have fun with my friends doing it. It's just really, really wonderful. And I hope that you all keep coming back for the fun and civility and the science. And the science, yes. All right, what is on the show tonight? I have some stories about trust, a helpful virus and bird brains, as you know I love them. Yes. I know you love them. I have, yeah. Wait, wait, wait, we also have an interview. We have a guest, hello. Yes, hello, we have a guest. We're gonna talk about viruses tonight with our guest, Dr. Efrain Rivera-Serrano. And now, Justin, what did you bring? Oh, I have, adding up the universe. I have vape juice hot take. Nature finds a way. And Neanderthals. Nice, always love the Neanderthals. I love, like you love brains, I love Neanderthals. Yeah, you know what I love. What's in the animal corner? Just some inspiration and also some fireflies or lightning bugs, which I'm obsessed with. And then I also have a really quick story about clave juice. About what? You know, it's a little thing, it's something to be concerned about. It's like, no, the number of days, but it's still, it's kind of important. So, just a little. Yeah, kind of. A little baby, yeah. All right, well with all these stories and a wonderful interview coming up, I would like to remind you, as we jump on in, that if you have not yet subscribed to Twists, you can find us all places that podcasts are found, Spotify, Spreaker, Pandora, Radio.com, Apple, Google. Just look for this week in Science. We're also on YouTube and Facebook and Twitch. You can also find information about the show at twist.org, T-W-I-S, dot-O-R-G. All right, so now let's dive into some of that aforementioned science. Want to talk about trust? Uh-huh. Well, let's talk about trust in science. How does that sound? I trust science. I trust science and, well, good news. A new Pew report, research survey. Yes, it's a great institute that has done many surveys over the years, and they survey public ideas on about, or how public feelings about trust. The survey, the new survey is out now. They looked at 20 global publics. That means they went to a bunch of different countries. They surveyed. Yeah, they surveyed. Going to other planets? Yeah, nope, nope. Just different countries, different, yeah. Looking at how different people in different countries look at science or how they think about it. They surveyed more than 35,000 people to find out those public attitudes on science. So let's talk about us. I mean, the US, yes. Oh, that's the one I was afraid of. Is that like US Weekly or US Weekly? I never can tell. It's sad, but that's the one, when you started talking about this, I'm like, oh, hopefully they left this out. Like they at least did one more. If you don't include the United States, it's looking great. Actually, and let me tell you, actually it is overall looking great. Public trust in science in the United States is looks like it's on a slight upswing, but it's not huge. I mean, it's always kind of been around 40% or so of the public. And we sit at 38% of the US public who have a lot of trust in science. As a group, about three quarters of the United States, 77% have at least some trust in scientists to do what's right for the country, at least some trust. And this is great because the views here in the US are pretty similar to other global publics everywhere else. We're right around the median actually for the amount of trust in science or scientists. We're not the worst. We're not the worst. In something. Right. Exactly. Where it breaks down is in the area of politics. And when you break Americans down by partisan identification and political ideology, 67% of Democrats have a lot of trust in scientists. 17% of Republicans do. So the ideological divide is huge. This left-to-right ideological divide is really strong in the United States, but it's not alone. Australia, Canada, the UK, Germany, Italy, many other countries also have similar political divides. The one thing that Democrats and Republicans are aligned over, however, is the value of being a world leader in science and the state of the United States in scientific achievements. We want to be the best. We think it's the thing we don't trust. Everybody's okay with that. And across the board, the two groups value investing money into scientific research. So I think the take-home message is there is trust in science. So the war on science is not as broad as you might think. However, there have been ideological divisions that have been played, certainly, and taken advantage of. And so there's work to be done in terms of science communication and building that trust across the board. Anyway, take-home. That's my take-home message. Yeah, I was looking at the Rice University Moonshot speech by Kennedy, as I occasionally refer to in my free time. And there's an interesting comment in there where he's really talking about science leading this next step for the United States as being a country that's going into this new knowledge. And as we gain this new knowledge, we're going to be showing more of our ignorance by exploring these new fields. One of the interesting things that caught me there is he says that today there are more scientists alive in the United States than at any other time in our history combined. And that it is doubling the statistic, he might have made it up, but I think I kind of trisk it. It was doubling at a rate, the number of scientists working in the United States was doubling at a rate 12 times the population growth of the United States. So there was this time when people were really on this press was being excited about it. And people were running droves to become scientists. They were really teaching this next generation to prepare for a future that was going to be science-based, which is how we got here to the modern age that we are in now. We got here through science. And the idea that there could be that much of the population that doesn't trust the thing that worked over the last 70 years, it's mind boggling. And it is mind boggling, but it is where we are at the moment. But interesting point in case anybody was wondering whether or not trust in science around the globe correlates with the prevalence of COVID-19, SARS-CoV-2 infection rate, it does not. So countries that have like India that have very high trust in science have a pretty high infection rate. And when the United States is not alone in terms of its infection rate and trust in science. So it seems to be a mixed bag. Well, trust and understanding are different things. And there's also the India, there's the huge confounding variable of like population density. Population density and infrastructure and things like this. Yeah. Yeah. So the trust is there, but there are still public health issues at play. There are a lot of variables at play for sure. But good news, it ish. I mean, there's work for science and science communicators to do for sure. So I couldn't see that chart. I don't know if you still have it up, Kiki. Can get it up. But if we only counted, if we only counted blue America, where, where are we? Are we ranking? Are we ranking higher? Are we up towards? Are we at the top? If we just ignore. Oh. Red America. We're at like 68, right? Right. 67%. So yeah. Which would put us if we only counted. Well, I'm just looking for a brighter spot. All right. Where are those infections happening? I guess. Yeah. We only count. We're actually doing fantastic. We're number one again. I see. I seem to remember somebody saying that we should only count some of the states anyway. So anyway, while we're on the subject of counting. How much matter. Justin. How much matters in the universe? I want to know. Do we know? Yeah, we do. We have the most accurate count. Scientists at the University of California Riverside, they just finished a very exhaustive task of accounting for every bit of energy in the universe. Let me guess. It's something to do with like Avogadro's number. I know it's California. So I'm sure Avogadro's got involved at some point. According to, this is an astrophysical journal. The team determined that that matter makes up 31%. 31.5%. Give or take 1.3% of the total amount of energy in the universe with the remainder consisting of dark energy. So 31%, that's not a bad number. This is quoting lead author Muhammad Abdullah. He says, to put that amount of matter in context, if all the matter in the universe were spread out evenly across the space, this is the physicist creating the spherical cow that we've talked about. Taking that spread out across the entire universe, it would correspond to an average mass density equal to only about six hydrogen atoms per cubic meter. So it's a very undense universe still. However, since we know that 80% of matter is actually dark matter, in reality, most of the matter consists not of hydrogen atoms but rather a type of matter which cosmologists don't yet understand. There was a graduate student at UC Riverside Department of Physics and Astronomy. So of the 31.5% of the universe's energy that is from matter, only 20% of that is the stuff that we can see and interact with. So very small amount. Now we're down to that one hydrogen atom per cubic meter. So one of the ways that you can determine the amount of matter in the universe is the number of galaxy clusters. You look at those and you weigh them. Higher percentage of matter would result in more clusters as it says. But it is difficult to measure the mass of any galaxy cluster accurately because most of the matter is dark and we can't just look at it with our telescopes. To overcome this, the team developed the gal weight system, a cosmological tool used to measure the mass of gals at the county fair. Ladies, guess your weight in you. Win a prize. What? Nope. No, gal weight. Gal weight is actually for a galaxy weight. Okay. There we go. A cosmological tool to measure the mass of a galaxy cluster using the orbits of its member galaxies. Quoty voice of Gillian Wilson, professor of physics and astronomy at UCR. We have succeeded in making one of the most precise measurements ever made using the galaxy cluster technique. Moreover, this is the first use of the galaxy orbit technique which has obtained a value in agreement with those obtained by teams who use non-cluster techniques such as cosmic, microwave background and baryon acoustic oscillations, type 1 supernova or gravitational lensing. So they created this model based on all these different looks of galaxy clusters that they could observe throughout the universe and they put them, compared that with a simulator that said, okay, well, if we had more matter, what it would look like, if we took away matter, what should that look like? And then they took their result and compared it to a bunch of other models that had already existed and they found, wow, it's overlapping. It's matching. So great confidence in their result and they believe they've come up with the most accurate measurement of energy in our universe. I think that's exciting. I mean, it's such an abstract concept. We're sitting here in the middle, or off in the edge of our galaxy in the universe and the idea of being able to actually calculate from our vantage point the total amount of anything in the universe. It seems like a very abstract concept in the fact that we are developing technologies to be able to image what's out there, to be able to see things better. It's really exciting getting better understanding of what's out there. More avocados, I mean avocados. Hey, Blair, you got to talk about birds now. Yeah, birds and climate change. It's bad news, guys. Oh, great. There's a whole universe out there. Well, Max Planck Institute of Animal Behavior in Cornell University worked together to look at temporal changes in birds. So kind of a synchronization problem is pretty common with climate change and animals that have kind of seasonal patterns. And so they were looking specifically on decades of data on weather, food availability and breeding and tree swallows. And they wanted to see what that did to timing of when to breed and when food is available and when kind of weather takes unexpected turns. And all of those kind of things to make a happy, healthy tree swallow population, they're getting decoupled. They're kind of, they're spreading farther apart. So this is what happens with climate change, right, is that it gets warmer sooner. That means that trees blossom sooner. That means that bugs who go to those trees, to those blossoms come out sooner. And then food is available sooner. And then tree swallows will say, great, it's time to breed. But then a couple weeks later, you can get a cold snap because it's March, not May. And then all of those bugs disappear because it's cold and there's nothing to feed the babies and the clutch can actually die. So this is kind of the big problem with this decoupling of seasonal expectations. And so they looked at the past 30 years of data and they found that over the last 30 years, the breeding of these tree swallows would be three days earlier, every decade for those 30 years, which doesn't sound like a lot, but it can add up. And even 10 days, even nine days, can make a difference in food availability for those babies as they're growing up. And they did find also that earlier hatchlings were at greater risk of exposure to inclement weather, which also reduced the availability of flying insects as well. So there's all these kind of dominoes that can fall as a result of laying eggs too early. And so this actually, the reason this is interesting other than just like, oh man, birds are screwed, it's also, it actually explains something that we've seen historically, which is swallows, swifts, flycatchers, nightjars, other aerial insectivorous birds are declining faster than mathematical models would expect in North America and Europe. And this is probably why it's because of this kind of exacerbated impact on the population because of decoupling of these environmental cues. So kind of having babies earlier in the spring, creating cold snaps, less availability of food, and that creating less survivability of chicks. So this can help us predict what can happen to these species in the future. And it's just another reason to kind of turn our sights back onto climate change. So, you know, it's a good reminder when we're in this COVID panic all the time that other things can kind of fall to the side, but especially with an election coming up in the United States, it's a good reminder that climate change is ever present and the decisions we make now can affect birds so it's a reminder. Yeah, because I think we're not going to be able to have enough bird training programs. No, no. And we also can't go grab all the eggs and put them in an incubator and then release them back in the wild. There's just not enough of us. Yeah, the human intervention on the animal side is limited. So yeah, we got to act on the climate change side. Yeah, we do. Well, speaking of, well, not climate, just the earth, we have other issues, plastic being among them. We love our plastic. There's a lot of it on the planet. How are we going to get rid of it? What are we going to do? Well, last year or 2018, actually, there was an enzyme, an enzyme that was discovered in a bacterium that naturally degrades plastic. Yeah, this enzyme, PETase, because of PET plastics, the the PETase is the enzyme that breaks down these polymers of plastic. And what these researchers just publishing in the proceedings of the National Academy of Sciences have found is that when they mixed PETase with another enzyme called m-hetase, which is a monomer hydroxy, blah, blah, blah, something is, and they found they doubled That's actually the name. They got lazy in the middle of defining it. blah, blah, it's fine. And then they did the experiment. It worked. They're like, we're stuck with the name. No, no, no, they're not. So when they added the second enzyme, doubling the enzymes, doubled the fun or actually doubled the digestion speed of the plastics. So what they found is that they were able to speed up the whole digestion process and what they are hoping to be able to do with, here we go, the PET polyethylene terphthalate deconstruction that is added to the monotoo hydroxyethyl terphthalate, that's the m-het, this double enzyme system. There we go. I got it. That by adding them together that they can hopefully develop a plastic recycling system where we will be able to take types of the PET plastics, turn them into PET monomers into monomers of plastic and recycle them into other types of plastics. So that's the idea. Someday recyclable plastics and hopefully according to research like this out of the center for enzyme innovation at the University of Portsmouth, we will get there. I think that's an important distinction just that I want to mention is every time we talk about digesting plastic I feel like we're still talking about breaking it down into tinier plastic, which in this case it's the tiniest I think we've discussed because it's getting down to the monomers which is really really great. Those are the little building blocks of those plastics. It's not quite the same as the polymers which are much more destructive to the environment. There's still things that we would then turn into new plastics. It's not like it's brought down into natural components that we could just release into the world. It's not like taking a cheese grater to the plastic or finer and finer grater and just making smaller and smaller and smaller polymers. It's taking it to the building blocks. It's like okay. If you're a 3D printer somebody who likes to make things you could make something, degrade