 This is TWIS, this week in Science, episode number 564, recorded on Wednesday, April 27th, 2016. The Secret Lives of Lab Mice. Hey everyone, I am Dr. Kiki and tonight we are going to fill your heads with cats. Well, one cat and mice. Lots of mice. And so much science, you won't know what to do with it. But first... Disclaimer, disclaimer, disclaimer! So much progress has taken place over the past few centuries that it is hard at times to consider what effort each individual advance required to reach the modern age. When we think of the great contributors to science, many names come quickly to mind, but chances are none of the names you may be thinking of belong to mice. And yet, many of our Nobel Prize winning human scientists, behind them each, there is a focused and dedicated team of research mice. Living lives even more dedicated to science than the humans who employ them. And let us also not forget the trusty lab rat, whose stoic and steadfast use of logic and mastery of emotional equilibrium is the basis of much modern psychology. And while our whiskered cousins may not claim credit for the results, the modern era of science and medicine would not have been possible without their dedication, brave commitments and heroic contributions. Research mouse, lab rat, we salute you, here on This Week in Science, coming up next. This week, there's only one place to go to find the knowledge I seek. I wanna know what's happening, what's happening, what's happening this week in science. What's happening, what's happening, what's happening this week in science. Good science to you, Kiki and Blair, and Cat. Welcome to this week. Good science to you, Justin and Blair, and Cat, and everyone out there. Welcome once again to another episode of This Week in Science. Tonight on the show, we are, as Justin said in the disclaimer, celebrating the lab mouse, the lab rat. Really all laboratory animals, because this last Sunday, the 24th, was World Day for Laboratory Animals. Today is also International or World Tapir Day, but we're gonna talk about lab animals unless Blair has a taper story. Yeah, unfortunately, the tapirs were not in the news this week yet. Not yet. So tonight, we have an interview with Dr. Cat Lutz from the Jackson Laboratory, and we're gonna be talking with her about the genetics of lab mice, and using mice in research. Additionally, I have stories about alien oceanography, brain thesauruses, or just one brain thesaurus, potentially, and lots of data for climate change. Justin, what do you have? What did I bring? I have a rat brain study. I have dirty wine, and I have a competitive soil story. Competitive soils. I didn't know soils competed in anything. Fiercely competitive soil. Good to know. Blair, what's in the animal corner tonight? Oh, I have how to measure stabbiness. I have deadly nightshade and big brains. All right, we all like big brains, and we also just like a lot of science. Let's get into the show, everyone. It is time to start off with our interview. We're going to be speaking with Dr. Kathleen Lutz, the head of the mouse models repository at the Jackson Laboratory. She is also a senior research scientist, and in her laboratory, she focuses on modeling human neurodegenerative disease in mice, emphasizing optimum use and best practices for research and preclinical drug testing. She works with the NIH and multiple disease foundations to improve existing mouse models, identify modifier genes, and generate new models that will facilitate therapeutic development. Perfect person to be speaking with. Thank you so much for joining us. Thank you for having me. It's nice to be here. You are so welcome. I reached out to the Jackson Laboratory because Justin here said, we talk about lab mice all the time. We're constantly talking about either stress in lab mice or results of experiments with lab mice, lab rats, et cetera. A world lab day came up, and we thought what a great opportunity to actually try and elucidate some of these processes and procedures that go on that seem like magic to everyone who benefits from the research that comes out of it. So how did you get into working on mouse genetics in the first place? Oh, boy. That's going back many, many years. I really did cut my teeth on working with mouse models of different diseases, but in a very different way than we do today. 25 years ago when I was a student, we didn't necessarily have a lot of the genetic engineering techniques that we have now. So we used to rely on spontaneous mutations in the very large mouse colonies at the Jackson Laboratory. So when you're breeding all of these mice, eventually you'll have a spontaneous mutation that occurs just like sometimes it happens in a human population. And you'll usually be able to see that visibly. So sometimes the mice would have a neurological disorder. They might be a little ataxic. They may be waffling. They may have a wasting disorder. A lot of them were the ones that we could visibly see. Their tails were crooked. Their ears were bigger or smaller. There was a co-collar mutation and so all of those things that we could see. And at the time what we could do is we could look at the phenotype of those mice, what we could see. And sometimes they were really related to diseases that we were studying, maybe the mice were obese, for example. And then we would sort of work backwards from the phenotype and say, okay, can we identify the gene? And that took a long time. I think that actually was a large part of my PhD thesis. In fact, the better part of six years. Now you can probably do that in a summer. You know, a couple of weeks with a good summer student. Is that all because of technology now? Everything is just so much, it's computerized or standardized. It's the technology. I think with any area, whether it's biology or science or computers, there's always some very big disruptive innovations. Things that happen in the field, discoveries, inventions, technologies, that completely change the way we do our work and we monitor our progress and the way we do science. And for a long time it was, you know, this is sort of the genetics approaches, those spontaneous mutations that I was just telling you about. And then in the early 90s, genetic engineering really changed with embryonic stem cells and the ability to do genetically engineered mice in a way that you could target a particular gene. Any particular gene that you wanted. And that was huge. And for a long time, we used those embryonic stem cells and those genetic engineering techniques and mice to really drive forward and manipulate the genes that we wanted to interrogate. So if we knocked out that gene, what would happen? If we made that particular gene a null or introduced a point mutation, what would happen? And then we could study the disease mechanisms that way. When I was in grad school in the 90s or late 90s, early 2000s, there was a lot of the knock-in and knock-out work that was being done. And one of the questions there that I've always found really interesting is the off-target effects on the phenotypes. So you knock out a gene expecting to have a certain, say, cognitive effect or behavioral effect. But then what other effects does stuff like that have on the health of a mouse? So that's a really good question and it's a really good point. Because mice aren't humans and humans aren't mice and there's a lot of years of evolution between mice and humans. And so while the genes are conserved and the proteins are conserved and we learn a lot about maybe the regulation of a particular gene, the pathways and the proteins that it interacts with, there are sometimes where we get results in mice that we don't quite expect. Sometimes that actually is very enlightening because if you're always looking under the street lamp, you're only going to find what's under the street lamp. And so when we do make a knock-out or a mutation in a mouse and it doesn't necessarily do what we think it's going to do, sometimes people would think, well, that's really unfortunate. But in the end of the day, it really just tells us more about that gene or more about that protein or more about that disease that we just didn't know before. So it's a big discovery and that's what science is. Yeah, that's an interesting way to think of it. I come from the behavior side of things and so it's always the, oh, well, that didn't have the behavioral effect that we wanted. Behavior in mice is hard. It's an art, I like to think of it. It's not as straightforward as people like to think and there's all kinds of things that affect your experiments as you know. Absolutely. So I guess from a historical perspective, we started out, as you said, kind of going just from natural genetic mutations and using those animals into this manipulation of embryonic stem cells, knocking in, knocking out. How has this affected how many strains of mice there are? I sort of picture, especially with the CRISPR-Cas9, that now there's orders pouring in from everywhere to get the specific thing. And I sort of picture like, why do they have to open another warehouse? Because there's these changes that they have to keep putting up everywhere. And I suppose some of it is like that, although I guess the ability to do knockouts and do specific things and not have to sort of wait for the manifestation of an obese mouse to just sort of present itself within a population and start to do the breeding that way. You, at the same time, can get all these other papers that researchers would have loved to have worked on if they had a model, but now there's a way to get that model. And you still have to do a fair amount of breeding and sort of still isolating that from that breeding pool, if I'm correct. It's not as if you're like, okay, we've knocked out the gene and these two mice and now they'll start the population and off it goes, all those mice are exactly what we want. How does that work? How does that process of you start with we're going to knock out a gene and how do we find the samples that we actually want to send to the researcher? Well, I think the interesting thing, since you brought up the CRISPR-Cas9, I'll just touch on that briefly, because that technology is the disruptive innovation that we were just talking about. It completely changes the way we do our work, how we approach science, how we approach therapeutic testing as well. So it's