 This is TWIS, this week in Science episode number 613, recorded on Wednesday, April 5th, 2017, taking a science swim with the fishes. Hey everybody, I am Dr. Kiki and I am back once again to swim in science-y land. Tonight on This Week in Science, we are going to fill your heads with surprise, fang-blennies and tiny harpoons, but first. Disclamer, disclaimer, disclaimer! They say that a watched pot never boils, but they never ask the lobster who has been watching it intently. And as we resolutely instead fastly move forward, without addressing greenhouse climidia, the changes begin to take place all around us. The end is not nigh. In fact, it is just beginning. It's going to be a long enough process that none of us here now will likely live to see the end result, but it is developing fast enough that we will all see with certainty where it is headed. The constant flooding of New York City, Miami and New Orleans, first frequent flooding, then simply underwater and abandoned for good. The state of California, the capital of California, and nearly 100 miles inland from the sea, swampy marshlands. In other parts of the world we will see much of the same as coastlines recede, as ports and harbors are swallowed up by rising waters and the dead seas come back to life. Most famous world cities have a close relationship with the ocean and all are at risk. The end is not nigh, but it is nigh to impossible to ignore anymore, though oddly we won't even mention it on this episode of This Week in Science coming up next. Got the kind of mind that can't get enough. I want to learn everything. I want to fill it all up with new discoveries that happen every day of the week. There's only one place to go to find the knowledge I seek. I want to know what's happening. What's happening? What's happening this week in science? What's happening? What's happening? What's happening this week in science? Yeah! Science to you, Kiki and Blair. And good science to you, Justin, Blair, and everyone out there. Welcome to another episode of This Week in Science. It's good to be back here with everybody. We missed you! I missed doing the show last week. It would have not worked, but... Hello, I am podcasting from the car. Yeah. Hello, it's me. I'm driving in the car, but I have science, don't you see? Wow, we are musical theatering on twist right now. Care of Blair, here we go. All right, this week we're gonna... We had science, it's not just musical theater. It's not just fun and games and jokes. It's science, lots of science. And so I've got some stories about CRISPR because we all love CRISPR. I've got brains and babies because that's always awesome. And little tiny harpoons. Little tiny harpoons. Tiny harpoons. Adorable and terrifying. Absolutely. Justin, what do you have? I have got strawberry alarm clocks, ancient Americans, and biochemically manipulated eyes. Ooh, I'm excited about that. And Blair, what does the animal corner hold in store for us? Oh, the animal corner reeks of fish this evening. And I also brought a cash cow just for fun. A cash cow? Yeah. Share. Yeah, sharing the cash cow. Delicious cash cow. Cash cow. A cash cow's like money. You're gonna give us money. No. Of sorts. Okay, fine. All right, let's dig into some of the science news that's going on. We've been talking recently about the replication of studies and how there seems to be something of an epidemic of non-replicability, reproducibility in the world of psychology and cognitive neuroscience. You know, specifically, we've talked previously about MRI, errors in the MRI calculations, and other things that have led studies astray. Well, a group of researchers have done a meta-analysis. They analyzed 26,841 statistical records from 3801 cognitive neuroscience and psychology papers that have been published fairly recently. And so what they, what? That's good. Big data crunching there. Those are many, many studies within this crunch. Yes, many studies. And so this is really, you know, and it's kind of, there's irony here in this study that is not lost on me. Hope it's not lost on you. But they were looking at these studies and they basically found that sample sizes in most studies in psychology and cognitive neuroscience have remained small. Irony there, right? Small. And because of that small, the smallness of the sample sizes, they predict that about 50%, there's a rate of about 50% for the whole literature of false positives, of false results. That's real terrible. That's a failing grade. That's a failing grade. And so this low statistical power that results from not having large enough sample sizes is basically leading researchers to making conclusions that aren't necessarily true, that later researchers trying to reproduce their studies can't reproduce because they, you know, basically it's like, we just needed more people in these studies. So the researchers say, you know, using their large data set, they estimated this statistically significant false finding or false report probability. They observed that cognitive neuroscience studies had higher false report probability than psychology studies, even more so due to smaller sample sizes. And so when you think about cognitive neuroscience, very often you're like, okay, brain areas, these are fMRI studies where they're doing brain scans. Again, it's very hard to get large communities of people involved in studies like these. Come on, into my, into my very tight machine. They need to increase the stipends. Higher stipends all around. There's that, there's also, I wonder how much of a pre-selection process is going on with their sample sizes. Like this is so complicated. You know, any individual study who's looking for people who have a particular makeup, who don't drink coffee, and who also sleep, self-report, sleeping well through the night, or like whatever it is, like they're also a lot of the times they're looking for a type of person to study. So it's tough. It's a tough thing to get the big sample size for some of these when they're trying to eliminate other factors in their, in their sample. They should make it a requirement for all undergraduates to participate in one study. That would be fantastic. Well, if you're, if you are in taking psychology classes, very often it is a requirement of a psychology course to be in a psych, to volunteer for a psychology study. Yeah, but even that's too limiting. Just everybody, everybody, the whole university, all the graduates have to participate in one study. Yep. And one of the most interesting findings from this was they looked at correlation between the statistical power of the studies and the impact factor of the journals in which these studies had been published. And they found that it was more likely for really low statistical power psychology studies to be published in very high impact factor journals. And impact factor is like, you know, science and nature sell, you know, these are journals with very high impact factors. So there's, they're looking at, they're potentially getting a, they're going for the sensationalist finding, the thing that's going to sell, that's going to be great, but not necessarily looking at the statistics in the way that they should be. So this is, this is I think a wonderful example of science correcting itself. And this is, these are scientists taking a hard look at the work of other scientists. So that potentially changes can be made to the process and we can move forward and improve the scientific method and actually publish high statistical power studies without false positive results. Yeah. And it's got to be a huge challenge for the, for that field to be able to, to come up with the numbers. You know, that's, I don't know how they're going to do it. Yep. Well, they have to, they got to do something. I don't find a way. I mean, I mean, really, I think you would have to figure out how to design is something that people could pop into say on a phone app or some, some sort of, some sort of test as much as you can get, you know, entice people in to do this on a wide level remotely where they don't have to be at the university in that controlled environment sitting down in that chair in that room you were describing. And, and, you know, you've got, you've got three weeks to work on this project at the university and you've got 20 people who said they'd show up and eight show up. Yep. Yeah. And it's, it's, it's a, it's a horribly difficult