it, recycle it and then make something again if you have these monomers that are available to you. Justin, you got your hot take now? Yeah, the hot take. This is a result of a vaping study have shown that significant lung injury can occur but it might not be the vape juices fault. Back off the CBD gummy gasm. Don't blame the cosmic cotton candy THC. It might not be the ice cream nicotine cookie dough oil that has been causing severe lung injuries because the materials used in the heating elements of some e-cigs and e-cig devices contained nickel chromium alloy heating elements that are now being thought to be the culprit of all the severe lung damage that we sort of saw spike in 2019. Nickel chromium sounds like a pretty bad combination if any of that is something that you are inhaling. Apparently. So the findings, they say I would know. It also sounds like a really bad band. Honestly, if you describe the material makeup in this form of anything we ingest or interact with, it all sounds bad until you're like, oh, that's salt. I get it now. It sounded like something really gross. Anyway, the findings were consistent in this with or without the use of nicotine vitamin E oil, THC oil which had been previously thought to be contributing to these respiratory problems. The early results published in the Journal of American Heart Association by researchers from the University of California Irvine School of Medicine and the Huntington Medical Research Institute were observed during a much larger study where they were exploring the effects of vaping on the cardiovascular system. While they were conducting this experiment, they observed the associated lung injury immediately after changing out their vaping devices. So it was a bit of a fluke that they even discovered this because they were doing this research and they actually weren't seeing, this is a year long study, they weren't recreating the severe respiratory problems that people had been experiencing. At some point, the device that they were initially using to do their testing went off market and they got a substitute device that was and immediately they saw the, there was, let's see, within an hour of beginning of the experiment we observed the evidence of severe respiratory distress including labored breathing, wheezing and panting, says Michael, claiming PhD professor of occupational environmental medicine at UCI School of Medicine. After analyzing lung tissue from subjects in the study, we found them to be severely compromised and observed other serious changes such as lung lesions, red blood cell congestion, obliteration of alveolar spaces and pneumonitis? Pneumonitis? I don't even know in some cases. One problem. What had happened is the old heating element that they used was stainless steel. No problem. The new one had the nickel chromium alloy immediately problems in their test. Yeah, one of the other interesting things is so there's still there's still warnings on the vaping isn't really all good for you. That's not what this is. Putting anything into your lungs other than just air isn't good for you. Oxygen at its base level is rusting you, but your lungs they help you extinguish gas. Anything, smoke or anything in your lungs is not good. Exactly. So this is definitely not a you should do this. It's safe. However, however if it's the thing that you're doing to combat being a cigarette tobacco smoker, maybe there's hope that this can be a thing again. Research is aimed to study the impacts of breathing the vapors from these cigarettes on heart function and a well established preclinical experimental model, but over the course of nearly a year none of the subjects exposed to vapors from the stainless steel devices with or without additives contracted respiratory distress and only one of them showed a less than 10% area of inflammation in the lungs. So the preliminary studies need to be followed up with additional studies to systematically try to determine the cause of the lung problem what's taking place with this particular heating element. But vaping by itself has been proven to cause increased blood pressure endothelial dysfunction and risk of mitochondrial infraction and stroke even. So it's not all good news for vaping that's not what this is. However, one thing I thought was interesting is there is a condition that has been called e-cigarette or vaping product use associated lung injury, e-valley which is recognized in the United States back in 2019 when there was like people were dying from this. It was kind of horrible. There was like a rash of this that seemed to all hit at once or at least hit the news all at once. What's interesting though is that was a runway it peaked around the same time when they changed out their device and got this new one with the nickel chromium. So there may have been an association there looking back that they're going to try to investigate as well. But one of the interesting things too I find is that they have said that people who vape have higher chance of contracting COVID. Yeah. However, the cigarettes and cigarette smokers are smokers in general. The symptoms of e-valley the e-cigarette or vaping product use associated lung injury mimics features of COVID 19 pneumonia. And so without testing if you had a patient who came and presented with these symptoms they might get classified as COVID even if it's this because it would look the same. It would present the same to a doctor. Interesting. So that also has to be looked at like are these, is there a higher instance of them actually contracting or is it this is the cause of this lung injury and now that means the study is still ongoing. This is a preliminary result but the reason they pushed it out so quick is they wanted to give a heads up for the vaping industry which is still a thing. Fix your vape pens. Hey, here's what we found. Yeah, get that out of here. Get that out of here. We're still studying but we have such a strong hit for this heating element. It's worth taking it off the market. And for it to be done before whoever regulates the VDA probably it can self-regulate the self-regulated industry. Here's this thing we found that might improve your product and help keep it from killing people. Very cool. Very cool. Speaking of helping and not killing I have a virus story but it's not the dreaded pandemic virus. Oh, no. This is a micro fungus. That's right. I mean a micro virus. I have to say the words right. Sorry. I will say the words. Live program. Words come out. Not ripped. Blah, blah, blah, blah. Micro virus. Fungus. Sclerotinia Sclerotiorum Sclerotinia Sclerotiorum This is not Harry Potter Wizarding World. This is a fungus. It's normally pathogenic to plants that it infects and more specifically it's necrotrophic. It's going to suck the life out of a plant. There's a study that was just published September 29th in the journal Molecular Plant in which the researchers infected Sclerotinia Sclerotinium Sclerotiorum. I would never get the thing to hover if I were a wizard. They infected it with a really small DNA micro virus. It made the fungus switch from being pathogenic to being a helper. The viral infection of the fungus led the fungal infection to help the plant grow faster and to improve its defenses. So it was better for the fungus. In the words of one of the authors the fungal virus might be a good thing for the fungus because the fungus now recognizes the plant as home instead of killing it. The virus turned a foe to a friend. Which I think is such a fascinating turn of events when it comes to biological interactions. When is a fungus a friend? When is it a foe? We know that there are lots of fungal interactions in plants in which the rhizomes in plants are going to help nitrogen fixation. This helps plants grow. How did these relations come to be in the first place? Did they happen because of a virus? Did they happen because of something like this micro virus? Are there other interactions that have changed the evolutionary trajectory of fungal individuals? I think it's fascinating. Not just fungal individuals. Everything. I was about to bring it but they found that mice pheromones originated from a portion of a gene that's used in blood cells that they think a virus a CRISPRid virus might have gotten in and tweaked and basically led to eventually the pheromone scent that mice use to communicate. Viruses do this sort of have these interesting effects. Did you just use CRISPR as a verb just to generally mean editing that would put a gene inside of another gene? No. I literally meant bacteria that broke down a virus and remained and reinserted. That's where CRISPR comes from. I was just wondering if that's how you were using it or if you were using it like Xerox. If you explained it long form bacteria have this way of breaking down a and then nobody was like oh that's also CRISPR? Yes. It's an accelerant sometimes to evolution and how it plays out in living things. So there's evidence that mouse pheromones were developed that way. Fascinating. They somehow track the origin because the sequence of the pheromones is a sort of grabbed from a portion of the gene that makes hemoglobin repeated in this weird way. And then it's something to do with also using a pathway that was once used for venom and also an ancient ancestor. It's like this whole hijacking of junk DNA that the mouse might ended up with a pheromone and it's stinking. We can use this. This means friend. I know that smell. Now you're my friend. All right. Oh thank you biology. The complexity is beautiful. If you just tuned in you are listening to This Week in Science. If you're interested in a twist shirt or mug or other item of twist goodness head over to twist.org click on our Zazzle link and browse our store. We have all sorts of twist items available for you to enjoy and that will also help support the show. So you can shop knowing that you're helping us out. Now I would love to introduce our guest tonight Dr. Efrain Rivera Serrano is a cellular biologist. He's interested in viral host interactions. He left the laboratory as of today for adventures in the world of science communications and is also working as social media specialist for American scientists. He also has many dogs. I do. Welcome to the show. Thank you so much for joining us tonight. No, thank you so much for the invitation. I'm really excited to be here and talk about my favorite topic which is, well, literally it will be dogs but after dogs it will be the viruses. We're not talking about dogs today. Not today. We can talk about dog viruses. No, we will talk about the viruses. So how did you get interested in viruses? Where did that interest come from? So I actually I think this links back to the story the last story that we're talking about because I actually started my journey studying plants. So I started Groutful with the thought that I was going to get a PhD in botany. So another grad. First I wanted to go to med school and then I fell in love with plants. That didn't work out. So I left for the masters in plant cell biology. And I didn't want to leave science just yet. So I started networking seeing what my other avenues will be. Leaving a program and then restarting again in a different field was definitely challenging. But I was lucky enough to be welcomed in the biology community. And that's really what I love about most of the virologists out there that they're just very welcoming and they're willing to teach you their way. So I joined a PhD program in biology. I was lucky enough fortunate enough to just have that East transition from studying plants in a herbarium to studying viral infections in the heart in mice. I loved it at first. I actually started rotating in different labs and that was my first one. It was a virology lab. I just cancelled all the other rotations in grad school where I just said that that was for me. When I was at any meeting the community were just so welcoming that I said like this is my place. So that I continued studying viruses for my post PhD and a couple years later and until today. That experience of going into rotations when you start graduate school some graduate programs require you to do rotations and others you can come in and just work directly with an investigator. I always think that those rotations are really important because you don't just learn a different skill to bring a different window into a different area of science. Yeah, definitely. And to me, again, I came to study viruses with a mentality of studying cells, albeit in plants, but just how cells work and that was my background. And just again, after talking about viral cells interactions just wishing your mentality and seeing infection from the federal side and less so from a viral centric side and being able to switch us around gives you a different perspective and just like any issue in diversity in real life. Yeah, so yeah, let's talk about that for a second. The perspective of the from the virus we all we know, okay, there's a virus. It's going to attack the cell. It's going to get into the cell. It's going to use the cell to replicate itself and then it's going to kill the cell most often. How do you how do you flip that around and look at it from the perspective of the cell itself? Yeah, so you can imagine. So when I'm teaching this I would say like imagine your cell as this is your house. This is your you know your happy place. And if someone is trying to break into your house, I always hate the story from the again from a viral centric side that the virus just comes in and does all this and the house explodes. But in reality, there's a lot of things that are in your house that are protecting you, right? We have walls. We have some people have alarm systems. We have weapons. We have and the cell is no exception. So I think the moral of a virus comes as this explodes and moves on is a very simplistic way when as soon as the virus enters the cell, there's a whole lot of things that the cell does to try to prevent that the cell is not a biosender it just reacts. I spent a lot of years just studying those quote-unquote canonical pathways. So like things that essentially almost cell in our body does that it's not special to our immune system but how are cells really responding and there are differences in different tissues and whatnot. But at the end of the day if someone is trying to break into your house there's a lot of things that are going to happen. You're going to have an alarm system. You're going to call 911. You're going to call for help. Maybe the neighbor's going to come help you and nobody's no exception. Except that sometimes the virus gets in and then you just walk past the living room, it's there on the couch and you're like okay you should go. No, but again again by the way And I'm going to clone myself like a hundred times this morning and so I hope you have enough coffee. Yeah, no, but again, I think in biology that's also another issue that we face that is that we tend to think very individualistic, so that same burden or you might not be able to stop it the first time, maybe it came and rubbed your house, but if you can let the neighbors know and call 911 you're preventing it from infecting others. So sometimes it does happen and the virus comes and if it infects it, I mean actually it's almost always because that first infected cell if it's not able to, it's very unlikely that it will just stop the virus right in. Almost always what it's doing is preventing it from spreading. So you might be, that burger might be breaking into one house in the neighborhood, but the whole problem, the key in the biology is to protect the host. It's fine if you lose one cell, it's not so much if you lose a whole tissue or an organ. Right, so how do, what kind of differences have we discovered in different tissues and how they respond to viruses? Is it like the same across the board? They just, this is, I'm the liver and I respond this way, I'm the heart and I respond this way or is it virus specific as well? Yeah, so you can, any different permutation that you can come in a matrix, there's a different, something different that can happen from a virus perspective, from a cell perspective, from and not just in an organ, like a liver has different cell types and each one of them behaves differently. So, and that relates not only to their genetic makeup, so like what proteins do they have, but also their kinetics, like some organs respond really fast. So you can imagine there's a lot of different star body just like what we're saying, as we're seeing here in the image, we can get exposed by microbes by essentially every route that you can imagine. And right now, as I'm sitting here, I'm being exposed, there's stuff coming on my skin, my skin itself is a barrier, I'm breathing in, there's stuff coming into my lungs. And so this is what happens, essentially, all the time, every time that you breathe, every time that you eat, this is happening. But almost always, our body does a really good job and that's the part that we sort of neglect. We tend to focus on the time when we get sick, but not every day that we're not, because our body is really good at it. So it's not the half, the glass half empty half full depends on how you see it. But yeah, to answer your question, yeah, there's different, there's, viruses are very different from different families, their genetic material is different, our cells are different, based on how the virus is in its genetic material, whether it's DNA, whether it's RNA, whether it's circular, whether it's senior, whether it's all those determine the type of response that our cells will have. And so our cells