orders of magnitude easier with CRISPR-Cas9 than it ever was with embryonic stem cells. Embryonic stem cells, you know, were good, but you lost efficiency along the way. You lost efficiency in the targeting process. You lost efficiency in the germline transmission and the percentage of chimeras. And then if you were so lucky as to get a correctly targeted mouse, then you would have to breed out the selection markers and a lot of other things that went with it. With CRISPR-Cas9, you can really have your founder lines in one generation instead of a year. And so the time that it takes to do those experiments has been greatly reduced. And so of course the cost has been greatly reduced, and now you can do a lot more with the same amount of money when it comes to the targeting. So that's really, really exciting. And I also think it opens up more possibilities because with embryonic stem cells, you know, we were really restricted a lot by the genetic backgrounds that we could work with because we just never got passed with embryonic stem cells that, you know, there are just particular strains of mice where you could make embryonic stem cells that would be germline-competent, but others would not. And, you know, we just never got over that efficiency. But now with CRISPR-Cas9, we can go into any genetic background of any mouse that we want and make these, you know, very, very efficiently. So that's, you know, extremely exciting. And so of course now this whole playground opens up of all those things that you wanted to do, but, you know, either didn't have the technology to do or the time where the money was a little consuming. But, you know, in that respect, I think that you still have to think very carefully about the models that you're doing and what you're making because, you know, sometimes you'll find your answer in a different model organism. Maybe you'll use zebrafish or flies or even maybe even do a cell-based assay. That can provide you with a lot of information. So you have to think about the temptation about going right into the mammalian system, right into the mouse. It's there and it's easy to do and it's great. But, you know, there will be a bottleneck down the road and that will be the space. You know, you mentioned do we have to build more warehouses. I think we do. But it's also money too because you still have to clean and pipe the mice. You still have to be really thorough investigation about exactly what's going on in that system because you don't want to miss anything and you don't want to jump to erroneous conclusions. And as we all know, we produce ability and being able to replicate these results are incredible. So you do have to, you know, think very thoughtfully about what it is you're doing and what the goal is, especially in light of, you know, this huge, like I said, almost a playground in front of you. There's too many things and too many experiments you should do. So are the orders up? I mean, are you getting many, many, many more requests for, I mean, I can imagine that there's a laundry list of researchers out there who had a study they would love to have done if it was possible to have the model. But now that it is, are they getting funded? Are they getting the green light to do their research, the grants, and then calling you? So that is going. It's a definite uptick. So I think, yeah, it definitely has. There's a lot more interest than we might have had before because of this new technology. But then the other part of it is you pair it with the other innovative technology and that's genome sequencing. And not that the sequencing of a genome is necessarily innovative, but because now the cost of sequencing a genome or even a whole exome sequencing has gone down, that means now we can start to interrogate these patient populations in ways that we didn't before. Think about diseases like Lou Gehrig's disease, ALS, Alzheimer's Parkinson's, all of these diseases where we used to have a loved one diagnosed with that disease. You know, we would do our best to care for that patient and that family member, but it wasn't necessarily the case that clinicians would try to gather these patients and try to sequence their genomes or their exomes to try to understand exactly what the pathogenic variant in their genome would be. And now they're doing that, and they're doing that with a great deal of success. And so once you've identified the pathogenic variant in the human population, of course, modeling that particular mutation in another mammalian system that you can manipulate more is very powerful. Yeah, it just unlocks all the ability to actually research and look for things that are preventative measures. Now it's not even the question so much of how is this happening? It's how do we actually now take that next step and prevent or deal with it or create a therapy for it? Can you tell me a little bit about the Jackson Laboratory Rare and Orphan Disease Center? Sure. So this is a part of the organization that we thought very hard about, especially because of these two different technologies. Most of rare and orphan diseases are monogenic in nature and that usually just means that they are caused by a single gene. And so if we do have the ability now to do this kind of genome editing for these single gene mutations, we now have the ability to help a population that may have gone essentially with an unmet need, a huge unmet need because the patient population is so small. And there have been some other really interesting developments in rare and orphan diseases and that is that the FDA and the government have gotten together and really have put some incentives in front of biotech and pharmaceutical companies to allow them to hold patents for longer to get accelerated approval for therapeutics. And when you're a biotech company, especially having those kinds of intellectual property and those patents is going to be what makes or breaks you as a company and allows you to move forward. So being able to... I don't want to use the word capitalize because I don't think that that's the right word, but so much investment goes into biotech and pharmaceutical companies. And most of that at the end of the day is not a widget or a gadget, it's intellectual property. And so they need to be able to profit from that in some way that they can go back and reinvest those dollars in the next disease that they want to. They want to look for therapies for. And so I think that the rare and orphan disease center at JAX, what we really want to be able to do is help those disease populations, those patients, those groups with this huge unmet need, where we can provide those resources to the biomedical community. We can work with pharmaceutical companies, we can work with biotech companies so that at least they have the starting materials in the form of the mice with the proper genetic mutations and the precise genetic mutations as well. And then they can start to interrogate whether or not their therapeutic is really going to have an effect or not. And then once they get a pre-clinical indication, that gives them and their investors and the FDA a lot more confidence in moving forward with the clinical trial. And then not that maybe I misheard, but you're not also raising orphans for research. But that's got to be a huge obstacle. If there's only a thousand or two thousand or ten thousand or could be even a hundred thousand really, and the global population that's affected at any given time by a particular mutation or disease, you're not going to get a biotech to pour billions of dollars into just those people. So there does need to be a way for research to be done than that to see, and then to see if there's already a therapy out there. There could already be a therapy out there that's already existing that's effective on it. So that's a brilliant, a brilliant benefit, GeneXus is applying that. And I think the other thing that while we seem to think of these diseases, they're rare in orphan diseases, maybe they only affect a couple hundred people in the population or maybe a couple thousand people in the population at any one given time. A lot of these diseases will have very common underlying mechanisms and very common then therapeutic strategies. And so while you're only going after one particular gene or one particular disease, the underlying mechanisms or the application of a particular therapeutic like an antisensit with a nucleotide or gene therapy, while you're only solving maybe that one particular disease today, you're opening yourself up for a whole suite of different diseases that may have an application with your drug or therapeutic. And quick question, that reminds me too, when we were talking about how the stem cell use was like, it was hit and miss but you learned other things from sort of that process. Is CRISPR giving us that same sort of look or is it not giving us much of an idea of what else is being affected in parallel? I think it's giving us a huge look. And I think that, so we mentioned therapeutics that, you know, might be able to cure a disease, but we also talked about things that could prevent a disease. And so one of the things that we're always interested in when we make a mouse model, so for example we have some mouse models of Lou Gehrig's disease, for example, where the mice are very susceptible to that disease and they get motor neuron degeneration and maybe behave classically like we would consider a motor neuron and we think, well, that's a really great disease model because then we can test therapeutics in it. What's even more interesting is the mouse, when you put that same mutation in a different strain or a different genetic background, it doesn't get the disease. And so now you're saying, okay, why is this mouse succumbing to the disease but this other mouse isn't? And it's the same thing for the patient population, right? It may be a mutation may be necessary but not sufficient to cause the disease and there could be, of course, environmental triggers but when you're looking at a mouse model that's, you know, the mice are genetically identical, the patients aren't, obviously. And they're also all in this basically identical laboratory mouse environment. Right. Yeah, we control the environment, yeah. Which is, I mean, I don't want to preempt this part but this is something that's been coming up more and more is actually