effort to do something in two controlled environments. So what you need to do is create noise, your tests noise, the tests that can, that can handle greater amounts of noise and just, just get it into the make it, make it the user friendly, easy access thing so you can get a really large number and hopefully the noise that's in that test disappears with the size of the population that you've got involved. Or you could just increase your stipend, offer beer. Yeah, that's free beer to those that come to the but after only after and then who shows up everybody who drinks beer and is broke. Yeah. So everyone in college is what you're saying. Not actually one, but yeah, yeah. Moving on into some other really interesting stuff. You know how much I love talking about advances in CRISPR and what people are doing with CRISPR and the Cas9 system, right? This week in CRISPR. CRISPR update. So some studies this week were very interesting paper published in Nature Biotechnology from a team out of Duke University. They have used a high throughput screening technique. So basically it's just like throwing lots of, lots of genes or DNA through a screening methodology, finding out what's in there. They used CRISPR Cas9 to identify regulatory elements that are in the in our DNA. So instead of looking at the coding DNA or the, you know, the not junk DNA, they looked at the stuff that's considered junk, which is a majority of our DNA. And so they started looking at specific regions around various areas of interest that they thought would be interesting. And so then they used CRISPR Cas9, which edits clip clip clip to clip clip clip and see what's in there to be able to determine what regions are actually important for modulating, for regulating the protein coding genes. So it's like, there's a lot of regulatory stuff that comes out of that non-coding junk DNA that actually controls the expression of the things that make you you, that make your body work. And so it's really unknown at this, at this stage how that system really works, what does what. And so this is a method that they have now used to determine. So they were able to confirm some known regulatory elements and they also revealed new roles for other DNA sequences. Some of them of the sequences that they looked at appeared in activator and repressor screens. So some of them were involved in both activating translation of proteins and tamping it down and repressing it. And some seem to play a regulatory role for a gene in one kind of cell, like say your kidneys, a kidney cell, for instance, but not for the same gene in another kind of cell. So maybe in your liver, the same gene, it wouldn't be regulated by the same sequence of DNA in the same way. And so there are very cell specific instances of regulation that are going on, which kind of makes sense. It's like you don't want everything always doing the same thing in all the organs of your body because the organ systems of your body are even though they work together, they're like separate groups, you know, they have different things going on. So the researchers say we know that there are several aspects of the epigenome that correlate very strongly with changes in gene regulation. And it's always been a struggle to turn those observations into a real understanding of how genes are actually regulated. We don't know yet if the particular epigenetic modification that we observe is the causal one, just correlational, but we do know now from this and from other work from our labs and others that modifying the epigenome does indeed have a role in regulating some of these target genes and another researcher brought up the idea that this throughput method, this screening technique that they're that they're working on, although it has limits at this particular point in time and they're working to scale up the technique and make it more available for for the entire genome. It could be used to go through genomic data like we've reported on before the encode project, which is has been trying to figure out what all the stuff in our DNA is for, right? What is it all code for? Or what does it do? And this kind of a methodology, this, this is a new tool in the toolbox that we can maybe figure out what's going on in diseases. You know, why does some G's get expressed or under expressed what's going on in the regulatory elements of our DNA that make things work or not? So it's pretty cool. And then along those lines as well. This is the surprise that's coming in. Researchers published in E life, which is an open access journal. So if you want to check out this article, you can go read it, read it for yourself. There is no no fee for reading. Researchers from Cold Spring Harbor laboratory used the CRISPR-Cas9 system to knock out a gene in cancer cells. So this gene is called maternal embryonic leucine zyprokinase, otherwise known as milk. And milk is a target for various therapies for RNA interference therapies for all just all sorts of things. They what has been thought from previous research is that milk is a very important gene for cancer cell proliferation. And so if you can target milk, then you can stop proliferation. And so there have been lots of studies and different things that have been done like RNA interference and people are working on actual therapies that target this gene, you know, thinking, okay, we're going to get it cancer cell proliferation will decrease. This is going to be great because it'll reduce the growth of cancers and maybe allow people to live longer being being able to allow people to get surgeries before things go go too bad. However, this paper, this paper, they use the CRISPR-Cas9 system to knock it out there, clip it out, just go into the cancer cells. And if, you know, they basically were like this cutting out milk out of the cancer cells, this was their control because everybody was so sure that milk was responsible for cancer cell proliferation. And so he says, he said, we had the researcher, Jason Scheltzer, he says, because there was all this previous literature that milk was in fact a cancer dependency, dependent. So in our initial conception of our experiments, we had milk in as a positive control. And then they expected it to inhibit proliferation, but the cells still proliferated even after they cut milk out and got rid of it entirely. So what they're going, everybody's like, what is going on? So now the hypothesis has changed that milk is involved in a pathway, but maybe the RNA interference and other therapies that have been targeting milk have actually been having downstream or even off target effects that have been showing the results of decreased proliferation. And so they went on and they looked at all sorts of cancer cells. They looked at 13 cancer cell lines. It was not the, it wasn't in charge of proliferation. There was no cancer dependency for milk once they cut it out in any of the cell lines. And so they were like, okay, this is what's going on here and nobody really knows. And so they, to find out a little bit more, the researchers actually created cancer cells that didn't have milk instead of just chopping it out. They're like, okay, we'll just get rid of it entirely, knock it out, cut it out. And then they treated them with a drug, a milk inhibitor that's called OTS167. It's actually being tested in clinical trials right now. And they found that the milk inhibitor was still effective even though there was no milk there. See, I would think that that would at least maybe not have an effect because it was, it seems like it was already targeting something. That's right. But it's, it's targeting something else. It's not there. And so it's, it's, there's something else that they weren't targeting that it's affecting. That's still having that result. But that's, at least they got a good drill down there. Yes. And so it was super surprise, you know, these, these researchers thought this was pretty well understood and that they could even, you know, use it as this is a control. And this is the lovely surprisingness of science. It's like, oh my gosh, we have something wrong in the way that we're figuring things out. And the scientist magazine reached out to the Japanese company that is a lab that is responsible for the development of OTS 167 and the spokes person from on co-therapy science has written back. We are not in a position to give you any comment about another group's paper. When the