essentially have evolved in ways to recognize anything that our body would not normally produce. So if you come for a virus, for example, and I have here a cartoon, you can imagine a virus sort of like, I think it might have a gene in a lamp, where that gene is protected into a protein shell and the gene is the gene being the recipe to make more viruses. And so it cannot really, it needs a trigger for that gene to come out of the lamp and the lamp being what we call the captive. And so viruses have evolved to release that gene only once it is inside the right cell. But once that happens, our cells just know, okay, the gene should not be here in the cell. Let's start trying to stop it because we know what's coming. And so that's sort of like the general thing that happens. And as the gene just tries to make more copies of itself, our cells at the same time are trying to stop that, not only again from that initial infected cell, but also learning neighbors within the tissue, like there's something going on in within me, you guys need to be prepared. So then all the other cells neighboring cells are priming themselves and getting ready. So again, going back to the neighborhood analogy, the alarm system is going off, you know, it's loud. So my neighbor knows that he needs to start looking the doors. Is there something around? So, well, that's sort of how the thing works. Justin, are you muted? Sorry. What is what is this mechanism of intercellular communication? And are they they're not they're not the is the defense against the genie or is it against the lamp itself? So most of them are really what they're sensing is patterns in the genie. So, for example, for a coronavirus that has an RNA genome, there's pattern, what we call like patterns in is nucleic acid that our cells have different proteins that say, okay, this should not be in our RNAs. Therefore, this is a foreign material, let's start activating a pathway. A DNA virus has different features that our DNA does not have. For example, if you have a virus that is a DNA that has a DNA genome, when it enters and that DNA is in the cytoplasm of the cell, our DNA should not be in the cytoplasm. So that by itself is a trigger in our cells. Like, why is this happening? And so that that's really how it works. And so to answer your other question, most of these are based on cytokines and chemokines, which are very small proteins that get secreted of the cell. So you can imagine this as like signal flares when you're in a boat and, you know, like iconic kind of thing, and you're just like doing a signal flares, that's really what the cell is doing. It's just launching and releasing little proteins that will then bind to neighbor cells. And they will respond to those signals as, okay, if I'm sensing this, if it's released by an infected cell, I need to be ready. There's something around this area that should not be here. That's interesting because like so with the flu, we know that there is a cytokine storm that can occur that is kind of the bad side, the downside of the cytokines and in what they're doing is leading to an increase in inflammation. And that inflammation is increasing heat that could potentially denature that viral, the viral DNA that could, you know, is part of that whole defense system for the tissue for the host, right? Yep. Yeah, correct. And again, it's like no different. Like, you can start blasting on alarm right now. There's someone coming into my house. And for the first 10 seconds, you'll be fine. Okay, I got the message. But when that firing goes on and on and on and on, like clearly, no one's really going to enjoy that. Because there's a lot of after effects. There's a lot of timing that has to be regulated. And although that firing has to be turned off, you cannot just have that alarm going on all the time, because you might not be able to hear the name of the neighbor, you might not. There's a lot of complications when that misregulation goes to a regulation goes wrong. Yeah. So we've got the the genetic material that wants to get into the cell so it can replicate itself. The capsid is that protein sheath around that genetic material. And sometimes viruses just have the capsid and the genetic material inside. But there's, but this doesn't look like the SARS-CoV-2 virus that we've seen pictures of with all of the little antigen sticking out the the receptors sticking out. Yeah, outside of the cell. What's going on there? Yeah, so you can have the two different varieties and sort of like an intermediate two. When you don't, when you just have that capsid, which is just a protein shell composed of proteins from the virus and inside of your material, that is what we call a naked virus. And that's why almost we don't like naked capsid. That's essentially a simple escape. But a lot of viruses also have another an extra layer, some even have multiple of lipid, the fat, what we call an envelope. And that is derived from the whole plasma membrane. So as some of these viruses such as the coronavirus egresses or leaves the infected cell, it gets sort of like engulfed in that plasma membrane of the cell. And so it attracts that. But in addition, as the virus is producing its own proteins, if you think about the coronavirus, it produces the spike protein, that's one of them. And that spike just sort of gets into the plasma membrane and sort of like you can imagine it as it but it's not taking only the lipid from the cell, but it's also taking its own proteins that were embedded into it. And so this one will have an extra layer. And then for these viruses, that's where they're sort of like if you imagine what the virus is going to need to infect an Excel, again, the go back to the burger analogy, you're gonna have you're gonna need a key and a door. So their key to enter the next house is going to be embedded into that envelope. So when the pandemic started, that's where all the discussions were, if you can dissolve that fat layer, that fat envelope, and take away the key with it, then that virus is inert. And it cannot enter a new one. So I had a question a lot of like, why, why are, why some viruses have an white, other stone, but it's, it's sort of like why fish swim and birds fly. It just to it to whatever you need better. So like a virus that, for example, transmits through the enteric route that has to go to your stomach. And there's a lot of acid there that lipid envelope would just get dissolved. But there will be more stable in for like people or transmission. So they don't need the envelope, they just need stability. And coincidentally, with a virus that spreads, for example, to coughing and to droplets of the air, they need a humidity, they don't go to the to the stomach pH, an envelope is more suitable for the for the need. So you can have, essentially, and like viruses like hepatitis A sort of has an intermediate phase. So you can have viruses that have the two phases that are semi envelope in the body, but then naked envelope in the environment for stability. So you can, if you can imagine if there's a virus out there that does it. So they're just basically the wonderful complexity of biology and chemistry. It's giving the virus is what they need. One of the things that has that's really interesting is modern microscopy and our ability to actually be able to see these viruses and see their shapes and what what tissues they're in. And you've done a lot of this fluorescence microscopy and taken really gorgeous pictures. How do you do that? How do you how do you find and show a virus in a tissue? Yeah, so in order for you to really get at here's the captive of a virus. And here is you have to go back sort of like old school and do electron microscopy, which you're looking at. If you think about the coronaviruses that are 30 nanometers, you need to really have a high photon microscope. And those are the ones that you tend to see like in black and gray shade. But that's when you really want to look at the structure of the virus. And here is like, I mentioned like the crown. But there are other ways that you can visualize sort of like in a macro way, where not only like yes or no, there's far as present, but there's a lot of things that the viruses are doing to the cell. And so ourselves, if you can imagine ourselves as a, as a fried egg and the fat or blood and being the white and the nucleus, the the yolk, the virus is doing a lot of things to rearrange that that space to suit its needs. So it's not just coming in and here's my unit of material, let's leave. It's actually making it its home. It's distributing cells that are organelles. And so that's what I studied. And for that, we use like for us in microscopy. So cells are clear, you cannot really see them to their, their inside, but you can tag them. So if you go right now, especially here, that is almost like midnight now, if I go to my backyard is pitch black, right? So I won't be able to see anything. But perhaps I can see some fireflies because they are producing life. And those are really easy to see. And so this is sort of like the same concept. So in here, we, we go back like physics and chemistry, and we're tagging different molecules, whether comes in the virus or we artificially tag them. But we are irradiating a particular light of a known wavelength. And by just physics alone, we know that this fluorophore would absorb the light and will emit a different wavelength. So then we can visualize that change. And so if you, and there's different spectrums of molecules that have these properties, that's almost them like, when you ignite blue light, and then they turn the release green light or vice versa. So you can start making all these different combinations and start illuminating the cell. And so this is done a lot just to look at the cell itself. But that doesn't mean that you cannot do it to visualize the virus that is inside the cell as well. And so here's we're looking at an example of how the microscope works. It's just a lot of physics and behind it and getting the right light. But the concept is that if you have a compound, for example, that binds to DNA, and it happens to emit blue light, when you shine it with ultraviolet light, because our DNA is in the nucleus, that's when you put that light on, the nucleus will light up. So I put something, if I put light in the pine tree that I have in my backyard, and I put blue light on it, every time I turn the light, I know exactly where the blue that where the pine trees that if I put red lights on a different tree that I know, so I can start labeling my whole backyard accordingly. So that's, and again, if you now if you do the same thing and put a light on the burger that is trying to bring to your house and you give it a yellow light, you may be able to track it as it goes around the neighborhood. And doing this combination is where you can see not only where the virus that I give in time, but where is it at? And what is it? Why is it doing to the cell? So we have an image here of a virus that in this case is in colored green. So you can there's a lot of different cells in the in the picture that we're that that an image that we're looking at. But and we're tagging different things in the cell different colors. So the nucleus of the cell is going to be blue. So that means that every little blue oval shape thing that you see is going to be the nucleus of each cell. And then we're different components in the cell different colors. But we're also wanting to see what the virus is that and we tag it with green in this case. One cell looks bad. Yeah. So the one cell in the middle is lighting green. So again, if I was to put a, you know, like vibrant color into a burger and that shines light to it. I know exactly in what house is that so I can tell you that that cell in the middle is infected. Now with this resolution, that's not a virus. That's just a full cluster of virus that we're seeing. But it gives you a lot of information. You can immediately tell you that the virus is in the cytoplasm is not in the nucleus. So can you use knowing where the virus is and being able to find and identify the virus to treat somebody who's infected with virus? Yeah, so that's sort of like the concept of taking like basic knowledge to my transition, more transitional research, because if for example, if we know that the virus replicates in this particular compartment of the cell, it needs it to that's where the replication of the genome, the genie has to be there, the genie has to make more copies of itself in this spot. Perhaps we can disrupt that spot temporarily. And then that hampers the replication process. Perhaps the virus needs to move from the cytoplasm to the nucleus, and it needs some some proteins to move it. If you disrupt that, it doesn't cannot get to the place where it needs to get. So you can target that with drugs. And then the virus essentially cannot replicate. So there's many different things that you can see. And a conclusion that you can make by understanding the requirements of viruses from a cellular perspective. But then then isn't there this whole other layer, that protein that's doing that transport probably has another function. Yeah, important that it was doing. So if you're shutting down that transport protein, what else have you now affected? So this is this is this is tough. Yeah, no, and that is that that is part of why viruses are so tough to to treat, if you will, because they their whole life cycle relies on host proteins. So there's two ways that you can target viral infections. So you can target components of the virus, a particular protein of the virus. If you target the protein that is required to make more copies of the gene, our cells don't have that protein, it's a very more specific targeted approach. So the chance of toxicity is less because it's a very direct approach. But you can also target, again, the cellular side and those again, as you mentioned, it runs with the problem that there's a sale in our body because ourselves needs them. And so there's that that two ways, and they're going to have pros and cons. So you can imagine, a more targeted approach has a pro of it's going to be very highly specific to the virus. But that means that it's only for that virus. Whereas if you were to use a more broad approach and just say this protein that polyvirus uses, hepatitis uses, blah, blah, blah, so you can repurpose the same drugs, as long as it doesn't have higher toxicity to our body. And you can repurpose it for multiple viruses. So it's a faster way of discovery, especially when you have emerging diseases, if you know that they belong in the same family is very likely that they rely on the same component. So you can just target in that way faster. Yeah. And we've and and that's something that's been that's being looked at for SARS-CoV-2 with the ACE2 receptor that we know is targeted by the spike protein. There are ACE inhibitors that we already use for multiple diseases that are being looked at as possible treatments. We haven't had enough of the large double randomized double blind studies done yet. But at least we have drugs that are out there. Yeah. Yeah. There's a question from from my droid, which is not my personal droid. That's the name in the in the chat room. Who's speaking of mRNA, how does mRNA COVID vaccines work? Or how would an mRNA vaccine in work? Yeah. So especially for if we go back to the DNA material of the viruses, some viruses have DNA viruses and some viruses have RNA or DNA material, some of them are going to have RNA material. And those within have many different different ways of exist. You can have an RNA that is in the right sense, what we call that means that it's ready to go when it makes proteins or it can be on the opposite direction. And then you have to retranscribe it. But for the most part, I mean, in our cells, mRNAs are made into in this particular orientation that derive our ribosomes in our cells, read and make a protein out of it. And so coronavirus is no exception. For example, there RNA is essentially a very long 30,000 basis RNA that just make a big protein that then gets cleavage into smaller proteins. And there's different ways for doing that. And so mRNA vaccine is essentially just that you just have the recipe that when you give it to ourselves, they're going to make it into a protein. Depending on the sequence that protein is going to be to be made. And so if you have, for example, they are the sequence mRNA sequence for the spike protein that the virus makes. In absence of a virus, you can just give that sequence. Our cells will read it, produce the spike protein. There's no virus out there. There's no the gene is not there. The other components of the capsid of the lamp are not there. But it is a foreign protein. What will we produce? So with the hopes that our body then will create antibodies against it because it's a foreign protein. So they know that it is for this virus. It could be the spike protein from a different virus. But that that is a concept. So you're giving your you're giving our bodies the recipe. This is how the spike protein of coronavirus looks like makes something that when if we were to get infected, you can stop it. And by stopping it, is it just is it going to interfere with the the translation? Is it or the the printing of the of the of the the viruses protein or RNA is it going to interrupt that surface so it can't get replicated or? Yeah, so because it's targeting in this case the spike protein and the spike protein is from that lipid layer of the virus, what our body is going to make it our antibodies which are proteins that we recognize in this case