the environment in which mice are kept and affecting the outcomes of research. Yeah, I was going to ask what temperature you keep your mice at since we talked about that last week. I mean, if a lab has a better result because they have classical music playing, it seems like that's actually in itself, it sounds like, oh great, they got a better result but it's actually kind of disastrous to think about if they're the only ones doing it and giving an artificially high result from that lab. Uncontrolled variables. Uncontrolled variables. So how much effort is going in to controlling these, what you were just saying, keeping that environment controlled? Yeah, so we're very aware of those kinds of effects and how they can really derail everybody's research and confuse the literature and, you know, was that a real result or was it? I think the important thing to remember is that in cases where you can't reproduce somebody's results, it's not necessarily the case. In fact, it's very often not the case or very rare that that person is just being fraudulent, right? They're not making up their data. They're not trying to get a nature paper, come hell or high water. I do believe, I think we're all in agreement that the results they got at the time that they got them were real. And so there's a lot of things that can, it's the environment. It could be the reagents that they were using at the time. So a lot of what we do is we get nice into the Jackson laboratory. If it's a, for example, a behavioral phenotype or something that we may think may be highly variable or a little bit persnickety, you know, depending on what person's hands they're in, we'll do a second site validation. You know, we'll get those mice in and we'll say, did we see the same exact thing? Most of the time we do in some very subtle phenotypes, we may not necessarily see it, but we allow people to understand what we saw. And of course this all comes out in the literature, eventually anyway, if it doesn't come out at, you know, people at meetings just talking about, oh, I couldn't reproduce that part, but I could reproduce this part. And I think at the end of the day, those phenotypes and the things that are going to be the most robust, you know, are going to sort of rise to the top. And we may have to just let some of those very variable portions go, but I think the consideration to try to have the most reproducible results that you can have, you know, right from the beginning, making sure that your experiments are powered the way that they should be, basically being conducted and blinded and controlled and just making sure that we're not introducing that variability in ways that are not appropriate. Great. Did you see the story last week about temperatures with lab animals and that maybe these mice were too cold? Did you have any ideas about that? Well, I mean, certainly there's a lot of anecdotal information out there from, you know, the sex of the animal caretaker to the temperature of the mouse room to really, you know, what noise is going on in the mouse room, which probably makes a little bit more sense. But then there's also variables, you know, some people will say, well, don't put the cages on the top rack if you really want them to breed, because there could be, you know, something about the lights. There's a lot of different, you know, but there are so many different variables when it comes to that. But I do think there is a lot more room for those kind of animal husbandry types of experiments and, you know, just because we're comfortable at that temperature doesn't mean the mice are comfortable at that temperature. And there's also, again, a strain-by-strain case that some of the mice actually like to be a little crowded. You know, they actually do better when there's more mice in the cage but for other strains, they don't like that at all and they do a little bit worse if you're measuring reproductive performance. So do you have these instructions then if somebody is going to be hoarding your mice like, you know, do not overcrowd this one. This is going to change sort of the viability of your experiment if you've got them overcrowd. I mean, do they get like a little list? Don't feed them after midnight. You'll never get them well. Did they get this sort of rundown of what to and not to do? Well, I think for most people, their animal husbandry is dictated by their animal care and use committee. And so their veterinarians and their staff will dictate what they think is an appropriate housing condition. And there are, you know, international guidelines along these types, but other people will say, oh, you know, as soon as the female mouse has a litter, you should remove the male because it stresses them out. Well, you know, maybe in some strains, maybe not in others, but we just find that if you do that, you just miss the next estrus cycle and you've just lost a round of breeding. But other people feel, again, do you provide enrichment to the mouse? Do you give them toys to play with? Those are the kind of things that actually really introduce those environmental factors that can really change your results. And that's my concern, too, is that if we don't have some sort of a standard in place, and there's international standards, but I'm not really talking about the just basic animal husbandry of the situation, but something like this wheel that you introduce for the mouse, something like this. And if you have found out that if you keep it cold and there's no wheel, you might have had a much lower result, which you might then use if you're trying to prove the negative. And then, hey, if you really want the high number result, let's get the wheel in here, let's crank the temperature up to 72 degrees, let's put the classical music on in the background, and we'll avoid the top cage. It seems like the standard needs to be something like this. I mean, if they're all going to be in a cold room, let's keep them all in a cold room, and that's the standard or whatever that is. I think there should be a maximum standard too of the type of care and entertainment they're getting. Otherwise, it does seem like you're tweaking your result, whether unintentionally or not. I think that, again, so you can control those things, and I do think that most people, for the most part, they do. We have, like I said, the ALAC guide for animal care and husbandry that basically sort of set the norm. So if you have a singly housed animal, you need to provide them with enrichment. That's pretty standard in uniform across all institutions, as is the way that we handle the mice and the cage changing and things like that. But the other part of it is there are other factors that are likely to be much larger than that that we can't necessarily control for. So maybe it is your reagents. Maybe it is the food that you're feeding, the animals. And even though in the chow that we give our animals, the protein and the fat content is controlled for what's going on with the way that wheat was stored or that corn was stored that year could introduce a higher or lower level of ribothylavins or aflatoxins or something along those lines. And then let's not forget the microbiome and the pathogens and the opportunistics that if you try to exclude every single organism and have just this pathogen-free animal, and we're not talking about bad pathogens. They would be dead. They would all die. They'd be unable to digest their food. And so I really think those microbiome experiments are really going to be interesting. So we can control for and we should control for the environment as much as we possibly can and standardize. But at the end of the day, I think there are going to be a multitude of factors and we're just going to have to do our best to control for it and make sure that we're running the proper controls in our experiments because you may not be able to get exactly the same result that the other person got. But between your experimental group and your control group, you should be seeing the same, maybe not value, but the same end result anyway. And is it more on the researchers who want to run particular studies to determine the exact strain of mice that they want to use and then based on that strain determine all these factors that we're talking about, whether or not they should be housed in a group or housed individually? Yeah, I think, you know, for the genetically engineered animals we've been a little bit, as I mentioned, constrained to maybe C57 Black 6 or 129 or the common inbred strains. And so in a lot of ways, you know, we have a small number of genetic backgrounds with a large number of mutations that are introduced onto them. By and large, you know, they can change from one mutation to the other, but most C57 Black 6 mice, you know, regardless of the mutations that they're carrying and that's a huge generality, obviously it's not a rule, you know, will give you the same litter size, you know, the females still don't like to be disturbed, you know, just leave them alone, let them have their babies and do their job and you know, you'll have a lot more mice at the end of the day. You know, whereas if you keep, you know, poking your head in the cage and it starts out and not like that, some models and some strains are much more sensitive to those kinds of variables than others. Yeah. So, yeah, you just have to, you have to know your mice and we certainly provide as much information as we can, you know, we have a whole database and a whole group of technical information support specialists, you know, who will tell you, you know, if your experiments aren't working or your mice aren't breeding or things aren't happening the way you think they should, you know, we'll give you the benefit of, you know, the 75 or eight years or more of experience that we've accumulated at the lab and pass that on. Someone in the chat room, Ed from Connecticut is asking to what degree could modeling, computer modeling even replace working with live animals? Is this something that, as computer models become more and more sophisticated, is this a direction that Jackson Lab, working on this stuff as well? Oh, yeah. I mean, I think that to not take advantage of the computational sciences and the computational network biology, we know so much more about the systems and pathways than we did before. So, to not be using that kind of computational