scientists tried to find, hey, what do you think about this research about your drug and how it still works, but it's just still does what we said it would how it works. Like whatever, we don't know what it's doing anymore. Yeah, we don't know why, but so now, so now what exactly exactly. Yeah. So now what they are really interested in doing is using this CRISPR-Cas9 methodology to target other genes and knock out other genes that are thought to be thought to be critical in cancer to do the drill down and really figure out, okay, what is what are the important genes when we are targeting things with our therapeutics are are are they off target effects or are they actually targeting what we think they are, which will be important moving forward. Yeah. Anyway, so CRISPR-Cas9 bringing us scientific surprises and kind of it's I think it's exciting. I think it's a neat development. This drug, it doesn't mean the drug is not necessarily going to keep going through clinical trials. If it does its job, it's a good job. It's great that we now know that it doesn't work the way that they thought it did and so we can it'll narrow actually it might might I mean does jumpstart a whole lot of other venues to look at then. Yeah, absolutely. What are the what are the off targets? Where what is happening? I love it. This is this week in science. Hey Justin, what you got? If you're a farmer, you want to get growing when the growing is good and if you're a strawberry, the growing is good when bees are about and according to new Cornell University research, the bees are all about apple blossoms. When the apple blossoms abundant so the fragrant flowers attracts pollinators, it attracts so many that if you've got another crop across round away over the bed, whatever it is, they kind of ignore them and it turns out that that crops such as strawberries have lower yields during apple tree blossom time. However, this is what the study found if growers time their strawberries to flower directly after a neighboring apple bloom strawberries produce higher yields than they would if there were simply no apple trees in the area. Yeah, so it shows as much as they can previous research showed that strawberries can have as much as a 40% yield increase when bees and other pollinators are there compared to them just relying on wind based pollination. So you don't want to distract the bees from the strawberries, but you want to attract them over so that they hang out in the strawberries for the after party. Right. Yeah. It's like, okay, because the bees are going to move on. It's like the apple blossoms are gone. They're just going to take off. It's like the taco truck right outside the night club when it closes at 2 a.m. That's right. Well done, Blair. That's it. So this is a quotey voice of Heather Grabb, Cornell University doctoral student of the lab of co-author Brian Danforth, Professor of Entomology. We are trying to figure out ways that growers can use ecosystem services to promote crop yield rather than relying on external inputs such as fertilizers, pesticides going on, planting natural habitats around farm fields can lead to lead to improved health of pollinators and a boost in their services according to the research. But for most growers and agriculturely dense areas, increasing natural habitats is not really an option. Those growers grab continues need some more sustainable agriculture options. If growers pay attention to timing, the wind crops are blooming and manipulate that by planting apple varieties and strawberry varieties that don't overlap. You can get a boost in yield that is almost as equivalent, the equivalent of having the natural habitat there nearby all the time. So I'm sure there's some like cranky old farmer out there listening this going, I've been that's how I've been doing it for the last 200 years, but you know, 200 year old farmer. That's why that's secret farmers who who work in sustainable crop rotations and agriculture live longer. Those who rely on the on the chemicals, maybe not. Right exactly. Yeah, I think, you know, there are lots of really interesting things that we should look at. It's stuff like things like this, the crop rotations to improve our yield so that we don't have to rely on the fertilizers on the on the pesticides on the, you know, all the all the things that we use, the pisons that we use. And if we are, you know, if we're able to make it a better environment for the insects that do the pollinating, right? Can you imagine like is creating an entire growing season, which is incredibly long. It's all year round almost here in California. Where your your timing, where the placement of your pollinator attractions are going to be like in an area where they can sort of be passed off from from this crop to that crop from that crop to the next to the next to the next. Then you have to eat your produce seasonally, which is something that you're not the best at doing yet or again. We don't have to. We've got trucks and planes and boats. Right. Buses full of strawberries. Maybe this is a time to revisit that conversation. California with its near, well really all year round we're growing something. There's, you know, California could do more than one crop of strawberries in a year. Like we have some that can bloom earlier, some that can that can be ready later. But it's sort of an interesting idea to really to for maybe it's not just one farmer but a group of farmers that kind of would have to sit down and get together and figure out the schedule for the year so that they can maintain the population of pollinators. And I think they're, you know, farmers who are getting into more organic methods, these naturalized methods where they are planting multiple types of plants side by side, you know, to increase the diversity of the actual insects that do come and visit the plants. And there, you know, there are a lot of techniques that are being that are being used right now. And so, yeah, those are good. But, you know, a lot of a lot of these colony claps, if you think about it, if there aren't natural habitats and you have all of the thing that draws them there showing up at the same time and then being completely gone, where do those bees go? Like where do they feed on? They've got to completely move or or just perish. Or perish. Why are we talking? Why are we talking? And no perishing bees. What? What did I miss? Where's, where's the, she's losing it over there. I don't know. I missed it. I was too busy talking. I don't know. I don't know what you missed. Sometimes I can't help myself. Watch the YouTube video, everyone. You're not sure what's going on. This is when to tune in. Do you know what time is the best time to tune in? Oh, I do. My favorite, my favorite part of the show, week in, week out, is the one that's about to come up next. Blair's Animal Corner. Oh, it's, oh, it's Blair's Animal Corner's next. Oh, never mind. It's open at all. Want to hear about animals. She's your girl. Except for giant pandas. That's part of that. Yeah, Blair. Well, we were talking earlier about, about medicine. And I wanted to bring a very interesting story about a researcher named Brian Fry from the University of Queensland. Brian Fry has been studying fang blennies. Fang blennies. I'm sorry. That's either like a cocktail or the name of a muppet. I think it's, it's my new nickname. Clearly. It's my Playa name. You call me fang. Blenny. Blenny. Fang blenny. That's me. Fang blenny's are tiny little fish. These tiny little fish have fangs. Little fangs. And some of them have some potent venom. Yes, believe it or not. Those might be venomous fanged fish. Venomous fanged fish. This is not a money python sketch. This is a real thing that occurs in nature. And researchers recently did a proteomic analysis of extracted fang blenny venom. How do you extract fang blenny venom? I'm so glad you asked. Yeah, seriously. I know with snakes, you have to take their fangs and get them through little nylon or something and milk them. Do we have them? So it's difficult to collect enough venom to actually do an analysis like this for a few reasons. One of them is that the fang blenny's are tiny. And so when they bite, they only inject a tiny bit of venom. So what they ended up doing is they would take little fish out of their tank, dangle a cotton swab in front of the fang blenny. The blenny would bite the cotton swab and then the cotton swab would