the spike protein. So if you have a virus that has spike protein making that crown around it, if you're vaccinated in this case for the spike protein, our bodies will create antibodies that will then sort of like bind to that spike. You can imagine I've got no neutralization. And so that if you take away all the keys from the virus that that needs to get into the cell and you code them for example and buy it around the body, then that virus cannot get into a cell. So it cannot do it Yeah, it's like it's like the way someone briefly described it to me was that it is making your body pretty much produce the effect of the vaccine. So it's like when you get a vaccine normally it's putting in that antigen that your body then has to be like ah what is this thing and recognize it and make that immune response but then what you're basically doing is you're going nope this is the thing just there's the antibody right there just there you go so your body has it already and if it sees it again it knows what to do. Can we can we really train that many or is that much cell tissue at once? I mean like it can does that communicate throughout the cells or does it have to get delivered to the cell each cell through a drug? How does that happen? Yeah so once are it's sort of like training our immune system and so our immune system is white blood cells that are just roaming around our bodies all the time and they create memory and so by doing this if you have a strong immune response and our body learns to recognize this is by protein when I see it I know how to destroy it and it memorizes it and that's memory immunity these cells are going to be their long live they're going to be circling our bodies for a long time and it depends and that's why there's vaccines that are you know forever and you don't need a booster there's some vaccines that you need booster so it really depends on that antigenicity and the immune response that that our bodies mount to it and so a lot of people don't understand like why I have to get a fully vaccine every 10 years but for this one or you know for hepatitis A it's like two every six months and in reality just depends on the antigenicity of how our bodies react to it but in the perfect world our bodies our immune cells will just memorize the sequence of a spike and parts of the spike proteins forever so and they'll just be running around our bodies and the whole concept is that when we get infected those cells that know how to attack it will multiply and divide because now they're needed and start producing antibodies to neutralize it and once the infection goes down and you know those different substances sort of like disappear but you're always going to have that memory in our body yeah that's what that's what's amazing about our our immune system is the fact that it's not just reactive right here and now that it does have that memory and yeah thank goodness for that the basic is actually sort of like if we go back to the drug repurposing right the pros and cons the system that I told you of first of how the alarm system right in the neighborhood works and how are all of ourselves essentially have it again it's not very specific it's your alarm system doesn't tell you this burger is coming versus this one is coming it's just an alarm system and so going wrong like a phytocrine storm then that's really why it's just a broad it's made to recognize a viral infection the system is not saying oh here's the coronavirus and here's the hepatitis virus and here's the herpes is just patterns just like a drug attacking or being a broader broader drug versus an adaptive memory immune system is a very very specific response recently there's been a lot of talk about how SARS-CoV-2 affects different tissues and we've learned that the ACE2 receptors all over the body and lots of different tissues and one of them is the heart and you were you have this amazing twitter thread that you wrote about about viruses in the heart and this was as you mentioned early on a very focus of your study for a long time and you were also recently quoted in an article by Ed Young in the Atlantic talking about what's going on with SARS-CoV-2 in the heart is it unique compared to other viruses so for our earth it's not or at least I don't think it is because we've known that viruses a lot of viruses at least over 20 human viruses are somehow I will prefer to use the word associated with cardiac damage because many cases are indirect but it's not the standalone case so viral myocarditis myocarditis comes from hiatus is inflammation myocarditis from the myocardium so the inflammation of that myocardium in the heart tissue can be caused by a lot of things it can just be a genetic error it could be caused by bacteria or parasites but a lot of cases especially in the U.S. and Western Europe are caused by viruses and sort of like for the longest time it is known but a lot of the literature comes like from very few labs because not a lot of people study them and in reality it's like when you think about all these viruses this is not their main side of replication they're just like a secondary organ or their effect is indirect so viruses that we tend to associate with myocarditis these affecting the heart is an indirect or a secondary effect it's not really whether replicating and they're only like they didn't just come to our body to replicating the heart right and I always say that is our heart is essential like a virus really doesn't I don't want to like humanize the virus but it's you know if you want to create more copies of yourself and in for a virus the most important thing that it wants to do is to spread from host to host if you just if you're a virus and you just want to infect this person you're dead you're never going to to survive in the population and so destroying an an organ that's essential is even if you were to do what you're probably never going to spread so you're never going to find the virus in the population right and so a lot of these viruses just have this off-target now we're seeing a lot of cases with COVID-19 patients that are coming as myocarditis is positive and so I think my my my whole take on this is because there's so many cases we are now seeing a lot of myocarditis cases and the reason is because pre-pandemic when you have a viral infection that somehow affects your heart for the most part they resolve on their own and so you get a viral infection some vards can get to the heart and destroy our cardiac cells many of which are not replantable so muscle cells in our heart don't undergo mitosis so like what's that going back to hascopiology cells divide maybe more copies of themselves so cardiac muscles cannot do that once they are differentiated for the most part overnight some percent they just they're they just do their thing beating so the bulk of the cells that we have in our heart right now are the exact same ones that we can when we're a kid they're just the exact same ones and so I had no idea yeah so they are just doing their thing the differentiated their beating and which comes with a consequence right if you lose them then they do not come back and so for the most part historically all these viruses that cause cardiac damage the the symptoms sort of like resolve on its own so virus comes either destroy some cells or our own immune system goes wild like a cytokine storm as we mentioned it starts killing the infected cells because if you destroy the infected cell that virus cannot spread it ends it right so our immune system is trying to do it the right thing it's just doing either too much or unfortunately we need those cells because they're not going to come back but for the most part the infection results and you're never going to see it you're never going to have a symptom and you just move on so a lot of the statistics come from both more than biopsy so someone passed away and they're doing biopsy on the heart and you can find all the cardiac lesions that reflect that at some point we were infected again because these cells are not dividing with because we're not because we're not replenishing all you're going to find is a false site these were this is a spot where muscle cells would have been now they're not it's likely that a virus killed them and but our bodies clearly infection it can progress to other conditions you can even to cardiac arrest and so but for the most part it doesn't but now we're seeing a lot of cases because we're in a pandemic a lot of people are infected there's an intricate relationship between the lung where coronaviruses are affecting and the heart oxygen and CO2 exchange so you have those you know that relationship there plus now we can talk about that later it's the age distribution that we're seeing historically because it resolves on its own and unless unless it's a biopsy you don't know that you had a viral myocarditis you never notice it you're only going to notice if you have a symptom and so that's usually on younger folks and likely because they have a heart higher cardiac demand it's very common on athletes because their heart is you know at its max peak compared to someone that that it isn't so even though you might not have a symptom right now if you start building all those cardiac lesions over time and then you push your heart really really hard that is that is why myocarditis comes to at a very high or frequent cause of sudden death because you don't know that it's there until it's too late that's what we need is some way to see what kind of cellular damage we have in the heart while we're still alive as opposed I mean you can go in and probably do electrical tests see how well the muscles transmit the electricity through the heart along their channels but we may be getting some information on this in the coming years because number of NFL players as in the past a bunch of basketball players have been come down with COVID how does that affect I mean that's that's not just an athlete that's an elite form of an athletic body that has been training a lifetime working that heart to do these things and as so often happens sports medicine teaches us a lot about how to fix ACLs and ankles and sprains and tendons and concussions and everything else and now we're going to put COVID on that list I guess yeah it is I guess it is fascinating but at the same time that I think the biggest problem was that the thing that we need to really consider again this has been going on for a long time it's just we usually just don't notice they don't unless it's a really bad case that you know you have cardiac issues or it may ask or whatever but I'm personally don't remember any of my 30 something years of life but I'm pretty sure that there's some cardiac illusions just by statistics alone and the number of infections that I've been encountering my life I'm sure there's some issues there but that's important to consider when you were talking about asymptomatic cases and the population that says well I'm I'm helping enough and I'll be okay if I get COVID and I'll just have a little flu like symptom and I'll move on but what we're what what we need to remember is that there's a lot of secondary effects and perhaps you were symptomatic and you were infected at some point and you never experience any fever any coughing but that doesn't mean that there was some damage to your heart either because the virus got there or because there was some mild inflammation triggered by our immune system in response to the virus when we try to stop it that damage themselves and some studies are coming to get at that but my criticism is that it's very hard for you to have a control group during a pandemic so and that's important too that's important to sort of get at because we don't know how many cardiac lesions were there prior to this one so like you're seeing a cardiac damage now and you're relating it to COVID cases but what if only 10% of your heart was damaged was caused by COVID but you had like 30 other percent because you were exposed to like Zika virus or Koksaki virus or whatever at some point and it just adds it just sets up so without a control group it's really hard to to know but again because a lot of viruses do it it's sort of like you're just hammering and hammering and hammering that's a really just the the concept that over time there could be an additive effect of multiple viral infections that just over time maybe there's it just builds up until finally there's enough dead cells or there's enough car tissue that formed that oh it's not going to work right anymore yeah and most of the I forgot a percent I think it was like it's doing something I forgot a but it's a high percentage even from those viruses when they're trying to generate materials of sequence okay well what is in that heart is often at least two or more viruses that were associated with it and that doesn't mean that you were co-infected with both it just means that perhaps when you were 20 you got this viral infection and then when you were 45 you got another one and then when you were 60 you got another one and that's you know but which one did the most you we don't know but again these cells don't replenish so you start you know taking some and taking some losing some losing some and that's especially in this I think the my cases and younger populations the chances of them and this is something that we don't know I hate scaring people but we don't know if you if you're like if you're like 20 something and you already lost like 10 percent you see have a long way to go and we're gonna continue to be exposed to viruses bacteria parasites right and so so that low that low immune response for the for those who aren't showing symptoms might actually be incurring the same kind of damage that takes place in somebody who's getting the cough and in a sniffle on the heart you just we just wouldn't know yeah so again so that is frightening if you speak into the if we're going to just focus on the heart for just one second there are viruses that can't get there I cook sake bars for example if I love dogs so like parbo bars like that's one of the vaccines that we use for for the dogs for dogs like there's viruses that are known to to directly affect the heart and what I mean directly is like they're doing something they're going out there and they're doing something destroying a cell or something but a lot of cases if not most of them are because of how our body responds to it so either because of these our bars are circulating our blood and along the whole blood gets to your heart right it's a pump so all the cytokines are going to get there all those immune systems are going to go there and do after traffic through to a body so if they see something there they'll just attack or our cells are going to respond like if the cells are decreeing cytokines our cells in the heart and they're going to the blood our cells in the heart also have those same receptors that our cells in the lung will have so they will say okay we got a reaction so it's a problem and most importantly another we have a cell type in our body that is called the T-cell so like B-cells make antibodies and T-cells but another type of white blood cells that a tough set of them are made to kill infected cells virus infected cells and so even if you have like a little bit of virus that gets into cardiac cell a T-cell will kill it again trying to trying to prevent the virus from spreading it will kill an infected cell and you might not have a massive inflammation because that cell was very directed but again it adds up so if you have another T-cell killing that infected cell to prevent from spreading and then another one you don't need a massive inflammation you don't need a lot of symptoms for that event to happen and so that is a progression of how it happened so you can have viral entry and replication that the virus is replicating in in the cardiac cells and in response to that if the cell itself cannot just stop it through the system that we're talking about the alarm system that's usually the first thing that will happen that the cardiac cell will be like maybe I can hand it on my own but if you cannot then an army of immune cells come and start creating an inflammation and start trying to ease the the viral tire burden and most of the cases that results and that's enough you're gonna have some mild inflammation you're gonna have some necrotic tissues because the cells were lost but then sort of like you just move along and worst case scenario is when it really goes bad and you just have massive inflammation there's just a lot of cardiac cell loss that cannot be replenished yeah and because it's your heart it's not there aren't necessarily the the inflammation inflammation that comes if it's mild there's maybe maybe your blood isn't getting where it needs to go quite as effectively but it's probably still pretty effective and so you probably don't really notice maybe not at the top of your game you're just not you know peak performance but but you're still okay right and if you have if you have an infection for example that affects your your lungs and your breathing is fine it's not right but you're just lethargic you're in bed anyway you're not running a marathon and pushing your heart so you might not even notice it you can have fires that affect your joints like a chikungui infection you just don't want to walk so if you're not walking your heart is not it's close to rest you're never going to see like oh my I have like a race mass or something and so that's usually the the part until again in the case of athletes until you really notice it because you're pushing it too