biology, you know, I don't think there's many institutions or universities that don't incorporate that, you know, into their science. It's just, you know, another way of doing science, it's computer modeling and you certainly still have to test those hypotheses at some level. And you also still have to fill in all that data that they're modeling in the first place. I mean, this is, I think what it is is this actually becomes more useful if you're considering running some research and would be able to go into a database and find that not only has this been modeled or this experiment been run once or three times, and you might still want to run it yourself. But the computer model can show you what those results are based on. Three or four disparate studies that all sort of touched on the same gene. But you absolutely have to have done the actual real world research in the first place. Otherwise, you have nothing to create that model on. That's very true. But I also think, you know, just to add to that, you do have, you know, these databases that have, you know, all of these really great computational software behind them. So, for example, if I wanted to make a particular mutation because I thought, well, we saw this, you know, allelic variant in humans and we think it's going to be pathogenic. Hey, let's make it in mouse. Well, before I do that, you know, I'm going to look at the level of the sequence and the genomics and the transcriptome. And I'm going to see if there is cryptic splice variants that exist in the mouse or the human that don't exist, you know, in the other organism or vice versa. And so, you know, you have to take into account, I think, a lot of those changes. And, you know, certainly the network, the networking of genes and proteins and pathways that you can get is really, really interesting. And again, though, you're right. You know, sometimes it will tell you the experiment not to do. Sometimes it will tell you the experiment that you think is going to strengthen your hypothesis. But then, you know, you really do have to do the experiment as well. Yeah. And I think there's a lot of computational genomics that is predictive as well. So being able to give you give you a better guess as to where to look than you would have otherwise. Yeah. And that's really a lot of what the Jackson Laboratory and the Connecticut facility. So we're talking a lot about the mice and the genetic engineering that goes on in the Bar Harbor campus, for sure. But we have facilities in Sacramento and Connecticut is our latest campus which we just opened that really takes advantage of the genomics and leverages what we know about the sequence and the genomics to really do science in ways that are much different than we used to do before. So from your position working in neurodegenerative diseases and also in these rare and orphan diseases and kind of seeing the crisper technology come in and disrupt, do you have any I guess any thoughts on where you where you think lab mouse genetics is going to be going in the near future? Yeah. I think it's going to be, you know, better. Having just worked in spinal muscular atrophy for the last decade or so working with those mouse models from the ground up doing a lot of that work in embryonic stem cells and now seeing at what pace we can accelerate that. Now that we have the models and now that those resources are more accessible to the scientific community I think a lot of that pre-clinical work will go faster. I think as a community we'll be more inclined to collaborate and form consortia that will help us solve these problems faster because I think the days of one mouse in one lab the lab that studies this particular mouse mutation for the last five years those days are over and that's good. I think it's a really good thing beyond just creating the resources we need to be moving towards using those resources and the applications that we need to get for these therapeutics that we just really and they're there and they're possible for spinal muscular atrophy I never really thought when I started working in that 10 years ago that we would have drugs and clinical trials that really were as powerful as they look to be at this point but they're there and I think with this new technology for these other rare and orphan diseases I think we're just going to get there much, much faster and that's an optimistic and I am optimistic about it because I do think it's going to happen but it doesn't necessarily mean that there's not a lot of work to do still behind it, it just makes the job a little bit easier but there's still a lot to do and I guess finally to ask as we end the interview so World Lab Animal Day we can take a moment to think about all the animals that help us to come up with our therapeutic treatments to come up with our understanding of the human body of the animal body systems how it all works and how we can fix it when it's broken do you see a day I mean, do you think at any point in the future will we know enough to get rid of the animal models or is the lab animal is the lab animal is it something that we should respect and understand and accept that we're going to be working with it for a long time to come well I think for sure we'll be using animals and research I think just from the standard that we're not ethically going to conduct these experiments in humans we're just not but to your point I think the idea of and we do this now, I mean I think every researcher I know in the United States and Europe and around the world are incredibly cognizant of the care of the animals how many animals we're using we certainly, the 3Rs with the reduction of the animals is very much in the forefront of our minds we don't want to be using animals unnecessarily in the research whether they're flies or mice or anything else for that matter so that really goes back to incorporating all the tools that we have we may do a cell based assay and make those mutations in a cell line before we even think about going into mice we'll do the computational work behind the scenes to make sure that we're not just taking a wild shot in the dark on a hypothesis they're going to be well thought out and I think that that's where we have good regulatory systems in place not only in the way that we use animals and house animals but in the way that we do our peer reviewed work on our grants if you're really not putting together a good hypothesis and there's flaws in your experimental design you better believe your review the committee will tell you that we're not going to fund you because this is why we think you're wrong and here are all of our suggestions and you can go back and sort of I can picture a day perhaps 100,000 perhaps much longer from now when a group of the ancestors of a group of escaped transgenic doogie mice are there accelerated learning and memory discover the archive of hominid research from their archaeologists and discover that everything they need to know about curing any disease that befalls them is there in that archive that they don't very much appreciate the work that's been done we're doing a really good job at curing mice of all sorts of ways and I think that's a good point too because I think in oncology that statement is more true than anywhere else where mice aren't humans and humans aren't mice and just because you get a positive finding in a mouse or a generative disease or a metabolic disease or an oncology indication you really have to think about mechanism you really have to think about your outcome measures and look carefully because the mice are telling you information they're not going to tell you whether or not you have a cure in front of you and for that the preclinical model is a way to give you confidence to move forward with the data that you have and the more thoroughly you can interrogate it and be your worst critic on what exactly does this mean are the same biomarkers there are the mice dying of the same things or suffering from the same ailments of the human patient population so those are the things that you really have to look carefully and be your own critic on that and then I think that we'll get to the point where we really believe that the mice do translate and they will translate if you're watching and listening close to yourself being maybe overly optimistic or if it's just not the right area to be interrogating or the right disease to be modeling then you may have to go with something a little different Thank you so much for your time tonight it's just been wonderful to talk with you about the work you've been doing and just in general how this all works Well I'm happy to have been a part of the conversation and thank you so much for having me this was fun This was great and for everyone out there if you want to find out more about the Jackson Laboratory you can go to jax.org that is their website and they're also on Twitter as Jackson Lab and Kat I don't know if you're on Twitter or anything but it was it was wonderful once again and thank you for staying up late with us My pleasure Thank you Alright everybody I hope that you have had your information filled for mouse research that was a fascinating fascinating conversation and this is this week in science we're moving forward with the show it's going to be a really long show to get tonight you guys in for this because do you know what time it is? What time is it? It's time for Blair's Animal Oh my goodness What you got Blair? Oh I have some scientists doing some really important research That's cool That is exactly how stabby is a puff adder Exactly how stabby is a woodpecker Exactly how stabby is a mantis shrimp I want to know Please tell me there's a high powered air gun involved So this is something I think the stabbiness we're thinking of this is something I've often wondered about when hummingbirds are fighting each other Do they ever like jousting and they just Oh this is a great question So Phillip Anderson from the University of Illinois teamed up with Jeffrey LaCosse of Charles E. Jordan High School in Durham, North Carolina and Mark Pankow of North Carolina State University Rally to measure is the best way to describe it It's how animals puncture things and what animals are the best have the most force for puncturing things So they did this first by trying to figure out what parameters you use to measure how things pierce things