absorb a little bit of venom. The swab would then be suspended in a solution that drew out the venom, of course, after putting the fish back in the tank. But then from there, they were able to do an analysis on this venom. What they found was that the venom had a lot of interesting things going on. It actually had neuropeptides that occur in cone snail venom. Cone snail venom, one of the most painful stings you can get in the entire world and also sometimes deadly. It also had a lipase similar to one in scorpion venom. And here's what's especially interesting, an opioid peptide. Even more interesting when they then injected the fang blenny venom into lab mice. Further experimentation showed the mice showed no signs of pain. So when you said cone snail venom, researchers, we've reported on this several times, researchers have been working on compounds within cone snail venom as potential painkillers. Yes. And so this is something that this is sounding like. This is something that would be a contender. Yes. And Brian Fry, again, of University of Queensland, the main researcher here and the main author said, for fang blenny venom to be painless and mice was quite a surprise. Fish with venomous dorsal spines produce immediate and blinding pain. The most pain I've ever been in other than the time I broke my back was from a stingray and venomation. Stingray sounds so benign. They don't sting. They are pure hell. All right, Brian, Brian, he's got a penis. Yeah. Hell raise. Yeah. So since they use rodents for this pain test, they don't know for sure whether the fang blenny venom causes pain in fish, but most likely based on the neuropeptide and opioid components and the fact that it caused a sudden drop in blood pressure. This is most likely to cause the attackers that get the venom. Chill out. Oriented and unable to give chase. Yeah. So they're slowing down potential predators, giving them a real mellow, right, gives them a chance to escape. And while as far as they can tell, the feeling of pain is most likely not produced, the opioids produce sensations of extremely unpleasant nausea and dizziness in mammals. So that also might have something to do with it. It might just make them kind of disoriented. Yeah. What's more, this was also very surprising to me. Nonvenomous fang blenny's and other small fish capitalize on the venom success by mimicking the fang blenny's. But what's so interesting about this is that most likely the venom secretions evolved after the teeth, which is so they had the teeth for biting. Maybe it was, maybe it was defensive to begin with. So the bite was defensive. I don't want to be eaten. I'm going to protect myself with my big fangs. And then venom. Yes. So this is really unusual mostly. Wait, does that happen? Great question. We don't know yet, but in most cases, like with snakes, for example, venom evolves first. Maybe the rear fanged. Maybe there's secretions, all this kind of stuff. And then the delivery mechanism comes later. But in this case, it looks like the fang blenny's got their fangs first and then found a way to enhance the fangs with their venom. And the researchers went into the study as according again to Brian Frye. He's quickly becoming one of my favorite people. We had no grand hypothesis, just basic wonderment. So now we'll be comparing and contrasting the composition of venoms from different blenny species. So basic wonderment. Isn't that just the meaning of science? It is. That's cool. Let's just keep following it where it goes. Absolutely trail lead. Yeah. And speaking of fish. Yeah, a very interesting study from ISPA. Oh my gosh. I'm going to try to say this now. In Instituto Universitario, Instituto Gulberkien de Sencia and Funda Kayo Kampal Mode. These are all research facilities looked at zebrafish and they wanted to see through a model of choice. They wanted to study behavior and underlying mechanisms in terms of neural mechanisms related to social behavior in zebrafish. So this recent study looked at the zebrafish and behaviors relating to fear in threatening situations in relation to other zebrafish. Basically, they found in general that zebrafish were more comfortable when they are around other zebrafish, but how could they tell? So this research was looking particularly at if it was sight, if it was smell. So in general, they exhibit less fear in a threatening situation when they can both see and smell their shoal, their fellow zebrafish than when they are alone. So social support in this species is directly related to how much behavioral fear they exhibit and looking at trying to figure out if it was visual or olfactory cues, they found that the visual representation of the shoal is more effective out of the two in decreasing fear response when they are exposed to a threat and that the efficacy of social support in these situations has nothing to do on with shoal size. They just didn't want to be alone is what it sounds like. Yeah, especially if you see a predator and you're in here a shoal fish, shoaler, shoal fish or wherever you want. That's where you hide with the other fish because chances are when the predator comes eating, it'll get the guy to the left or the right and you'll be okay. Well, there is that. I saw Finding Nemo and then the Dory movie after that fish really do have great friends. They do, it's true. So, but what's interesting is looking at the fish brains, right? The social support phenomenon in the zebrafish triggered a specific pattern of activation in specific brain areas in the pre-optic area and in the amygdala. These are also involved in the same phenomenon in mammals. So this suggests that the brain areas in zebrafish as an ideal, they could actually be an ideal model organism for further research on social support that could then be extrapolated to mammals like mice like us. So it just, it goes to show you a few things. First of all, the zebrafish is a good experimental model for future experiments, but then on top of that, it proves that this potentially is very far reaching back of course, we all came from the sea. So this could be something that is, is persisting from all the way from when we lived in the oceans as the great, great, great, great, great, great, great grandmother fish. Right. It would be really interesting to see, I mean, now that they know areas like the amygdala are being triggered, this pre-optic area as well, even though the zebrafish don't have the cortical structures that we have, it would still be really interesting to see if hormones like serotonin are released or if cortisol release decreases when they see their conspecifics, you know, others of their same species or their friends from the shoal, you know, it would be really neat to see the actually see hormonal activation or regulation as well as the neural regulation as well. I'd love to see that. Yeah, absolutely. Not to mention that the more research they do on the zebrafish and these areas of the brain that can then lead to actual health care in humans with depression related to those issues, right? Yeah, you know, it's great. This treatment is going to be perfect. We tested it on a fish. Yeah, it's good to go. Plus, just if you were, if you were curious, I didn't mention that terrible pronunciation that I gave earlier. That's from the research facility in Portugal. That was my attempt at Portuguese. Apologies. I was like, I was a little bit like, is this, did she just skip from her story into doing some sort of Rosetta stone? Yes, I tell you. Yes. Anywho in Portugal, they're looking at zebrafish trying to make us all a little less lonely. Wonderful. And you know what? I hope nobody feels lonely tonight because we're all here talking about science moving on forward and we're going to take a quick break though. So don't go anywhere because we're going to be back here to talk about more science after our break. So stay tuned for more this week in science in just a few. Hey everybody. I hope you're enjoying the show so far. I would like to tell you a few things first. What are you doing June 10th and 11th if you're in the greater Philadelphia area here in Philly? If you're around there, you should come see us. We are going to be broadcasting live from the greater Philadelphia Expo Center at the young innovators fair and we would love to see. Twist fans come out young twist fans, especially if you're out there, we're going to be telling you more about this as the event comes closer. But as of now, the dates are June 10th and 11th 2017 in Philadelphia. The young innovators fair and we do hope that we will see there also coming up in a couple of weeks. Not so far off our robo games. Are you excited about robo games? I'm excited about robo games. I'm going to be at the robo games. I'm going to be doing some live broadcasting for the robo games crew interviewing the bot builders, the winners and the losers. Everyone and I do hope that you'll come out to see this amazing international robotics competition with over 50 different events. So many different ones. 