hard and in a pandemic where I think my transformation is happening and all that they might not even know that that happened and perhaps they're the heart is still recovering because the pandemic is not over and so even if they got an infection like two months ago when what happens is that when you lose those cells muscle cells even though they don't come back the other cells in our heart that take over that spot to like patch it so like if you get a cut in your finger right it's going to be open and then you're going to have a scar some other cells are going to start like patching it but you're going to see that scar forever right because it's in a different orientation it cannot stretch as well it's the same thing happens in your heart you're going to lose your muscle cells some other cells if it's going to take over but it's not going to be the same in we all probably have scars from where a kid said we would always have them and it will never be the same tissue so gosh I feel like all our listeners after this are going to be thinking all right do I have heart damage or do I have COVID anxiety or do I have political anxiety or is it the smoke that I'm breathing in or is there just yeah no what's wrong with me but I always like I always like to say there's a reason why we don't know this until postmortem it's because our body is really good at you know stopping it and moving on and we this is biology we adapt and we move on and so is that finding that balance of yes this is happening we all need to be and I care about this topic because it really affects the way that the young crowd thinks about us into my infections and oh I'm good I'm done but I also so I want them to protect themselves for others but also for themselves for that perspective but I also like to acknowledge that again our body is really good at coping with it right you didn't have any symptoms and most of us haven't had a heart issue even though we have had probably an inflammation in the heart at some point right now and so it's not like we're all just going to die of a heart attack because long and behold our bodies were made we've been coping with viruses many many years our bodies our bodies if it was that bad that one virus will kill our heart and kill us we would already be dead of the species by now and so yeah and and you know if the way to have a healthy long life is to avoid exercising too hard I mean this is that actually I think I think I got a couple of questions like that and I'm like well I mean and especially if you don't know that you have like you're just going to like stop living like that's not especially when even after this is before the pandemic during and even after these ends this is not the only virus out there and I just told you that a lot of viruses do it so even after this one ends there's still the viruses running around every day you know and so we cannot we cannot just stop living because you know yeah keep moving move as much as you can it's good for your we're a little meat machine right there's a there's a question Blair wants to ask so whenever we have a virologist on the show I have to ask and especially since you were talking about how kind of viruses I know you are kind of anthropomorphizing but they don't want to kill their hosts it's very reminiscent of parasites of course and so I have to ask I don't want the like the textbook answer I want your real answer do you think viruses are alive I know where this is going to be alive yes I knew where this was coming to I think well you really want my answer yeah this is a debate yeah we're gonna laugh anymore you can say whatever you want no I saw it you know the whole debate was like on twitter yesterday too and I was like well let's get away from this one sorry fair to it it again no it depends on again you're gonna go into the time you like you defend on how you define life and whatever of course but again I personally think that and this will link back to the mRNA vaccine question because of if you were to take an RNA virus that has a genome is basically an mRNA that when you put it into a cell it has a recipe to make more copies of itself if you take that in principle and here's something that we do in the lab we can synthetically recreate a sequence of a coronavirus in the lab we can take adenine we can take one like every single nucleotide that makes RNA put them in the sequence that we that goes to the virus in vitro like there's nothing here but building blocks just like one of the stories that we talked about if you put all these building blocks in a test tube in the right sequence put it into a cell that cell will make virus meaning are we really creating life I you know I and if you were compared to a parasite we cannot do that we're a parasite we cannot do that with an obligate bacteria we cannot just create a bacteria in a test tube or provide a sequence that will make it yeah tell that to george church keep working on it not yet not yet not yet but you can with a mRNA virus like I can just go just like how we buy DNA sequences for PCR and I can just buy a sequence of a virus and that alone is going to make a virus so like that's a fine line but I'm like if it's really alive and we are creating life in a test tube like from sequence alone and I don't like that concept so that's why I feel like I don't think they are alive because I can I can buy them like and I can't it can't I like this is the sequence you can see it when and the cell makes it and so wow that is my but that one's temporary that's a nuanced answer that's very different from the like the pin pedantic answer I usually get that's just like oh they can't replicate on their own so they're not but ever that no it's more chemistry time sensitive yeah because they're molecules but if we get to the point then when we can design a bacterium send it off to the chemists and get that sequence back and then produce it does that then change your opinion or does that mean that life doesn't it probably would yeah yeah okay it probably would yeah okay because till I see that I'll be like the fact that I can just purchase it like a chemist can make it yeah it's and at least for like RNA viruses you know there's so many different right but I've studied RNA viruses specifically for since I started that's the only so I'm very RNA centric and just the concept of like oh just go and buy the sequence and give it to the sales and they'll make it like it's really sad that's what it feels like if it was through life and we're we can purchase it and like awfulize it and over powdered and that water to reconstitute it like is it really seaman can have you been this is the first answer to this question that has actually shaken my like very adamant belief that viruses are alive this is like the first time I'm like oh maybe not oh something to think about there you go here's an interesting thing though this is a question from our guest from when somebody in the chat room earlier Mike Shoemaker who's asking the common coldest coronavirus and we have not been able to cure that assuming because of mutations why would covid be any different but then if it's mutating if it's sort of evolving to you know through natural selection and through through mutation that sounds like life on the one hand but his question is why why if we haven't cured that one how come this one would be any different I guess I guess somewhere in there there's we have some coronaviruses that we've been able to to stop maybe not the common cold one but there have been some that we have or is it none of them none of them none of them this is gonna be the first one that we have to stop we don't have any coronavirus vaccines none none yep and they either like circulate and they just magically disappear or or that's it and magic that's what we're relying on that's really just crossing my fingers and toes here when when we started and people were like well there's this is Covid-2 what happened to Covid-1 and people were like well it just came and like that's it like it just disappeared like it's just and so you know virus is its host so getting back to yeah the virus mutates virus evolves and so that is a very strong future of what we define life it can only do it in a in a in its host in its host so like I actually got that question from twitter like someone messaged me like can the virus replicate the genome in its own capsid and mutate there and so that is like a big no no it cannot do it and so a virus in itself but that genie is dropping a lamp cannot mutate it cannot evolve it cannot do anything it's chemical compounds sorry virologists but that is a chemical compound until until it has to evolve because there's in and that case is where paradigm comes from because it will then act like as a life entity and it will mutate and evolve to cope with all the pressures that our bodies and ourselves are putting to it almost always randomly but you know to be fair to be fair our own lives while a virus needs a host our own own existence is dependent on being a host to all the the microflora and I got so we have to be hosts in order to life so is that really life if you need all these helpers constantly doing all this work for you does that really count then because by yourself you would just die but what if life anyway yeah it is it's all of it it's all of it together it's just yeah but to me like it's not whether they're alive or not it's you know it's really what they're what they're doing and a lot of people just think of viruses as these negative things and they just come and do their things and destroy our bodies but not all of them are like that or they can be as we mentioned the purpose to do some more things that we discussed like plant viruses there are viruses that have been quote-unquote repurposed to destroy cancer cells so like those are uncoolidic viruses and a lot of people don't know that uncoolidic virus therapy is a thing that you that you can design a virus that specifically targets a tumor and so if you put that virus into our body you can destroy a whole tumor so like not all viruses are bad there's viruses in the ocean doing their thing there's viruses helping other organisms like I know and I know we're getting towards the end here but one of my the most fascinating stories I think that we covered on this show years ago was how infants don't have an immune system built up yet and they're they don't have they're not you're not born with a great amount of microflora but up until about the age of two we have the highest viral load that we experience throughout our life and it drops off as our immune system as our microflora pick up and take over but that our first immune system is children as infants is a viral immune system it's going in there and destroying bacteria that could be invasive because there is no other line of defense but those viruses to attack them so in some ways that we are absolutely reliant on viruses for our immune system in the first place yeah so there's people tend to prove viruses that again we are all very human centric and but there are viruses that we said infect cancer viruses that destroy bacteria and there's some cases where those viruses are really good for us because they kill the bacteria that is bad for us and so we just have to stop considering our species as the center of the world because there's a lot of positives and you know they didn't viruses is just didn't come to exist and to wipe off and just be the bad guys there's pathogens are an accident yeah you have nature pathogens are just like a one-off accident miscommunication something's wrong it's not intentional it's all a system it's all a system it's everything using everything else being a part of everything else the ebb and flow of energy I know I'm sounding kind of new agey here but really you know trophic levels and and molecules and electrons yeah that's a really good question and the last philosophical venture that I want to leave you think about I actually got that question one time it's like why are immune system has not evolved away to like stop going wild and like in many cases killing us like it just goes so rampant in an inflammation that we die and again I if you then go up in the macro it might be that it's killing you as the one host but it's so that you don't spread it to the whole population so again just like in ourselves you might lose one sale but you're saving the organ you might be that in case of running ball that for example it might be that you just die so fast because our body just goes wild but in reality perhaps trying to stop it from if you kill the host at the hole then you stop spread and the human population so it's species survival so so then so really what we need to do yeah the good part we need to do is make the coronavirus more lethal no so that it kills people quicker before they can go and spread it that's what I finally make sense we're not gonna we're not gonna do that clean up function experiment no thanks I don't know if it works you gotta think about the herd you know not individuals yes um I heard I heard you there Efra thank you so much for joining us tonight I know it's it's getting rather late over there on the east coast where are people going to be able to find you moving forward yeah so I'm always I want to say always I mean always on Twitter so they can find me at naked capsid I as I'm changing jobs I left so tweeting about viruses but if anyone has any questions about viruses my inboxer is open I have a website that is linked there to my Twitter page too and so you can click on there there's a contact if you don't have a Twitter and you want to message me then there's a contact there with my email information and whatnot I'm always happy to answer questions even from the what you might think that's the most basic question in biology that you want to understand feel free to do so so those are usually the two go to places to find me fantastic and you're venturing into into more into communications now I think that's going to be bright future because this was fantastic interview learned a lot today thank you so much yeah no thank you yeah so I've been doing from Twitter time communications so it's not my first time I've been managing different Twitter pages for self-biology journals and stuff like that so that's what I'm moving next and it's if you think about every time that you're on social media whether it's Facebook or Twitter or Instagram and there's let's say the cell journal and there's a tweet that comes saying the paper well there's someone behind it that writes that tweet that read the paper wrote a tweet and tweeted it and for some journals that's me that that's what I do so that means I have to read a lot of papers way outside my area and like condense it so that that's the communication part of what I do now and that gives me excited because like every day I need discovery that I get to summarize and share with the world so that's exciting and as we talked about earlier there needs to be more sharing of the science with the world so that we can get that trust up right more sharing more communicating thank you so much for your time and for joining us we have more stories that are still to come will you be saying with us or I can hang around for a little while yeah yeah okay fantastic all right back out for a sec I'll be right back you'll be right back okay well we never stop this show is going to keep going right now oh yeah that was a fantastic fantastic conversation and we will have the links to Dr. Rivera Serato's information on our web page thank you all for listening to twist you are the reason that we are able to do what we do every week that's right bringing you the science down to earth views the news a somewhat sane perspective and hopefully we combat a little bit of that misinformation that is out there by bringing you some credible information in the world if you would like to be a part of bringing more of this sanity in science to the world head over to twist.org right now click on the Patreon link and choose your level of support be a part of bringing the science to more and more people thank you we can't do any of this without you thank you for your support all right Blair is it that time the time in the show where I play the music for Blair's Animal Corner what you got Blair? I have a story that's a little early for halloween bear with me here all right I'm ready a wild story I said a lot of time on the show trying to demystify snakes and talk about how they're not scary but I have one particular snake that I'll go ahead and say it turns out they're very scary the snake from Thailand they're called the small banded kukri snake and they have been documented on three occasions doing something we have never ever seen snakes normally they swallow their food whole they either constrict or they will inject with venom and then they will they have these kind of backwards pointing teeth and they'll swallow their food whole they're not chewers but on three occasions this snake was found cutting open the abdomen of a large poisonous toad inserting their entire head into the abdomen of the toad and then pulling out the organs one by one to eat them well the toad was still alive is there a video? what? I do not have a video there's a picture but it's it's quite graphic I'll just say if you're listening or watching if you're watching the video we now have a frog with or a snake with a frog on it wearing a frog as a hat right so this was this was seen from the Asian black spotted toad which as I mentioned is poisonous so it secretes a toxin from their parotid gland which is kind of behind their their