So they started by using an arrow shot from a crossbow ballistics gel and ballistics gel is usually used to simulate human flesh Usually used on myth busters This is where I've seen it It's on myth busters exactly So it's a replacement for human flesh So the way things are punctured is actually it turns out very complex which they figured out using high speed video on these arrows going into ballistic gel So first the object let's say the arrow hits the target with enough energy to initiate a crack in the target surface This is where our body would get a cut That impact creates stress waves which moves through the target material like sound waves and these waves interact with the edges of the target in formation or a wound After the initial impact the arrow must open up new surface area inside its target deepening the wound breaking molecular bonds and overcoming friction to penetrate more deeply and the target material builds up elastic energy as it deforms at a certain point the elastic energy in the material causes it to push back against the arrow and if the elastic energy is large enough it can eject the arrow or this is where the arrow stops So the arrow's shape its mass and its speed also all play a role as the composition of the target as does the composition of the target So knowing all of this this team figured out the best way to measure and continue to call stabbiness is by kinetic energy That was to figure out I think you should call it their keekiness Yup So they were more keeky if they had higher kinetic energy and all of us physics buffs out there know that kinetic energy equals anyone, anyone half times mass times velocity squared half mass velocity squared So the object's mass is related to kinetic energy but velocity speed is always squared in this equation so velocity is super important in the kinetic energy question So looking at animals like for example as it loads the trap jaw ant the Portuguese man of war the woodpecker the mantis shrimp, the puff adder these guys have a huge difference between all of them in mass So what they found was that velocity how quick you're stabbing somebody has a big effect on the kinetic energy and how effective of a poke it would be and so just as they expected the velocity increased as size decreased So the speed at which they attack varies with size for an example the trap jaw ant shuts their mouth their jaws at 60 meters per second so that sounds very fast it's very fast but the puff adder only does it at about 2.6 meters per second see this is already isn't the puff adder though isn't it a defense for the puff adder no the puff adder is a viper I'm picturing a puffy why am I thinking of like a puffy fish oh puffer fish no the puff adder is a venomous snake oh an adder I got it so this is their fangs they need to they need to be stabby so that they can get their fangs deep enough into their prey's tissue to inject venom so it's very important that they're stabby the mantis shrimp was only about 3 meters per second so remember we have the mantis shrimps with the clubs those are usually the ones that I talk about on the show but they're also the ones with the spears and so they go 3 meters per second the woodpecker 7.5 meters per second the hydra or the portuguese man of war is 37 meters per second so that's the little nematicis the little stinging cells like on a jellyfish that's really fast and then even faster again trap jaw ant 60 meters per second that's about 130 miles an hour wow that's pretty fast so the smaller they are the more stabby they are which is probably really important because they need to impart greater force to have more of an effect yes exactly so it's all about the kinetic energy and so if you're tiny you need to be faster in order to still penetrate a surface your stabbiness need to be faster gotta be fast and stabby stabby if you're little you have to be more like kiki yes exactly and so Ed in the chat room is talking about orca jaws but remember an orca is huge so because he has all these muscles orcas have all these muscles huge in themselves their teeth don't actually need to be as sharp and they don't need to close their mouth as fast yeah they could slow to you yes but because of mass and also muscle we did not include muscle in any of this so you're talking about a jaw closing and biting power that's very different from stabby power because stabby you're not occluding things it's not like two teeth that are going up against each other you're just poking it's very different so there you go you would need a narwhal running into something to measure stabbiness now would you rather be stabbed or eat deadly nightshade probably be stabbed because my chances of survival would be higher unless I have some antidote to the deadly nightshade where am I going to stab or I'll go with the nightshade maybe I've been micro dosing myself with deadly nightshade for a long time before having the nightshade like Iocane powder exactly yeah so deadly nightshade deadly deadly nightshade it's so called and used in stories all the time because this is a very famous poisonous plant and it's a poisonous plant that makes berries that look very alluring and so back in the let's call them the dark ages children would wander off and eat berries and that was because the deadly nightshade was protecting itself with poison so the idea was that if animals that try to eat the nightshade die then maybe someone else will see that and stay away from the nightshade and nightshade once you know what it looks like is pretty different looking from other plants so this means that in theory because it looks distinct that means that if you know that that plant is dangerous you won't ever try to eat that plant so there's that side of things but there are other animals that have figured out how to eat deadly nightshade or some invertebrates that can eat nightshade and nightshade has been found to have a pretty interesting response to herbivory and it's something that we haven't really seen before so researchers from institutions in Germany and the Netherlands have found that nightshade make a special nectar like liquid that attracts ants so why great question what is going on there so the nightshade when something starts to bite away at it then they exude this nectar like liquid turns out to be essentially just sugar water it's even way more simplistic than any sap you've ever seen and it's essentially just water and sucrose and this is specifically made by the nightshade to attract ants the plants that had sucrose on their leaves attracted more ants than any of the other plants and the researchers also did this with nightshade plants that hadn't been chewed on yet they sprayed them with normal water and indeed ants showed up to the nightshade plants that had the sucrose water on it and they found that when there were ants on the nightshade plants it greatly reduced predation by slugs the other main predator that this nightshade has is flea beetles and they cause the most damage the ants couldn't drive away the flea beetles but they did remove beetle larva from stems where they had buried themselves after calling up and out of the dirt when they had been hatched so the ants do protect the plant against beetles in future generations that's brilliant so I wonder if by removing them if they're just removing them out of the goodness of their heart saying this little thing's in the way I want to have a nice smooth stem or if the ants are taking them home and using them as a proteinaceous food source food source but it also could be it's been worked out over many many many many years an evolutionary handshake exactly so that's the question which came first the sucrose or the ants so as far as we know this is the first instance of a plant exuding material from a wound for the purpose of protection right because we hear a lot about other compounds that are used to keep predators away lots of bitter compounds lots of not sweet stuff but all the stuff that is either poisonous or bitter or is somehow communicating that animals need to stay away and we've also done a lot of stories talking about plants releasing chemicals or some sort of signal to warn other plants exactly but this is the first time we've seen a plant exuding something found to attract another animal to protect them that is definitely new oh this web of ecology I love it so the deadly plant is now covered in sugar water resisted if you can kids oh gosh those nice yummy berries that just gets worse this story about the nightshade alright everyone this show is not going to get worse and worse we have lots of science news out there in the second half we're going to take a quick break right now and we're going to come back because I have stories about alien oceanography and the rain thesaurus yeah so hold on to your hats everyone this is This Week in Science hey everybody if you are enjoying this show do hope that you take a moment and either give us a good review on iTunes or a thumbs up on YouTube or wherever you're listening to us tell other people that you're listening to twist because that will help us out a lot put us out there in your social networks and let people know that you like twist and we're a show worth listening to it'll help it'll help and you will be the one helping additionally if you can help support us we also have merchandise that you might like to take a look at if you go to our Zazzle store there's also a link on twist.org to our cafe press store but the stores that we've got zazzle.com and cafe press they are where we hide all of our 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the PayPal buttons which you can click and donate pretty easily we also accept donations through patreon.com slash this weekend science is where you can find a way to support us there and you'll get little gifties in return at various levels of support on Patreon whatever your preference head over to twist.org the links are there check out the most recent show also let us know what you like what you don't like because you are our executive producers you make this show happen we thank you for your support we really could not do it without you we are back with more this weekend science fantastic okay I've got a couple of cool stories alien oceanography I teased it I'm not going to keep you waiting I think it's time to talk all about it did you know