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Yeah, one has real power who needs if you could travel my thought to a mystical place, why go to book signings and buy for shelf space? Why would you wait for your agent to call you and try to convince you he's worth 12% and we're back with more this week in science. Oh, yeah. Hey, Justin, what you got? I got a new discovery out of Case Western Reserve University School of Medicine. They are shining a light into the biochemistry of vision by way of a light sensing pigment found in everything from bacteria to vertebrates. We find it can be biochemically manipulated to reset itself in the study just released from the proceedings National Academy of Sciences. Researchers used a modified form of vitamin a called locked retinal to induce a recycling mechanism and engage proteins central to human vision. Human see as we all know most of us to with the help of an extremely sensitive protein in the back of the eye called rhodopsin which attaches to the retinal molecule to sense light light photons enter the eye get absorbed by the retinal rhodopsin complex activating a cascade of downstream signals that constitute what we call and recognize as vision. Importantly, the retinal awaits light photons while maintaining a particular chemical configuration. It's not important, but it's 11 cis retinal and transforms into a second configuration all trans retinal after is absorbed after it absorbs a light photon. But this transformation is a one-way ticket requires an army of specialized proteins to convert all trans retinal back to 11 cis retinal inherited mutations in any of these specialized proteins causes retinal degenerative diseases. Researchers who want to treat such diseases must repair bypass the mutated proteins to maintain this retinal conversion to humans and they do so typically by giving people lots of drugs. Quotey voice. Our study shows how a chemical modification the retinal can activate downstream visual signaling and photo silica and if photo silica manner this chemical modification allows retinal to self renew using thermal energy and hence does not require any additional enzymes. Gladi said that is the researcher of this involved in this newly discovered mechanism may enhance curtain approaches to treat retinal degenerative diseases and other nerve cell disorders. Researchers can biomechanically tinker with retinal and retinal bound rhodopsin molecules to improve their ability to turn on and off proteins in the eye. They discovered the self renewing mechanism in bovine rhodopsin which apparently is very like human. Researchers use purified proteins in their laboratory to show their modified retinal binds to bovine rhodopsin and successfully activates specific human eye proteins in response to light when complete it uses thermal energy to slowly return to its inactive form that can be repeatedly reactivated again by light. So so it's glad to although one way reaction mechanisms are usually in the function normally in the human body that cannot renew their activator molecules and hence are dependent on continuous menstruation of drug molecules to treat the disease symptoms. So this is that workaround but with this they've got a self sustainable way of of maintaining eye health. That's that's great. I mean yeah. Wow. New methods over eyes new methods to tinker with the eyes and help keep people seeing more longer. Yeah. I love it. What about dinoflagellates? I seem to. I know we're talking about tiny things. Yeah little teeny tiny single celled organisms that live in the sea. Kind of good like this. Yeah. They've got flagella that help them. Oh sorry like that. Those are still I was doing Celia. This is flagella. The jelly there. It's like tail. It's got a little tail exactly the flagella and so anyway these little single celled organisms they eat other single celled organisms. So there's still like predator prey stuff going on between some of the bigger dinoflagellates and other of these little single celled organisms. The beginning stages of the game spore. They're like the t-rexes of the microbial world. Kind of and but it's more like they're in this research we find that they're more like the harpoon throwing fishermen of the microbial. The flagella going like this. It's like this. Yeah. So there's this one particular kind of dinoflagellate and it's called polycricus of kofoidee. Oh are you speaking spark in Portuguese? I don't know. No. Polycricus kofoidee. That's like well there's way too many vowels in that. But it does have an organism, an organelle that it basically uses as a harpoon. There's a little tiny arrow or dart that gets shot out of this organelle but it's not just an arrow. It's a harpoon because it's connected to a line that is still connected to the polycricus kofoidee. So they can use it to reel their prey in after they impale them. And so these researchers decided that they really needed to go learn more and take a look and this is I do want to take a moment and thank Matt Stafford for sending us this study because this is a pretty cool study. And so we've got some video here of these little dinoflagellates floating around and going after their prey and using their using their harpoon to be able to to attack. And so what you see is a little dinoflagellate that's just like doop dee doop dee doop and then the big dinoflagellate comes in and stabs it and then swims away really quickly and basically drags it with them. You're coming with me. Hog time that other single celled organism. Yes. And so there's a an actual that's it's a there's a there's pressure involved here in releasing the dart and there is there's definitely this is fishing fishing for other dinoflagellates. It's very stuck a hook in it and stick away now I'm about to engulf you. Yeah. And so what they looking at it they found that there are three parts. So there's the dart. There's a nematocyst which is a larger dart and has a tube attached to it that functions like a hypodermic needle. That's exactly what Nigerians have like and this is another and this is another point to the study which is very interesting. I'll get to that. Yes, but it injects an unknown substance. They don't know what substance it injects into the prey and then there's the toe line that's used. And so they found that there is very little relationship between these dinoflagellates and nadirians and so what they think is this is an example of of this is just coincidental evolution. Oh, it's convergent convergent convergent evolution that they have done something they came up with a similar solution. And then there's another another kind of a dinoflagellate a neotodinium and it had a weapon that the team said was kind of like a gatling gun where instead of harpooning and towing the prey just shoots multiple rounds of stinging nematocysts which is just fascinating but there are some on there's here's a 3d rendering of the nematocyst discharge and in this it's a they show this rendering of what looks to be a bunch of rope attached to a needle of some kind and how and then that discharge it gets shot out to attack a prey. It does look just like jellyfish or anemone. It does fascinating and then we have who else do we have we have some some some other hunting hunting videos these kofoiti hunting some poly poly eedra so there's a bunch of little tiny things in focus and not in focus these these videos but this is just a very interesting they've done scanning electro micrograms of the cells and it really is like it's a it's a dart. Gosh. I wonder if it hurts. Well that that's what we don't know what kind of we don't know what kind of substance it is so maybe it's an opioid but I mean we're talking about single celled bacteria so I don't think they don't have any necessarily have nerve cells I don't think we're talking