eyes kind of near their neck if a toad even has a neck kind of just head but anyway so yeah so they they secrete this poison so there's now two theories as to why these snakes might do this one it could be that this is their way of avoiding the toxin so they are cutting open into the toad to avoid the poisonous secretion on the skin and go straight to the vital organs that would make sense okay other theory comes from a fourth observation in which they saw a snake actually eat a toad whole but the toad was much smaller so either the toxin isn't as potent when they're small and it gets more potent as they grow big and that's why they couldn't swallow these bigger toads whole or they were just too big to swallow for these small snakes and so that's they're just I guess they're getting real desperate I don't know but yeah so so there's something weird going on here again this is only four total cases that were observed so it's very very preliminary but it still is something that just has not been observed before and kind of shake some of the expectations that we have for snakes and the way that they eat food I mean it's really different from what we normally expect the whole I'm swallowing my prey whole thing yeah for those of you that are now terrified of the idea of the snake that eviscerates and disembowels they are harmless to humans you're way too large they are tiny snakes so far though the one thing though is if you were bitten by one of these snakes you'd have to wear a bandage for pretty long time because they have a really powerful anticoagulant that they inject into the bloodstream when they bite and this is important to death you wouldn't bleed to death you put on a bandage you wrap it kind of tight it would eventually coagulate we're big enough it's fine but if you're a toad it's helpful because when they spend this extended period of time with their head inside the body of the toad they don't want clotting to occur so this kind of helps allow them to get to all of those organs it's something that I do not want to see ever on a hike no no never so just beware if you're ever hiking in Thailand just if you see a toad on the ground just assume it's a friendly happy toad and be on your way don't take a closer look is what I mean wow yeah okay so that's a that's a new thing yes yeah I'm traumatized let me now bring you to something fun and exciting which is fireflies okay I like fireflies I like fireflies California girl didn't really go to the south at all growing up and so I didn't see fireflies until I was an adult and I was I was visiting my friend in Atlanta and we I just saw something out the side of the car when we were going to dinner I was like pull over and I jumped out it's they're amazing I'm so fascinated by fireflies they're magical and this is a study looking at fireflies in Great Smoky Mountains National Park and a very particular thing that fireflies do which I did not know which is in this national park thousands of male fireflies will congregate and they will flash together synchronized is this a mating thing great question so this is studied by the Department of Computer Science and Bio Frontiers Institute at the University of Colorado Boulder they wanted to see how this synchronization happens how they manage it and why they do it it is definitely related to mating it's a mating display but are they doing it because it's just part of the way that their body functions is it an internal rhythm or is it something that they do to communicate with each other and they actually got to use 360 degree cameras in order to kind of see this from all different areas and they also had a pop tent so that they could catch all the fireflies and then release them one at a time to see how the kind of the flickering display changed depending on depending on how many fireflies were out and they don't behave the same when they're alone versus when they're in a big group so that definitely means it's some sort of communication it is not an internally wired rhythm yeah like the temperature gets to a certain degree and then that leads to how frequent the things are but no that was eliminated yes so so they they have a few quick bursts and then they have a several second pause and then more bursts and then pause and it they say it looks kind of like a wave of light passing over the hillside which just sounds beautiful I would love to see it someday and so they it seems to be kind of a competitive edge between the fireflies so as they they kind of all start to flash they they they're big copycats they all kind of do it together to try to to do one another exactly yeah I'm gonna say match wits match lights with each other when they are competing for a mate it's probably it sounds kind of like it's kind of like the the firefly version of lecking where the birds the the male birds all come around the female and they're like all of them displaying and showing off I'm gonna puff out my chest ooh I'm gonna puff out my chest too oh I'm gonna I'm gonna move my head back and forth oh yeah good idea I'm gonna do that too yeah yeah got that so part of where this computing department comes in from from this study is they actually hope to use this group dynamic to help design swarming robots which sounds terrifying I have no idea you're gonna go from fireflies to robots okay it sounds very scary I'm not necessarily with it but I'm sure there's a good reason to have swarming robots I just can't think of any right now no if you have if you have a large number of robots that are acting autonomously or if one of the robots has instructions and the other ones can act based on what they see the other robots around them doing then you don't you can have larger groups of robots acting in concert then you could potentially you know it's easier than controlling them all from a distance right yes I'm thinking of the latest spider-man film I don't know anybody saw that but it's where they had a bunch of drones kind of working in concert to make holograms and things like that and definitely yeah they reminded me of bees for sure yeah I I just imagined swarming robots in outer space that's just where I imagine them I mean I know there are lots of uses for them down here on the planet but I just think of them swarms of robots in outer space yeah from strobing fireflies in the bayou to swarming robots in outer space they're all connected or we could or we could replace those those cardboard cutouts of fans in the in the stadiums with robots that you know couples start cheering for a play all the rest of them cheer somebody starts booing it's a pretty good idea I like that trademark that immediately yeah yeah Goldezator in the Twitch chat room is saying if one robot fails the rest of the swarm can continue smaller robots are simpler and more reliable there you go yeah yeah um I was gonna say this is this week in science if you just tuned in and if you like the show do you want to help us grow get get a bigger audience we would like that get a friend of yours to subscribe to twist today that would be just wonderful and very helpful thank you yeah and if they happen to just leave their YouTube open because browse over to the other who can sign hit the subscribe button for them and then it'll be like a nice surprise it will start popping up in their feed they won't know why but if they enjoy the show they'll stay yeah Justin tell me a science story oh I probably have one of those you sure would uh if nature communicated better uh it may have a if they had a newspaper that it put out newsletter twitter account of its own one of the most prevalent content subjects that would be trending would be about who is eating who currently in the world of nature scientists at NOAA northeast fisheries science center have developed such a source of who is eating whom off the northeastern united states oceans the predators were divided into 48 predator-sized categories and 14 prey species fish predators included but are not limited to Atlantic cod Atlantic herring haddock goosefish Pollock spiny dogfish winter flounder in the yellow tail flounder prey species included such fish food favorites as squid zooplankton shrimp like crustaceans shellfish brittle stars sand dollars and sea urchins among the studies findings most of the fish responded to changing abundance of prey by switching prey they went through a sort of learning period when the prey in the highest abundance began to be targeted that response helped do a couple of things first of all it meant that they had the most stable food source but it also then helped stabilize the prey populations so there's sort of this equalization thing taking place within these fish where they because we were talking about the birds earlier how the birds if they if they lose their food source because it's global warming they the clutches can die from starvation in the fish world they would just stop eating insects and go on to berries or something else they would just sort of it looks like they have this and it's very interesting they just go they will change you know we think of predators as often being sort of very specific feeders on specific things but it's plastic they can they can change so this is actually a pretty huge study this goes back to surveys that were data that was collected from back into the 50s and 60s into the 70s so this is a pretty comprehensive long-term study really interesting the findings are published in fish and fisheries and it looks at these at these 17 species of predator and prey what why is why is it that nature can find these balances so simply and humanity can't sort of sort this out like I don't fish so much smarter yeah I mean that's it's it's something that when we had differently modeled societies there is historical evidence that we were better at switching prey species and switching our resources based on seasonality and the environment that we were in native peoples are known to have really used fisheries very well and actually helped certain fisheries to thrive in in their management and use of those resources over time so yeah it's I think it's more a modern conundrum and maybe it's something that's based on how many people are on the planet because we've gotten to this point where it's just really hard and we're all in cities and how do how do we manage all this stuff but I think nature and humans as part of that historically we've done a good job but we aren't anymore I mean how many times on the show have we said like oh we thought we knew what this animal ate but it turns out you know we found out that deer sometimes eat meat which blew my mind when we figured that out so yeah I think Nate it's exactly that nature's a lot more flexible than usually or ever Jane Goodall was on The Daily Show with Trevor Noah recently and one of the one of the things that she sort of pointed out was that like if chimpanzees were as intelligent as humans they would likely be just as destructive to the environment you know that desire to take on a resource when you can control it is just too tempting for most life forms but I do like I do like this study for another reason too because we've talked about how fish are going to have to be migrating as ocean temperatures change this is a really good sign that at least based on the northeastern fish species are really off in the Atlantic that there is the ability to change strategies that there is ability to shift to the abundant food source for the predators hopefully the prey species can be as agile and shifting what they're eating otherwise the whole system's going to fall apart but but that is at least good news for fish populations in the face of global warming and changing ocean temperatures as their population of fish that they encounter changes strategies might be able to keep up in real time so that's fantastic yeah hopefully with climate change and all the other pressures that are out there it'll all continue to manage but maybe we'll get better at managing come on humans sustain abilities fun yeah it is it is didn't you have a story about Neanderthals oh uh yeah I've got that too here let's see this is uh so there's there's been some constant improvement molecular technologies that have allowed the scientists at Max Planck Institute evolutionary anthropology to in the past determine with some high quality sequencing genomes of several Neanderthals which then led to the discovery of the other extinct humans the the Nisevins now they've gotten to the point they finally basically got the Y chromosome looked at in Neanderthals which is not something that we've had before and it's reinforced some hints that they had gotten previously about modern human Neanderthal interactions but by comparing the okay this is from say by comparing the archaic human Y chromosome and the Y chromosome of people living today the team found that Neanderthal and modern human Y chromosomes are more similar to one another than they are to the Denisovan Y chromosome does that mean that we are all the descendants of Neanderthal? No it actually means something crazier that some modern humans around 370,000 years ago contributed heavily to the Y chromosome lineage of Neanderthals we've had a couple of hints of this before there have been some some hints that there was intermingling with modern humans in Neanderthals around the 200,000 year mark this is putting it around 370,000 years that modern humans contributed to that Neanderthal lineage so this is yeah oh is by well now established that all peoples of non-African ancestry carry a small amount of DNA as a result that this there's just one this one incident or the most of that mingling was thought to be in that 50,000 ish year ago range but the Y chromosome sequence now pride dividends in the Neanderthals and early modern humans met and exchanged genes before the major out of Africa migration potentially as early as 370,000 years ago certainly more than 100,000 years ago what's kind of also interesting about that is that's putting it in a time frame earlier than we think of modern humans as being modern humans so it's there's still so much that we don't know about how modern modern human Neanderthal interactions took place but it is it is more and more evidence that within the Neanderthal lineage itself there's a good braided stream to the point where it makes you then start to pause a little bit about what is truly Neanderthal DNA that we've looked at as Neanderthal and is a co-contribution from modern humans how much is that we attribute to being Neanderthal genes could be archaic modern human genes it gets very so what we really need is more a better look at Denisovan because the Denisovan Neanderthals are much closer aligned in many other ways so that's the that's the part of the puzzle when we get the Denisovan aspect in there it made me that the Neanderthals more of a hybrid of Denisovan and archaic modern human then it is its own branch of humanity lots of fascinating interesting things that are going to come from this going forward but yeah I can't wait to see you know as we get our technology improves and our ability to look at these questions you know what kind of answers we will find about what the you know how the braided stream really how it was really braided however how all these ancient lineages came to mingle how you know which what which lineages died off and how and what genes were contributed and part of the noise in that is also being able then to separate what's in the Neanderthal from what's human I got sort of an anecdotal example humans what are they even I'm very very good friend of mine is is scandinavian lineage of going back for like it was far back as you can look of being danish didn't travel much did the 23 and me came up with like 12 percent british well that's because likely there was some viking ancestry that left and went to britain at some point so then you have to say well is that 12 percent british genome which they identified amongst british people actually from britain and then you know and it only depends on how far back you put the slider of you looking 300 years ago or you're looking 500 years ago that all you know changes who's from where anyway so it's all kind of ridiculous at some point but uh but yeah now we have to start looking at how much of our DNA genome is just current modern human that also was in neanderthals anyway it's it's a lot of fascinating fun to come from this I love it I love it neanderthal why chromosome it's ours it was the humans let's talk for a second I've got two stories before we close out the show let's talk about brains because I love love the brains so in a new state a new study published in nature this week researchers at the rikin center for brain science in japan have described an area of the brain that is called some SUM this is an area of the brain in the hypothalamus that is related to memory formation specifically involved involving social novelty now what does that mean that means meeting new people well in this particular situation it was meeting new mice because they were looking at mice in the study they took mice and gave them different kinds of novelty they either got contextual novelty so a new running wheel in their cage or a ball or new fluffy bits to play with in their enclosure or they got social novelty and the social novelty was exposing them to new individuals who they had not met before the SUM they recorded from and discovered they looked at brain activity in a large area of the brain but focused in on this area because they found its activity was much much higher when social interactions were new when there was novelty there was not as active