that the we are doing oceanography on an alien world we're looking at oceans on an alien world and whereabouts is this alien world that you speak of really not that far away it's over on Titan oh the Saturnian moon of Titan the Cassini mission has been exploring Saturn its rings and its moons for many many years now and over several years it did fly by over Titan and took lots of nice pictures and looked at temperature infrared information did radar mapping of the surface and under the surface it was a while back it was found that Titan has lakes or giant oceans that are about the size of the great lakes at the north pole and also at the southern pole of its moon so the moon really is kind of like a world like earth it's got a high nitrogen atmosphere like earth it's got a lot more nitrogen than earth does but high nitrogen atmosphere the difference is it doesn't have oxygen in the atmosphere it has methane and ethane and it's thought that the methane and the ethane falls out of the sky like rain well it also collects on the surface of the not the planet on the surface of the moon and in looking at this some researchers recently published their findings that these lakes are completely these oceanish lakes are completely filled with methane they thought they would get measurements of methane and ethane mixed together but they didn't it was all methane so that's an interesting question that they haven't answered as to why where did the ethane go additionally because of their radar measurements they were able to bounce radar off the bottom of these lakes and they found that they're not hard hard pan bottoms but actually rather soft so there are materials or sediments at the bottom of these bodies of water and then also you would think that there is runoff from the rains as it falls onto the surface of the moon and those would create little rivers streams that would run into these bodies of water and you might find similar kind of heating and cooling of the land around around these oceans as we do here on earth where the sun shines on the land, warms it up a little bit more than the bodies of water because the bodies of water or in this case methane on the moon are are temperature reservoirs and heat up as quickly as the hard rock surface well what they found is that the surface around these oceans heats up at the same speed as the oceans themselves which makes them think that there are wetlands so kind of like marshy wet areas as opposed to very specific streams and hard land and beaches that you're not going to find beaches like we have here on earth on the edge of these oceans of methane you're going to find marshlands like in Florida yes swampy without plants right there's that there's that but otherwise I'll buy you basically yeah yeah there's this really interesting finding and I was really struck by the idea of these bodies of water on a a planet like moon in our solar system but it's still alien it's completely different you know similarities are there but it's different seas of methane you know marshlands but without any marsh reeds or animals yeah forget Mars I want to go there yeah I want to go there and I want to drop down some sort of some sort of rover marsh rover some sort of hovering by you like a fan boat like a fan boat that's the one like a fan boat rover to go around and do some investigating yeah I mean it would be amazing to get something on the ground there roving or on the water roving but it's a it's a it's a wonderful time now we're able to take information like that the Cassini mission has found and also from other missions that are going to different planets and you know not only are we doing geology and geochemistry on Mars we are also doing oceanography on Titan it's just a very very very fun way to think about Titan also has up to a thousand times the oil deposits that we have from the hydrocarbons most likely hydrocarbon marshes yeah but we need a pipeline we need a pipeline forget Keystone the hydrocarbons it's not it's not a fossil fuels darn maybe oil deposits there yeah and then another really interesting story that came up this week I thought was so fascinating is researchers at the University of California Berkeley have created what they're calling quote unquote a semantic atlas of the human brain you know we've talked about we've had conversations about what area of the brain likes up when I say apple and you think about an apple you hear me say apple what part of your brain lights up does the same part of our brains light up in the same way that's what these researchers have done because this is that whole if we had a direct to direct ethernet connection between our brains would we understand each other at all because my apple could be where your blue is or something like exactly stuff and they've looked at this is what they looked at their study process was really I would have loved to have been a subject in this study but it's been published in nature and they recorded I believe they said six individuals so it's not a large sample set so we're not like this is so there's seven people all together seven native English speakers so these aren't just people who learn to speak English after learning a different language these are people born and raised speaking English so who knows how really globally this research can be taken they had them lie in a functional magnetic resonance imaging machine and had them close their eyes put on a set of headphones keep their head very still and listen to stories from the moth radio hour for two hours the entire time they were tracking what parts of the brain increased their blood flow in response to certain words and what they found is beautiful and fascinating they discovered that the human brain from these seven individuals there are parts of the brain that are common across all individuals there are that respond to the same words or the same categories of words and there are individual differences at the finer scale resolution of how that's organized so in I'm showing a video right now it has a bunch of words painted painted over the picture of the brain a model of the brain and we can see that there's a word top and the word top will be found in an area of the brain that's related to clothing and other things like that additionally there's top as in location so related to up down a place in space a house that kind of thing there's also top in relation to other words that you could imagine top being related to and so they found as I said there's a global similarity so things related to visual imagery were found closer to the visual portion of the brain things related to say auditory words I don't mean things I mean words that were more evocative of hearing were closer to the auditory cortex words were spread out all over the brain in different places but this just goes to show that there is some kind of mapping that is relatively conserved across individuals in how the human brain decides to put words together there are definitely there are definitely individual differences so not every brain is exactly the same but certain categories do tend to appear in certain places and how big was the sample size for this? 7 so not large at all and I'd be interested if there was a cultural difference too and that's not something that's been looked at yet at all so I think it's very interesting for starters that there's definitely this consistency and that's what I would be really interested to see is how much the consistency is conserved across language barriers across cultural barriers across gender barriers across all these different things it could really change where you store things in your brain couldn't it I mean we don't know and sort of what I took away from was not a consistency I took it somehow I'm taking it differently I'm saying this would make this sort of brain to brain direct communication thing even more fallible because it's not so much just about where it's stored but it looks like what the continuity is is sort of on the line of this is a food item which elicits parts of the brain that react to a food item this is a word that means listening and now my audio cortex is sort of getting involved in what that means but it doesn't seem to say that we are an individual word has any direct context between two brains other than it may be reflected in certain parts of the brain where those connections are more likely to be made based off the words meaning so but there definitely is something to come out of this that we will find as Kenneth Wang who's a program director at the National Science Foundation's information intelligence systems division says to show how data driven computational methods can help us understand the brain at the level of richness and complexity that we associate with human cognitive processes and it's going to be really interesting to see how this is going to be able how this will inform artificial intelligence and language processing how will it inform the way that we design computer programs to understand human speech I think that will happen first before we start really doing you know direct brain to brain imaging like we've talked about before kind of at that far future science fiction level but it's I think it's have you ever gone to the websites that are like the visual thesaurus where you're able to you can put in a word and then it shows you it shows you a visual map of all the words that that word is connected to and so you actually can visualize it that way and you can go click on one of the synonyms of the word and that will take you to another bubble of words and so you can end up diving really deeply into this intricate connection or network of words that are connected together and see how they're connected in this visual spatial representation and that's basically what they've done here but in the brain and so it's creating the connected network of words and conceptual concepts within the brain which is going to be so cool and as hot rod said is in the chat room so our brain is a dictionary with an internet connecting all the words and Blair has brought up the visual thesaurus for us to take a look at and it's and your stab of course you did, you're feeling so stabby today and then if I click on jab oh poking poking's over there but that starts taking you someplace else yes yeah that's cool I ran out of my free trial that was awesome though