about pain so much anyway cool little microbes of the sea they're stabbing and darting drag you they're fishermen they're tiny fishermen of the sea I love it the ocean it's such an alien planet. Even a microscope just when you when you look just at tiny stuff there's all sorts of stuff going on you don't even know about I'm missing out on most of what's happening on this planet. Thankfully thankfully very thankfully we're starting to learn you know Justin what else have you found out that you want to share. This was a study of DNA and ancient skeletal remains and they added that to the evidence that adds to the evidence that indigenous groups living today in southern of Alaska and the western coast of British Columbia have been there for a really long time. Team looked at genomic data from Shuka Ka which in the native is native tongue there for a man before us. This is an individual whose remains were found in a cave in southeastern Alaska and they dated it about 10,300 years ago. They also analyzed the genomes of three more individuals from nearby coast off British Columbia whose remains date between 6,750 years ago. Earlier studies had focused on mitochondrial DNA. This is that which occurs outside of the nucleus of the cells and is passed only from mother to child so it's it can be mothers all the way down but every time it hits a son it doesn't pass on to the next generation and the mitochondrial type of the Shuka Ka person belonged to was observed in another ancient skeleton that dated about 6,000 years ago. But of course could not be a direct descendant right it would be like their aunt maybe had many many daughters that descended to this person. But in this idea of research has also then turned their attention to nuclear DNA which offers a little bit more overview of the relation in the history of the ancestry and what they found was within that DNA of these these three samples. There were multiple lineages there so this isn't all just one very small group but it looks like a little bit larger group that was initially there. The descendants of these are still living in the same region today. According in a few actually were co-authors of this study. This is this isn't a fascinating study first for the fine but for me mostly it's the participation that's going on between the native community and the scientists. This has been a long time sort of controversy of doing studies on remains that were thought to or known to depending on who you asked to be native and the fact that they're sort of opening up and embracing these genomic studies as another way of learning about the ancestry and and and it's also convenient to an extent that it shows that they've always been that we are the people who have always been here and that hasn't changed and the genetic data in this group in this group in this area is is is illustrating that. It's nice to see I think it's the the idea of the genetic continuity that they're telling with this tale that there was people people came to inhabit the area what probably 14,000 years ago or so and they've kind of been the same people ever since and the new genes coming in. Yeah, right. And then there's also that because there's also helps because in initial studies when they had just done mitochondrial it looked like at around 6,000 years old ago about 6,000 years ago the like the the mitochondrial lineage of this Shuka Ka person sort of drifted started to vanish it was like it's not really that so much but this is showing that the the relationships are there these are it's like even the 3,000 or the the 1750 year old specimen is related 6,000 year old specimens have been related and the current people they're related so they're all still related but just that maternal hap a hap the group going down from mother to mother the mother you know might have hit might hit some bottlenecks of sons where it just couldn't get beyond or or what have you or just might be rare in the population today than it once was. Yeah, it's just interesting. I mean the populations and we're probably so so long ago were probably very small so he wouldn't have as much genetic mixing and you don't have people meeting up meeting each other as much you might think but that's the opposite of what this is saying though because it's showing multiple lineages it's you know this is it's it's we don't know what the population was I don't think for this area but the numbers might have been quite quite a bit bigger and and may have been spread out over a larger area than than we may realize. Cool super cool and moving on from the genes of the ancient indigenous populations of the Pacific Northwest. Let's start talking about antibiotics and babies. Yeah, we've talked about antibiotics and the the there's a hypothesis that babies given antibiotics could have experience health issues as adults as older children that they could experience even behavioral changes as a result of antibiotic dosing. And so there is there's some some research that backs this up and so there are some earlier studies in mice and also humans that that bacteria the microbe in our guts actually interact with this gut brain axis right we've talked Justin's brought up a bunch of these stories I've talked about it this gut brain axis of the communication between the bacteria that live in your gut and the wiring in your brain the chemicals that are released in your brain to change your behavior. And there's a study in 2014 that found that eating two servings of bacteria filled yogurt a day for four weeks changed brain chemistry in a dozen women but again very small study. So we don't know the replicability of that and then there was a study of 871 kids found that found a correlation not causation but correlation between behavioral problems and depression around the ages of seven to 11 in kids that had gotten antibiotics in the first year of their life so researchers McMaster University decided that they were going to check this out a little bit more research on antibiotics in mice has historically involved high doses of antibiotics and it is showed that high doses of antibiotics can cause long lasting brain and metabolic changes in mice adults and adolescents so these high doses can have an effect and these researchers said well what about low doses and so they didn't do a study on human babies they did a study on mouse pups and they took 72 mice and they exposed them as pups to penicillin it was penicillin these low doses via their mothers before they were born and also after they had been born and this is through blood and also breast milk and then at age six they tested their behavior and their physiology and they look to see what was going on they found that those mice that had been exposed to penicillin were less social also a little less anxious and more aggressive than control mice and then in an aggression test they found that 42% of these mice that had been exposed to penicillin were feisty they're only about 9% of feisty mice in the control control group and then they said hey let's take a different group of mice and give them a probiotic lactobacillus remnosis at the same time that they're given the penicillin and see if it can block the effects and what they found is that it did block the effects of the antibiotic not completely but partially so not as much of the behavioral change was seen and then they looked at the when they looked at the brains they found that the blood brain barrier of these mice that had been exposed was thinner which is exposed to the antibiotic exposed to the antibiotic their blood brain barrier was thinner and what that means if you have thin blood brain barrier that means that stuff can get through the barrier more easily it's not as strong a barrier and there was also an increased expression of inflammatory molecules cytokines in the brain tissue so there's evidence that there's stuff you know cytokines are evidence that there is stuff that shouldn't be in the brain getting into the brain and causing inflammation this inflammation could potentially be having these downstream effects on the behavior and the sociability and aggression we don't know that for sure again this is still a lot of correlation but and and we don't know if it would have the same effect on human children as it does on mouse pups but so if I have a child and it's sick no antibiotics well that's the that's the the question that many people come