during the contextual interactions or if they were meeting a familiar mouse friend so what they did that really dug into this to discern how it works of course there was some there was some manipulation involved so because we have optogenetics now this wonderful tool involving blue light that allows researchers to turn neurons on and off they used optogenetic light stimulation to stimulate the areas of the brain that SUM connects to and they found that when it was active it was connecting to memory area a memory area of the brain known as the hippocampus it's involved in consolidation of new memories and so when a new interaction new experience happens the the neural activity is going to put connections into the hippocampus and then the hippocampus is going to take that information and send it out to other areas of the brain to make sure that the memory turns out becomes a long term memory if it needs to be so that it can get stored and there were two areas of the brain involved when contextual novelty the new running wheel or a ball or whatever was involved there's the dentate gyrus part of the hippocampus and that's kind of the the the I guess the the part of the hippocampus it's on the way out that's like information goes into the dent the dent goes into an area of the hippocampus called CA2 and then it moves out through the dentate gyrus and then it goes out to other areas of the brain so contextual novelty stuff was connected to the dentate gyrus social novelty novelty was connected to the CA2 when they used optogenetics to turn on or off the dentate gyrus or the CA2 connection they were actually able to make the mice behave as if they were having a new social interaction even if they weren't so they turned on that sum to CA2 connection when mice were with a mouse that they'd been friends with for a long time and instead of going like hey fred what's up good to see you again they were like oh pardon me would you happen to have any great poop on you know they acted a little bit differently because it was a new social interaction and so by sorry I don't know where that came from but I believe the 90s is where that came from yeah it might have been earlier than that it might have been much earlier than that for the kids listening for the kids listening the poop icon is a form of mustard and there used to be a television commercial where somebody would come up approach a stranger and ask them if they happened to have that land of mustard on them at the moment and to which of course they always did because she doesn't carry mustard with them wherever they go and I love asking strangers or mustard yep pardon me it's not the world used to work but anyway by doing these manipulations they were able to confirm that mice have an area of the brain that is specifically involved in meeting new mice and humans may have an area like this as well that may be involved in helping you through those new social interactions so that you can remember new individuals if they are going to be important to your future dealings I need to figure out how to flash that portion of my brain with light in just the right way to actually remember people's names when I first saw them yeah I think that's a completely different area of the brain that just has the magic erase marker in it always nice to meet you I immediately forgot can you tell me your name again oh it's gone again sorry I'm just glad that there's finally a therapy that might be developed for for introverts yeah maybe I don't know if that's what it's good for but yeah potentially and my final story for the night is bird brains because you know how much I love the bird brains not just brains but bird brains and we have talked a lot on the show about you know how birds think and how birds have much smaller and from an anatomical perspective what you know anatomists would call a much simpler brain we have a convoluted cerebral cortex which we have always thought to be responsible for our higher cognitive functions and for things like consciousness but we have a really hard time asking other animals whether they're conscious how do you go about finding out if another organism is conscious of their day to day experiences well ta-da science researchers have figured out a way to start getting at this question with carrion crows it's not tickling no it is not tickling yes so they looked at it was a very small sample size they trained two carrion crows to do a very specific kind of task it's a delay it's a what was let me close the window that I was just opening so that I can say exactly what the type of test was well they it was a delay and this doesn't really matter what this piece a delayed stimulus detection task this is what it is delayed stimulus detection task but what they wanted to show was that there is a subjective part to birds perception and that there is an area of the brain to confirm that that there is an area of the bird's brain that has the capabilities that we ascribe to our prefrontal cortex so the area of the brain that they looked at is a area in the back of the brain so we think of our prefrontal cortex it's up in the front of our brain the neocotolateral cotolateralis it's an area of the bird pallium which is a laminated structure it's not convoluted like the bird like the human cortex it's very smooth but this area in the back of the brain is thought to have the same cognitive capacities of perception as our prefrontal cortex so they put electrodes in there they trained these birds to look at a mark on a screen and then they trained them on a yes or no task so if they saw the light turn on the mark turn on on the screen and then there was a delay and then they were trained to respond a particular way yes or no if they saw a certain another certain stimulus so it was basically like hey here's this box now wait a second and now we're going to tell you what you should answer the part of telling the birds what they should answer was to remove randomness and that the birds might just be learning some kind of trick to the answer so by telling the birds this is what you have to do they were learning the strategy and learning how to play the game but they had to rely specifically on what they had seen previously before the delay so they knew exactly what the birds were seeing because of the electrical electrodes in the the back of the brain it's like oh if there was a box there on the screen do do do do visual cortex information went into the brain the brain lit up and it was like yes it was there if it was not there there was no activation in that part of the brain and if it was shaded at somewhere in between 100% brightness and zero it would the the neurons would light up somewhere halfway as well so then they said let's do this thing let's do this test and they had them either see the box or not see the box and react in the way that they were supposed to react and because of the way that they set the test up they were able to determine that the birds were not just visually responding to a stimulus but actually subjectively aware that the stimulus was there conscious of its presence and making a choice to click their answer to click the to click the response box because there was that delay the birds were taking that their perception and acting on it in a conscious fashion and so this study they say it confirms that crows carrying crows have consciousness now okay lots of animals you look at that Blair Efra you have your dogs I've got my cats I look at my animals and I've been an animal biologist for years I'm like but I still look my cat is conscious my cats know their name they're not just doing tricks they know what's going on right but they're also mammals a bird is a completely different it's a different group of animals and if consciousness is something that we share with birds that means consciousness itself goes back to an ancestor sometime before the split yeah it could be convergent or it could be it could be convergent but it could be convergent I tend to agree with the first premise so now the question is do you know if we look at this you know does this mean all all birds are are conscious does this mean that if we you know go back then uh the the crocodilians are they conscious like how far back does it go and what areas of the brain and what brain designs what structures and you know how does how does the structure lead to the function what amount of brain and wiring networking within it allows consciousness yeah there's consciousness you like there's lots there's lots to that right there's like a sense of self there's like an understanding of your impact on your environment or your population so then if you start thinking about animals that live in cooperative groups there's been lots of study on lots of different kind of levels of organization in the animal world about how especially with altruism like animals that help each other in groups if if an animal is is better at helping other animals they get helped more and if they're not as good at helping others then they get helped less which also kind of implies a sense of self and a consciousness because you're like you're there's oh well you're not gonna help me so I'm not gonna help you yeah which indicates an understanding of your own self so I feel like this is one of those things that the more you pick away at it the harder it gets to find a find a hard line in between this consciousness and not my favorite maybe there is no hard line I mean maybe it is a gradation I mean yeah my favorite example would be learning and the act of teaching like yeah I'm sort of picturing orcas doing things dolphins using tools or using strategies to to attack prey that then the young observe and then repeat so there's a there's both there's and especially with the orcas just because I've been watching too much orcas stuff lately reading too much orcas yeah they will do sort of faux hunting where they allow the young to sort of take the lead and then we'll kind of then show them how it's done and then let them go do it and then show them how it's done kind of go let them do it and that's both an awareness of one is learning I have to pay attention to this other individual and try to recreate what they do but also that awareness of I'm going to illustrate I'm I'm intentionally going to demonstrate and then allow my pupil are offspring to attempt to replicate and see how they do and then I'll show them again and so that sort of exchange you know and I I'm picturing this as I'm trying to come up with examples and they're all mammalian and then there's there's and then there's birds Blair can you think of anything is there is there a crocodilian thing because crocodilians can do a group hunt yeah and we've we've we had a really cool story so many years ago now where the the kind of the bigger crocodiles would sit and wait and the smaller more spry faster crocodiles would help chase prey to that crocodile that was waiting so there's teamwork going on yeah so in I mean when you're talking about animals that exist in social groups there's I mean definitely awareness there has to be some kind of conscious right and maybe it's not conscious but this study suggests that you know this is much more widespread than we you know than we have the evidence to think or to have thought before and that there's conscious awareness of self and other like you were talking about because you have to be able to exist in that group and work with others to exist in that group and if you're not you know not aware and conscious then but awareness and consciousness are like two different things right psychologically but I think it gets yeah it's just very interesting question the idea of being conscious of a perception to be able to hold on to it make a choice based on it and act on it there's I mean it's a there's a lot there's a lot in there I mean I have I have another today I was talking to a classroom of students about bearded dragons and how they like wave at each other to be like hey this is my space and you know if you're if you're a smaller bearded dragon than that big bearded dragon that waved his hand you're not going to challenge his space so how do you have enough sense of yourself to go okay I'm smaller than that dragon and that dragon just signaled to me that that is his space so I'm going to leave him be and try to find another space there's just yeah it's if you're picking at the scab it gets harder to there's two more examples I'm going to leave you because again it's satisfying and but we want to end the show I know we're gonna end the show there's two videos that people should try to find on the YouTubes one is of an otter and one is of a penguin and in each of these cases these animals are in the water when an orca comes comes comes by and leap onto a boat to avoid being eaten now they're in close proximity to humans which normally they would do anything to avoid but they're jumping on where the penguin is just basically jumps into the boat with a bunch of people and is like hey how y'all doing yeah so what are we doing are we fishing are we sightseeing because yeah it looks like a nice park you got here and it's just like sort of like really trying to ingratiate itself with the group there as quick as possible as this orca is like coming up and like looking like where'd you go where'd you go just I'm just looking like a human over here that's all doing my best to fit in aside from the natural fear of a predator driving this there is also some okay that's bad that's bad but this isn't as bad that's much worse and I'm gonna take care of myself by joining this and avoiding I think this yeah it's really hard to look and that's too you know that's a mammal and a bird it's really hard to look at the animal kingdom and really think that we are that different sometimes people forget sometimes people forget and it's worth reminding every once in a while are you gonna say we're we're animals yeah we're not yeah it's we're not really no I I love telling that to a classroom of kids and them all going no we're not we're we're mammals so that's an animal shouldn't be so strange yeah I mean our parents tell us our parents tell us I mean I tell my son don't act like an animal you know yeah I am one can't help it okay think that does it for our show for the night fellow animals we have science and we have made it to the end thank you for listening I hope that you enjoyed the show it's time for those shout outs what a shout out to Fada for helping with social media and doing the show notes thank you so much Gord thank you for manning the chat room identity 4 thank you for recording the show and as always I would like to thank our Patreon sponsors and the boroughs welcome fund for their generous support also Efra Dr. Efrain Rivera Serrano thank you so much for joining us tonight on the show you're welcome it was great all right time for me to read those Patreon names Donathan Styles aka Don Stilo John Shiolly Guillaume John Lee Allie Coffin Maddie Perrin Gaurav Sharma Josiah Zaynor Mark Shoemaker Sarah Foear Farr Donald Mundes Gerald Sorrell Steven Albaran Daryl Maishak Stu Pollock Andrew Swanson Fred S. 104 Corinne Benton Sky Luke Paul Roanovich Ben Beldnell Kevin Reardon Noodles Jack Brian Carrington Matt Bass Joshua Fury Shana Neena Lam John McKee Greg Raleigh Mark Hesonflow Jean Tellier Steve Leesman Ken Hayes Howard Tan Christopher Wrappen Richard Brynden Minnish Melizon Johnny Gridley Flying Out Richard Porter Christopher Dreyer Mark Miseros Mark Miseros Sardium Greg Briggs John Atwood Robert Rudy Garcia Dave Wilkinson Rodney Lewis Paul Matt Sutter Phillip Shane Kurt Larson Greg Landon Mountain Sloth Jim Drapeau Sarah Chavis Alex Wilson John Ratnaswamy Sue Doster Jason Oldes Dave Naver Costie Ranki Matthew Litwin Eric Knapp EO Kevin Parrichan Aaron Luthan Steve DeBell Bob Calder Marjorie Paul Stanton Paul Disney Patrick Pecoraro Ben Rothig Gary S. Ed Dyer Tony Steele Ulysses Adkins Brian Condren Jason Roberts and Dave Freidl Thank you all for your support on Patreon. And if you want your name to be read at the end of the show, you can find information at patreon.com slash this week in science or just click that Patreon link at our website. And on next week's show, we will be back once again. When will we back, Justin? We will be back Wednesday, 8 p.m. broadcasting live. That's 8 p.m. Pacific time. Broadcasting live from our YouTube and Facebook channels and from twist.org slash live. Hey, I know you love looking at our beautiful faces, but if you want to multitask and you want to listen to us as a podcast, just get the audio only. You can search for this week in science wherever podcasts are found. If you enjoyed the show, be sure to get your friends to subscribe, grab their phone, hit that subscribe button as well. For more information on anything you heard here today, show notes and links to stories will be available on our website, www.twist.org, and you can sign up for our newsletter while you're there. That's right. You can contact us directly as well. You can email Kirsten at Kirsten at thisweekinscience.com, Justin at twistmeaning.gmail.com, or Blair at BlairBazza at twist.org. Just be sure to put twist, T-W-I-S in the subject line, or your email will end up, I don't know, inside a capsid in a test tube in a lab, and we'll never see it. You can also hit us up on the Twitter where we are at twist.science, at Dr. Kiki, at Jackson Fly, and at Blair's Menagerie. We love your feedback. If there's a topic you'd like us to cover or address, a suggestion for an interview, a haiku that comes during the night, please let us know. We'll be back here next week. Oh my