that's fascinating it is fascinating and Jack Gallant says that they're definitely going to need to conduct further studies across a larger more diverse sample of people before we'll be able to map the individual differences in more detail and so that's where I think some really interesting stuff is going to come out going from seven people with kind of like okay I can see how these things are kind of mapped similarly in the human brain to a massive sample set of hundreds of brains that's going to make such a difference in the richness of this data but I'm so glad people are doing it yeah cool and writes for robots of course wants to know where the swear words are kept which I think it depends which ones right that all depends is it going to be the words next to mom or is it going to be the words next to you alright science Justin what you got okay so why does one person who tries cocaine get addicted while another might use it and then simply leave it alone why do some people who then get addicted manage to kick the habit while others who have been addicted continue to relapse and why is it that some families seem more prone to addiction than others there are of course a myriad of social environmental psychological factors in each of these individual cases however it may also have a lot to do with specific genetic factors that vary from individual to individual according to a no study with rats study was published in the proceedings national academy of sciences by University of Michigan medical school team and they're saying for the first time they've shown in selectively bred animals that the propensity for addiction is linked to differences in expression of genes for specific molecules in a specific brain region and they've also indicated that an epigenetic marker can predispose an individual to addiction and relapse should be sort of interesting if you can then take this information what through the genome of somebody who's an addict or even or at youth you could identify who's most like who really needs that just say no program who's really not genetically built to deal with addiction they used two special breeds of rats one breed called BHR for bred high responders these are rats that tend to explore and seek out novelty while the other they called the BLR for bred low responders now they don't in fact they say the BLR rats often act anxious when presented with new situations and prefer enclosed spaces even when they can see food in an open area they looked at the impact of drug use and addiction on gene expression epigenetics and the nucleus accumbens of the rats which is I suppose the brain's pleasure center where response to drugs like cocaine occurs normally dopamine system in this area responds to naturally pleasant experiences such as listening to this weekend science and prompts us to pursue them again and again and it's like the drug gets into the system and sort of hijacks the whole enjoyment portion of it and is just saying do this again do this drug this is the only way you get this do this again do this again researchers looked at the rats brains for genetic instructions needed to make a key pleasure receptor this is D2 D2 that allows the brain to receive signals sent by the dopamine chemical or cocaine we're depending this is what is that receptor signal in the brain that's listening for this they found that more addiction prone high responder rats had lower levels of D2 instruction to begin with compared to the other rats in the area of the brain that we were talking about the pleasure center the addiction prone rats were also more likely to carry a specific mark on their DNA called an epigenetic tag H3K N or H3K 9 ME3 which I'll never hear again that kept their brains their brain cells from reading the gene for the D2 receptors so they have this epigenetic tag which is sort of blocking their ability to create the D2 instructions to begin with but after they became hooked on cocaine the addiction prone rats had the same levels of D2 as the less addiction prone ones and when the cocaine was taken away these rats were more likely to relapse to addictive behavior interesting so they didn't sort of have their pleasure center receptors in place and then they got the drug they became in place became active and so the addiction was the sort of the only way that they maintained that pleasure center after that so is the take home here because they're able to look at these these rats and connect this with particular genes I mean could we start could we start looking for particular genes in individuals to find out whether they would be more or less addiction prone so yeah I mean there's that there's that part so there's a preemptive thing like I was saying you would test 12 year olds I suppose and start that sounds like a personal personal security like hey just test me because you need to know yeah well I'm sure we all know that everybody knows somebody who at least knows somebody who's struggled with addiction I've known a lot of people but does that mean that everybody should be tested at a particular age no but it does mean I know people who have chose to not indulge in pretty much anything because something runs in their family and A this is proof that it can run in your family which I think is very interesting that we've always kind of suspected this that it is an inherited trait a kind of a likelihood to become addicted or you know people say they have an addictive personality that could be genetically based but then on top of that this is a way that you can then potentially if you think that you're predisposed if you want yeah and finding and discovering that you have a genetic weakness towards a chemical or towards a drug or towards you test kids for allergies now what food not to give them alright well you test them for something like this and you can say hey look it might be just an additional counseling or education on it you know they separated the boys and the girls in like fifth grade they can separate out those at the high risk for a special class on how to manage your future on this planet because this is an exceptional risk for you that it might not be for your peers so when and that's the thing when I've known people with you know addiction problems and the like it's not like I or anybody else around them wasn't engaging in the same behavior so it's it you know there is all the other factors there's this sociological psychological environmental but there are people who are going to get addicted harder and faster and more severely than their peers so and this this kind of stuff I think but that's the first that was the treatment for relapse is probably where the most interesting right that's the second part right the first part like yeah I mean you could preemptively sort of have foresee what's going on but also yeah if we figure out then how to how to create therapies that address these specific receptor like the D2 perhaps keep it act find a way to keep it active with supplementing it with something other than this drug then we're creating therapies that prevent these relapses you know so this is a fantastic study and it's right on the heels of sort of what we were what we were talking about in our interview is not just being able to find the connections between things we can actually use this sort of information to develop the therapies well and I also see this information as being socially helpful in that I think there's still kind of this pushback of wanting to characterize people with addiction sometimes as being you know not having the strength or having a character flaw but other people will tell you it is an illness and this is a great example of exactly how it is an illness it's a problem that can be stemmed in their genetic makeup and it's not something that can be so simply simply written off as a character flaw or something like that there's actually a predisposition in there and I almost wouldn't then qualify it even as necessarily an illness but acknowledging that the environment will affect different people different ways and that we do have weaknesses that our friends and neighbors don't and that weakness isn't necessarily an illness I mean in the way I'm now sort of thinking of this and picturing this the addiction and everything is I guess you could categorize that affect in life as being you know most but this is really sort of like not having not having the proper spyware on your computer and that everybody can go to the same to any other disease right you're predisposed you have a you know that going into it there's certain things you're not going to go out of your way to do right just like if you're told you could be predisposed to other diseases correct you're right I'm continuing on the lab animal and cool research for treating human front there's a very exciting study related to fragile X syndrome fragile X is a genetic disorder it affects one boy in 4,000 and a girl in 7,000 so it's more common in boys than in girls but it's specifically caused by a mutation in a gene that ends up through a sequence of steps failing to make a protein called FMRP and some researchers have shown that if you delete the gene that makes FMRP in a part of the in the hippocampus where it's responsible for memory formation it causes memory deficits in mice and so they created a they created a knockout model we talked about they took this gene out they deleted this gene from mice and created a mouse model for fragile X disease with this mouse model they've been able to actually pinpoint this chain reaction of stuff that starts with the loss of the protein FMRP and ends up with a loss of memory so if you don't have the protein you can't form memories right no FMRP in the hippocampus no new memories formed and when this happens you know with fragile X starts being observed in babies when they're very young so this is something that you want to try and catch and treat as soon as possible the researchers found that they're able to use an experimental cancer causing drug and not cancer causing cancer treating drug called nutlin 3 and it's an it's an experimental cancer drug still so it's not completely through all of the regulatory process however because it works on certain aspects of the signaling cascade of this chain of cellular communication events they were able to they thought hey why don't we try using it in these