up against you know there are some kids that your infections I mean you can either run the course of an ear infection your child is miserable and potentially could burst an eardrum and it could have terrible effects on their ability to hear depending on how on how bad the infection is how bad the burst is and if you have multiple of these ear infections or even sinus infections you know they're all sorts of things that if they occur the easiest way to fix it is to give an antibiotic you have an ear infection you see the symptoms you go get the antibiotic you fix your kid and everything's fine so so what we really need to do is formulate a better probiotic yeah that's what I was gonna say is just not not open the antibiotic and and pour it into a bowl of yogurt now but this is but the yogurt's not necessarily a thing because we and this is the thing we've talked about on on the on the show before when when babies are born they have a really great diversity of bacteria within them and they also have a the largest load of viruses that they're they're going to have and as as they age by about age to those viruses that they're they're full of that they're just teeming with these viruses these viruses are all eating bacteria and as it turns out they eat the bacteria that perhaps those children don't need and then at some point the viruses sort of fall off and the bacteria that this filter of viruses has decided this is what belongs in this human and I say to the sides sort of casually that that's that bacterial load that that develops into a nice happy healthy human being okay so in fact the child with viruses got it right no that might actually help right if a probiotic the probiotic might be also coupled with a constant a constant constituents of viruses that the a child would normally have been born with to help rebuild that correct balance again yeah I mean the thing is we don't know what viruses are good or you know would be helpful and that is something that yes love the idea it's like it's at this point science fiction because it's not that's not something that we are at the we don't know what virus it's like I mean we're still doing that when we talk about probiotics and yogurt absolutely minimal evidence on bacteria helpful or not but I can I can I can guarantee you with some level of hesitancy that that if we did make a good study across all newborns up to about the age of one to two I guess it's maybe maybe at eight months you could even you can get a really good idea and you find out what viruses are present I bet you they're pretty consistent that that virus load is probably pretty consistent within children across the globe and when you discover further what those viruses eat and what they leave what's left over is probably the ideal probiotic for a human being I mean that's that's that's what I would I would love to yeah for somebody out so definitely more children no I research is needed more children and I needed for research and more research needs to be done I mean if that's your contribution to science Justin I mean go for it well I mean this is I mean this is how this is the natural immunity system of us it starts at a virus load figure out what and those viruses are eating they're actually filtering they're getting rid of everything that that that the bodies the sister ecosystem of our gut is is designed or or set up to get rid of so you heard it here Justin's working on the sample size problem himself exactly hey did you know that 70% of the plastic in the ocean or it of trash in the ocean start the question over did you know that 70% of the trash in the ocean plastic thanks Justin love how you can finish my sentences and we're gonna get us along that's gross and not surprising at all yeah so their researchers have put together a database it's called litter base it's really called litter base and litter base has a bunch of maps with the database and they actually draw on information from over a thousand studies from the date from 1962 2017 and they are basically tracking where trash has been found in the ocean you know like the garbage patches the gyres but beaches around the world and also on the on the floor the seabed of the ocean and so this some of the most polluted spots they are said to host more than 10 billion pieces of litter per square kilometer and they include beaches and patches of sea off the coasts of South Korea and Jordan and close to 70% is plastic and microplastics are the biggest problem in that because plastic doesn't go away it just gets tinier and tinier and so the database because of its reliance on maps and other information show that more than 1200 aquatic species are coming into contact with the litter eating it all living in it getting tangled in it but if you are interested in finding out more about the extent of trash in the ocean you can go to litterbase.awi.de and it's a portal it's a portal and a database for trash in the sea and you know who could probably use it really well is a group nonprofit that was at the American Chemical Society meeting in San Francisco this week it's a Santa Cruz based nonprofit called Clean Oceans International they have partnered with an organic chemist to develop a a smaller more portable way to turn hydrocarbons hydrocarbon based plastics into diesel fuel yeah so this isn't the concept of turning plastics into diesel fuel hydrocarbons into diesel or other types of gas is not new but what they are doing is he the the guy who started this is Captain James E. Holm he was out on a boat off the coast of Panama and he started seeing all the trash around him and he said the people that live in that area don't have plastic packaging and they don't have Oreos and potato chips and so the plastic had to come from someplace else us and you know so civilizations societies that do use the plastic packaging and so he's been at sea for a very long time and he came up with this idea he's like hey I know this can work so he found he founded this nonprofit and has partnered with this organic chemist to scale down the reactor to convert between 100 and 10,000 pounds of plastic daily and that would generate 10 to a thousand gallons of diesel fuel and the idea is that it would fit in a 20-foot shipping can container or even on the back of a flat bed truck and they're working on trying to make it even smaller than that so it could be put on ships that are already floating around the ocean the ships could harvest plastics from the ocean and turn them into diesel fuel and then burn the diesel fuel to find more plastic and make well if they could yeah they could burn the diesel fuel in that plot you know the plastic that hydrocarbon plastic did come from fossil sources already petroleum sources already so it's you know but it's it would be helping the ocean take that we want to get these plastics out of the ocean sure you seem skeptical Blair it's a little bit like instead of swords into plow shares we're gonna we're gonna turn swords into machine guns yeah it definitely is kind of an out of the frying pan into the fire situation I mean you're making a whole bunch of greenhouse gases with by burning this plastic but I think that you know it's important right it's important to remember that that that also will change the oceans chemistry and cause issues with the ocean as well by burning those fossil fuels so the I think it's even more important to remember to buy less plastic yeah yes I mean the I ideally then if we can stop the plastic waste yes from getting to the oceans in the first place that is any trash can we keep from throwing it into the oceans so this this can help fix the mess that already exists but it's not a blank check to continue making a mess exactly yeah but I mean I could imagine you know if you have robotic ships trolling around the ocean picking up plastics creating fueling themselves it could be Patrick sent me a video of the Baltimore Harbor and they've got this this little bargy thing that's that looks cute because it's got a canopy and it's got like looks like big friendly eyes but it goes around and it's got a conveyor belt and it scoops up the surface trash from the Harbor there and and and puts it into a into a container that's kind of yeah just kind of goes around gobbling up garbage off the surface I mean I could I could see that getting employed in a small area Blair tell me about Badgers oh Badgers they're so cute and they're in