gosh, it's almost October, and we hope you'll join us again for more great science news. And if you've learned anything from this show, remember... It's all in your head. So I'm setting up shop, got my banner unfurled, it says the scientist is in, I'm gonna sell my advice, show them how to stop the robot with a simple device. I'll reverse all the warming with a wave of my hand, and all it'll cost you is a couple of grand. This week's science is coming your way, so everybody listen to what I say. I use the scientific method for all that it's worth, and I'll broadcast my opinion all over the air. Cause it's this week in science, this week in science. This week in science, science, science. This week in science, this week in science. This week in science, science, science. I've got one disclaimer, and it shouldn't be news, that what I say may not represent your views, but I've done the calculations, and I've got a plan. If you listen to the science, you may just get understand. That we're not trying to threaten your philosophy, we're just trying to save the world from Japanese. And this week in science is coming your way, so everybody listen to everything we say, and if you use our methods that are rolling to die, we may rid the world of toxoplasma, got the eye. Ay, ay, ay, ay, ay, ay, ay, ay, ay. Cause it's this week in science, this week in science. This week in science, science, science. This week in science, this week in science. This week in science, science, science. I've got a laundry list of items I want to address, from stopping global hunger to dredging Loch Ness. I'm trying to promote more rational thought, and I'll try to answer any question you've got. But how can I ever see the changes I seek when I can only set up shop one hour a week? This week in science is coming your way, you better just listen to what we say, and if you learn anything from the words that we've said, then please just remember it's all in your head. Cause it's this week in science, this week in science. This week in science, science, science. This week in science, this week in science. This week in science, science, science. This week in science, this week in science. This week in science, this week in science. This week in science, this week in science. This week in science, this week in science. Oh yeah, we've come to the end of the show! No, not elect more. Oops. Not more Scientologists strength. No. No, no, no, no. Happy October, wean. That's right. Tomorrow it's October, and I know I haven't done things that I should have done already. No way is it keep going. I'm having issues getting things done. What? Same. I keep wondering, seriously, it's like people are running at this breakneck pace to continue to make things normal. They're like driving themselves to oblivion with normal distractions, and I just am tired, and I'm feeling like, I do need hugs, thunder beaver. I like the bumper sticker theme that you designed identity for. That sounds great. That sounds funny. Oh, Fat Bear Brackets. We should look at that as a group. If you don't know about the Fat Bear. You didn't know about the Fat Bear competition? No, no, Fat Bear Week. Their social media team is really good, but also they do fun stuff. They don't take themselves too seriously, and I love it. Yeah, so okay, here I'm going to screen share for those of y'all who don't know Fat Bear Week. Fat Bear Week is the competition to choose the fattest bear. Thanks, noodles. Yes, yes, and so there is a bracket. So there's a single elimination tournament for each set of two bears. Vote for the one you think is the fattest, the bear with the most votes advances, and one will be crowned. So okay, so we've already got a couple of days worth of polls. So here's the bracket. There we go. Fat Bear Week bracket. So today's closed, I guess they're on Eastern time. Yeah. So you can download a bracket, make your own predictions for who the fattest bear will be. So we have, let's see, oh, check back for voting results. So we haven't gone very far, but we've gotten. Oh, the one at the bottom. 151 got chonk. Yeah, so these bears are like how ready are they for the winter? They're chonking up for their hibernation. Those are some good boys and girls. I think, yeah, I think Justin, I think you're right. The one, I don't know, the bottom's pretty big, but the one at the, that one there, 151. But the 856 bottom one also looks, yeah, that's a good competition right there, but I think the one at the bottom. But you know, that one, it is a bear rump shot. It could be the angle. Bear rump. I got a couple of questions in the chat room here. One is, what am I doing and where am I? I ask myself this every morning. Are we supposed to answer this question or is this for you, Justin? That one's for me. Where am I? What am I doing? I'm in currently in Denmark. I am taking classes remotely and looking to be re-entering the workforce flow thing sometime at the end of next month, perhaps. But yeah, I've been, I've been taking a pandemic cation to a place where there's less cases and frequent testing available, which it's, it's a, Denmark is nice. If you've never got a chance to travel anywhere again, not a bad place. Also, let's see, random genre talk. I have a question for Justin in his study at the beginning about the matter percentage of the universe to black holes count as matter, matter or energy in this calculation. So that's a great question. What about the geodes that we were talking about? Those are matter, right? But it's dark energy. That's the dark energy, which is the mass, the predominant form of energy. So as far as the black holes, I don't know how exactly they would account for this. However, they are, the study was based on observing galactic galaxies. All right. So if you have, I suppose if they're galaxies, how the massive, most massive black holes at their core, so that matter and energy should be accounted for just by the fact that you're looking at these galaxies, because at the center of each of them is the biggest form of black hole that we know to exist. However, yeah, I don't know about the free floating black holes that might not be associated with the galaxy that maybe took up everything that was around it, but I don't know how, you know, when we look at that spread of matter, the way it's, well, what's the, what am I trying to say the words with the, how it's sort of all connected into the threads and webs of matter that is dispersed throughout space. Now to assume the black holes would be there because they need the matter to begin with. So they should be in and amongst those galaxies clusters. So based on that, I would say that that's how they've accounted for black holes as, as the matter energy. But, but that calculation they were doing was matter as energy. So I don't know if do black holes count as matter or energy in the calculation. I suppose it would be both. This bears number is 747. And is that because he's a jumbo jet? Yeah, it kind of is. That's another rump shot largely though. Let me show you my favorite. I'm Holly. Holly is my fave. Oh, look at her go. Oh, Holly. I don't even think Holly can walk. I'm just gonna hibernate right here, folks. That's it. I'm done. I love you, Holly. You're my fave. What was Holly getting a hold of? That's a lot of salmon. Seagulls. Seagulls? No, the seagulls are hanging out. They're like, Holly is a good source of food. I will. Holly has been, has been eating other bears, no doubt. Yes. And then, yes. The looking at bears and listening, listening to stories about matter in the galaxy. Yes. It all makes sense now. These tendrils of connection. No, Shoebrew. We're not talking about the debate from last night. Nope. No, no want. No want. That's why we like fun science. I wouldn't actually bear rumps. I wouldn't mind talking about the debate. I really wouldn't in the after show, but there wasn't one. I know commentary of, I don't know who won that debate, but one thing's for sure, America lost. Yeah, I don't, yeah, I don't really, I don't think that the one happened. Lots of shouting occurred. I don't even watch it. Yeah, exactly. What? I don't know. Fat bears. That's all I know right now. It's the most important thing. Oh, oh my goodness. How's everyone holding up? All good out there? Yeah. All the good out there in the world. I think Justin, you are starting to get your, your coffee is working. Get a day ready. Dopped working. Yeah, it is almost eight o'clock in the morning where, where I'm sitting, uh, had a pot of coffee and I think I'm almost ready for a nap because that's something's wrong. That's like every week. Oh my goodness. This week I've been very tired. We've got some kind of a little cold bug in our house and we don't know how we got it, but guess who has two thumbs and went to get a COVID test today? Oh, well done. How's your brain? It's fine. They did not do the nasopharyngeal swab. They just did a nostril swab, although they did, it wasn't, it would, they went up there like, let me get up in there. So it's, it's kind of interesting. I got tested here. 72 hours. We'll see. Yeah. I got, oh, that's a good, that's a good turnaround. Uh, that's a, that's a turnaround. I had her as 24 to 48 hours here. I think we got it, the results within 24 hours. Um, but it was a, a back of the throat swab. They did not put the, I was all like cleaning out, you know, before they did the thing. Like I don't want them to come out with, put the thing up and then come out with a big bogey. Right. That's just going to get in the first time, I'm sure. I didn't want them to find anything weird in there. And then there, no, it was, say, ah, and it went in the back of the, and that was the, the way the test was done. When they, when they did mine, they were like, you will gag. Don't be embarrassed. Oh, so you got yours. Yours was also the, the throat. They did both. They did both nostrils and my throat. Yeah. Oh, interesting. All the day. But this was, this was back in June. Yeah. And I had all of the symptoms except for the only thing I didn't have was the dry cough. So, but that didn't happen. I didn't have any symptoms, but I had been on a, I had just gotten to the country. So you, you have to get tested at the airport when you leave the airport. The brushwoods, Brian and Bonnie have COVID. Oh no. Yeah. Bonnie, yeah. Bonnie's having it worse right now, but yes. Yeah. They're making their way through that. Supposedly, hopefully all their kids are okay. So they have what three daughters like that, but yeah, I can't imagine having They all start with the letter B. All through. I hope so. Yeah. I can't, I can't imagine having a large family and trying to isolate and like deal with that and parent and home school and that would be quite a lot. It'd be quite a lot. Yeah. Their last test was negative. Yeah. Anyway, tests. We need more tests, everybody. Can we get more tests? And Gara Sharma in the chat room says he needs to go get his flu shot. Yes. Get your flu shot. If you're a person who can get a flu shot, get your flu shot. Get that flu shot. Yep. I got mine. I got mine. I got mine. I got mine. I haven't gotten one yet. I might get one relatively soon here though. Is it going to be the same flu shot if I get one here? Northern hemisphere. It's northern hemisphere versus southern hemisphere. So it's probably the same because people don't travel different hemispheres. Yeah. I don't know. They travel within more. Yeah. Most travel. Right now nobody is. Right now nobody is. So it's probably, this time it would be perfect, but interesting. Yeah. I knew there was different shots, but I didn't realize how it was broken down. It's seasonal. So the way that it works is because Australia and Southeast Asia, they have their winter and whatever strains seem to really happen there are the ones that we expect will start to happen in the northern hemisphere when our indoor season starts to happen. And it's not that people don't travel back and forth. It's just that because of the nature of the virus, it is more seasonal. You can get the flu just about any time if you don't have immunity for it, but it's more likely that you'll get it during the winter because of all the factors that are involved in allowing for the transmission of the virus. Humidity, cold, all that kind of stuff. Yeah. You there, Justin? I know. Your brain ended. Did I literally freeze real time? So this thing happens where I was reading something. I was reading something and it's, this has not been a problem in the past, but my older brain, if I'm reading my auditory, since it's shut down, I can't hear anything. So I was reading something real quick and then I completely lost what was no longer able to multitask. This is what, this is what this is aging brain. This is what aging looks like. Were you saying something to me? I'm sorry. No, would not at all. No, no. Also, it also could just be COVID brain. See, I'm like a couple ticks behind now too. But there's lots of really good articles about how like, hey, even if you feel like you've like found equilibrium in the time of COVID, you still probably have at least 10% of your brain that's constantly focused on the fact that we're living in a pandemic. And so it's harder to multitask. It's harder to get things done in a normal amount of time. It's harder to feel motivated and it's because your brain is constantly busy with something it wasn't busy with before. I just really, I really like the idea of just everybody taking like everybody taking a vacation for like a month. Let's just plan for it and just, can we all please just not, not do for anything. I don't, I don't want to do anything. Only healthcare workers go to work. Uh, grocery stores can be open like three days a week. Right. We don't need them open. Plan ahead. Just plan ahead. Close down for a month. This is the thing Justin's been talking about forever. I know. You're shut down. I'm not saying it for getting rid of the virus. I'm just saying so that we all have a vacation. Yeah, it is weird how like, we didn't get a summer vacation at all and yes, but yeah, but we need a do nothing November. We're distracting ourselves with work and it's right because now also like people like myself who had an office, I have the lines between work and not work are blurring more and more and more. And at the beginning of things I was like, okay, I'm going to work at nine quote unquote finish work at five like very clear line. Those lines are blurring more and more every day and it causes problems. Uh-huh. It's like, that's cute. Make soap November. Well, that sounds fun. Oh, I like internal monologue short stories. Carol Ann, you sound that sounds fascinating. Yeah, multitasking is a myth. That's for sure. That's true. It's true. People say we can multitask, but no, we can't not very well. Um, are we, are we, are we tired? Yeah, give the pint of blood today. You might need tomorrow. Yeah, if people can go give blood, now is the time to do that blood shortages. And if you are able, that is something very helpful. No, no vacations on cruise ships. Mm-hmm. No, no, bad. Not right now anyway. I would like the Lysol cabin. Their environmental impact is off the charts. So generally cruise ships, maybe, maybe we're done with them. Just a sailing vessel. Yeah, you could go on an eco cruise, which is like 50 people or less. And those are very cool. But those giant cruise ships, maybe, maybe they've had their time. They're good. Walking dysentery ballast invasive species delivery systems. Oh, I miss movie theaters. That's the one I do miss a lot. There are a lot of movie theaters are now doing private rental showtimes. So like, I have a coworker who who was able to rent out a theater for $99 for a showing, the entire theater. And so you can have up to 20 people, which like, he's an essential worker. And so he and a bunch of people who are going into work together every day and are already kind of in this pod are all going. So that's pretty cool. But he invited me and I was like, well, I'm still kind of working at home. And I also have other, you know, the other thing is I have a social engagement this weekend. And so I'm trying to not I'm trying to have like one every two weeks, if that right. So like, it's two days in a row with different social circles. No, I'm good. You know. Yeah. So this is that this is a reality that this is a reality that I have. I have declimatized from since being in Denmark. It is not there. Here. Yeah, there are you can go to a restaurant. They have they have implemented a face mask only recently at restaurants for when you're standing. You have to go in with one on. But then you take it off, of course, right away when you when you eat. But staff and waiters and stuff. Staff and waiters and stuff. These people are now wearing them. But it's yeah, I'm going to have to reintroduce myself into all of that. Turn back on that part of the brain that's always thinking about this. I haven't been. That's nice. Nice. I would like to not do the thinking. Okay. I think that's yeah, that would be nice. I like the not thinking I would like to turn my brain off for a while. Maybe with some sleep. Oh, got you. All right. In that case, I think it might be time to say good night. Oh, I was too late. She's already. Good morning, Justin. Good morning, Justin. Good night, Kiki. Good night, everyone. Have a wonderful week and we do look forward to seeing you again next week with more science and I hope that you stay well and you know, stay well, stay safe, stay healthy. Thank you for being a part of the night with us tonight or the morning wherever you are. Good night, sweetheart. Well, it's time to go. Boom, boom, boom, boom.