the Weasel family and we know about weasels right there they're not to be trusted so looking at behavior of scavengers in Utah's Great Basin Desert University of Utah biologists were expecting to collect data on things like vultures but instead they made an amazing discovery about Badgers so for the first time ever researchers got evidence of Badgers burying entire cow carcasses oh I saw something about this yeah so there's been some badger behavior witnessed and recorded before where they they'll cache they'll hide a maybe a rabbit carcass or something like that but nothing this big this is so much bigger than a Badger and one Badger is doing it all by themselves why is this important well actually this has a huge ecological impact so the first is taking the carcass out of the environment and hiding it where only the Badger can get to it monopolizes that carcass so it removes a lot of nutrients out of the area but it benefits the area as well because burying the cow underground is kind of like putting it in the refrigerator it's keeping it from rotting very quickly it's kind of preserving the meat and it allows the Badger to slowly eat off of it and this removes pathogens from the environment so the positive is it doesn't get other animals sick particularly other cattle other livestock and it reduces attraction of larger predators to livestock areas so actually potentially this action this very selfish action by the Badger may be a beneficial behavior to ranchers it's pretty interesting that's fascinating I mean I mean first off I mean the Badgers could bury a cow yes just that's a large animal but then the implications for the ecological effects are pretty interesting as well absolutely and you know it's a it's a it's been buried part of the ecosystem yes yes and here's a picture of a Badger who looks very satisfied with himself or herself having buried a cow and now walling about on top of the burial site in this case he buried the cow in January and ate it through March I mean it's something finding a large animal like that and having a carcass of an animal that large is going to but yeah it's going to feed that Badger for quite a while Badgers Wiley Badgers they know what's up I'm going to eat a cow I'm just going to bury it over here burgers for the next several months Badger Badger Badger Badger Badger Badger Mushroom Mushroom a cow if you're just tuning in I can't help you I have no idea what's going on it's remember it was that meme before memes existed from like the labels Mr. Weevils I think fat has put a link in the chat room to it after the show you'll have yeah yeah yeah you kids who were born after the year 2000 you'd even know what we're talking about look at Badger Badger Mushroom look at look it up alright everybody I think we have come to the end of another show don't forget two weeks April 21st to 23rd you've got robo games in Alameda County Pleasanton and then young innovators fair coming up in Philadelphia in the beginning of June 10th and 11th and will be at these places and I'd like to thank people who sent us story ideas David Eckerd sent me the story on the plastics in the ocean as I said Matt Stafford sent the story related to the microbial harpoons some good stories out there keep them coming you guys we do love sharing them with everybody and I would also like to thank our patreon sponsors I'd like to thank Chris Clark, Paul Disney, G. 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Science. Science. This week in science. Explore the world of tiny hands. In the after show of the twist. You have made it through the show. Now it is the after show. Did you like the show? Look there. It says hi to you. It says hi Blair. No. Hi Blair. No. I've got little hands on my fingers. No. Dick tell I was present around ACS in San Francisco this week. I had press credentials and was busy doing some interviews with nanotechnology people. So I did a little bit, but I didn't actually. Busy doing some work and so I didn't get to actually go to as many. Go to the ACS actual meeting in a go to the ACS actual meeting and see the science that was happening and it was it was different. So I was there, but not really. And now I'm home already. Yeah, it was it looked like it was a great meeting, you know, people being all chemistry, doing the chemistry talk. What's with this robot thing? Oh, the robot thing, I'm gonna be I'm gonna be doing something. So I'm telling people about it. I'm. Yeah, Kai loves to watch robots battle. Nope. I don't know. Somebody left me these tiny hands. Who could it have been? Somebody gave me these tiny hands. Who would write my name on a tiny hand? And you know, did you see it the whole time? Yeah, sitting back there waiting for you, the whole show, little tiny hand back there, back there, saying hi. Oh, here. They're too much. Too much. The greatest. I wish that I had had time to go to more of the American Chemical Society meeting. That would have been awesome. But you know, you do what you can with the time that you got. What a good philosophy on life. You do what you can with the time that you've got little bits of wisdom from that seems like a Kenny Rogers song or something. Do what you can with it. I was on a team that won pub trivia last night. Congrats. And one of the questions was, I think it was a 23 year old man in Nebraska legally changed his name to what? What a 20 year old man in Nebraska, 23 year old man in Nebraska changed his name to I think I remember this story when it came out. But I don't remember. I don't know. He changed. It was something ridiculous. T Rex. T Rex. That's right. His name was was like Joseph Gold or something like that. And he said that he wanted to change his name to T Rex because it was more interesting. Well, that's a good reason. Do what you want. Do what you want with the time that you got. Yes, Joseph Gold. Okay, let's see. Entrepreneur. No, Tyler Gold, 23. Oh, so he was already a T something. He was already a T. T Gold. Yeah, he needed a way to stand out from the crowd and a way to get noticed. So he did what any reasonable businessman would do. He changed his name to Tyrannosaurus Rex. Gold explained as an entrepreneur, name recognition is important. And the new name is more recognizable. He also noted that the new name is quote cooler. Yeah, that is true. That is a cool name. That is a cool name. So unfortunately, I've got to go to sleep at the time I've got left. I am like barely conscious right now. Yeah, I'm doing it. Now much of an after show. I know I'm I think I'm done. Oh, tired, Justin. Turn the lights out. You guys keep talking. Nope. No, this is not this is not the twist McGuiden show. No, you're not just gonna you don't get to just pass up. Pass up. Everybody clap your hands. Clap your hands. Everybody clap your hands. Stop it. I hate it. I know I love it so much. Tiny hands. Great me out. Oh my goodness. Did you think Dr. Strange? Yes, I did. The tiny hands. Tiny hands. I think I curled up as tiny as possible at my theater seat when the tiny hands happen. Spoiler alert, everyone. There's tiny hands and Dr. Strange. Spoilers. Oh, goodness. Okay, sleepy people. Yeah, I'm sleepy too. I'm had a busy week. We went to California. My dad got married. I drove back from California 12 hours on Sunday. And then Monday. And then and then Monday flew back to California to San Francisco. Logistics. Logistics are difficult sometimes. So you do things. And now and that I was, yes, doing things in San Francisco. Great visit. But now I'm home. It's time to go to bed. So energy for the rest of the week. I know you're probably jet lagged, right? I mean, you came all the way to California jet lagged. Oh, goodness. I'm smart. I swear. Did you see identity force comment? How did tiny did you curl up there? I'm ignoring it. Good night, Fada. Hot rod. There's a brain scientist who does periscopes. Awesome. That's cool. Say good night, Justin. Good night, Justin. Say good night, Blair. Good night, Blair. Good night, Dr. Kiki. Good night, Dr. Kiki. Good night. Thanks everybody for watching another episode of Twists. We'll be back again next week. We hope you have a wonderful week and that we connect with you on the internets in the in between. We'll be round and round and about these parts. Have a wonderful week and we will see you for more science next week. Don't forget to tell a friend about twists. I gotta hit the right button now. Good night.