fragile X mice so they gave about 10% of the dose that you would give to a patient who's undergoing cancer therapy they took a very much smaller very small small dose and they gave that to the mice for two weeks and when the mice were tested for memory a month later they actually were able to remember what they had seen and smelled in initial memory forming events so this experimental cancer drug somehow it pinpoints some aspect it gets in the way of whatever gets messed up by the deletion of fmrp and it continues the signaling cascade so that it's as if the fmrp was still there yeah so now it's an idea the idea for this is that if they can get through all the testings right now this is a mouse model there are lots of hurtles that are ahead potentially this could be a treatment for fragile X and it could also give fragile X children also show autistic syndrome symptoms so it potentially could give a lot of insight into the autism that comes along with the fragile X and these individuals so mouse model moving into human treatment so this is another really cool really cool story and then we talked about also this one isn't into animals yet but I actually hope that it will be soon we talked about last year a new antibiotic called tixobactin where the researchers found bacteria fighting other bacteria in dirt and they were able to isolate this bacterial compound that they were one species of bacteria was creating to destroy other species of bacteria that were getting into its space they found it and using the tixobactin as it was naturally taken from the bacteria so if you just get the bacteria to make the tixobactin the tixobactin is amazing at being an antibiotic at killing bacteria so this is it was very exciting the problem is it's a new class of antibiotic one that has not been seen before or developed before and so we don't have a way to make it so the next step was to synthesize it and see if we could synthesize it in a laboratory could we make tixobactin without the bacteria and some researchers at University of Lincoln in the UK have produced two synthetic analogs that are show very very similar potency to tixobactin and are only very slightly different from the original molecule and that they've come up with a synthesis pathway and so what this means is they've got a synthesis pathway that can now be be used they've also discovered the part of the protein of the the compound this molecule what part of it actually seems to be the active portion that interrupts the bacterial interrupts bacterial activity so they're very excited about this there's still of course a lot of work that needs to be done to move forward we're probably not going to see tixobactin and it's like in the market for you know at least 10 years but as we're looking toward the future and humanity dying from all sorts of bacterial infections this is a very exciting development that we might rapidly be developing a new antibiotic nice yeah also in the soil this is a scientist university of california riverside discovered a string of beneficial nitrogen fixing bacteria has spread across california this is bacteria called brady rhizobium it forms tumor like nodules on the roots of plants and it's able to fix nitrogen by breaking it down when it forms some plants can easily metabolize what they're trying to figure out is how is it what is it about this bacteria and there's a several not versions but several strains that have spread epidemically you might say across california this one is actually rather beneficial to plants it's you know it's doing nitrogen fixing it's making healthy plants where it goes but what they were looking for is the relationship how is it getting everywhere and what they sort of discovered is it's not that it has this beneficial arrangement with plants that symbiotic sort of portion of its genome is activated when it's doing this and when it's involved with plants but in the soil when it's not engaged in this these sort of pathogenic bacteria that have spread within the soil actually they've discovered just better at utilizing the carbon in soil they're just better at actually just using the resource of soil to feed itself and the symbiotic thing is just sort of what it does when it's got a chance it's not always what it needs to do it's just something that it can do it's just really great for it's one of those things to look at the symbiotic relationship between the plant and the bacteria and you think this has evolved over a long time and this is how they've survived but actually the competitive advantage that this bacteria has isn't what it does with the plant but it's how it just absorbs carbon to begin with and it might be an interesting thing to look at in the future as a bio-fertilizer this is something that we've tried to get away from using fertilizers that create pollution these bacteria can possibly either be manipulated or utilized in a way to fertilize crops without having anything that doesn't belong in the soil and one last soil story that I'll be actually done for tonight this is a quickie I just have to say I'm very excited about some of this research this wine research being done in Oregon I am all over that Gregory Redilac University Oregon Scott Burns Portland State University they were looking at the link between the taste of wine and its soil properties there's something when it comes to tasting wine there are those who extol the galt de terriere and then there are those who either don't know what that means or really don't know even how to pronounce it properly the word was supposed to be but they looked at the concept of tasting the geology behind the wine by comparing soil properties and vintages for Pinot Noir soil properties they say particularly pH levels in the soil affect the wine chemistry so while the wine drinking the wine, sipping the wine one cannot actually taste the soil from when it came it does modify the taste so if you're used to a slightly different pH for your favorite wine it could be the soil that it's grown in that is giving it that particular flavor right but when they say there's hints of chocolate they actually put chocolate in the wine right no I'm kidding it's a joke it's in the barrel oh they soak the barrel in chocolate no not at all it's all the pH of the soil apparently I bet a crow would know or a raven a crow or a raven would know so this week in not surprising news corvids are smart yeah they are how many times have we said that yeah so ravens a recent study from Lund University in Sweden shows that ravens are as clever as chimpanzees in a very particular test so the large-scale study looked at a tube an opaque tube with a treat in the middle and a hole at each end and the animal had to try to get the food out and then they repeated it with a transparent tube and the normal impulse would be to go straight for the tube where the food was run into the transparent tube try to bite through the tube or something but the ravens knew better they had impulse control they did not go for the food that they saw they went in through the side and they got their food and this was something that they did it at a level that chimpanzees did in mammal tests so they are very smart they also are looking at this as an expression of brain size again which is something that we keep coming back to and the most recent time that we talked about it we said comparably in a species the size of the brain of one individual is compared to another does not indicate how smart one animal or another is but in terms of the size of a brain of a species compared to the average size of a brain of another species often larger does mean smarter but not every time and this is a great example of that not every time at all and I'm going to say I've said it once and I'm going to say it again bird brain not an insult that's right unless you're talking about an ostrich brain yeah well there's there's that I said that you guys I won't tell I won't tell Hubble has been looking out at our solar system and has looked at a Kuiper belt object very similar to Pluto's called Maki Maki and this was a it's a one of the Pluto like objects that's out there in the Kuiper belt and Maki Maki has been determined by Hubble's observations to have a moon as well so it's it's called MK2 it's its nickname right now its designation is S because it was discovered in 2015 136472 one yeah Maki Maki is interesting because it has a very reflective surface and so it actually is very bright for an object out there in the Kuiper belt similar in that way to Pluto so it's thought that it's covered with methane on the surface kind of like snow that would reflect light but MK2 is really really dim it's 1300 times fainter than the planet it orbits around it's about 13,000 miles from the dwarf planet and it's thought to be only about 100 miles across so not very far across at all you know you could get across there in an hour and a half around the moon in an hour and a half the researchers are still trying to determine whether Maki Maki has a circular orbit or whether it has an elliptical orbit and whether or not it has a circular or elliptical orbit will let them know the source of the moon so circular orbits tend to be objects that resulted from collisions whereas elliptical orbits are more often objects that were captured as they were flying by so the question is where did the moon come from and so now they're just trying to determine the exact the exact course of its orbit around Maki Maki neat and also because it's very dim what is it made of why is it so dark why is Maki Maki so dark I do not know or Maki Maki's moon Maki Maki's moon mk2 exactly why is it so dark I do not know super curious and my final story climate data we're always talking about climate data and people collecting climate data and there are always these arguments of like oh we don't have human records going back far enough and well you know but people have been writing things down for a really long time and researchers going back into historical records have found climate data of lakes and areas that that froze so in one case priests in Japan keeping records beginning in 1443 about Lake Suwa in the Japanese Alps the priests started taking records to take record because the male Shinto God Taken Minakata crosses the ice to visit the female god Yesakata Ome at her shrine causing a ridge known as the Omi Watari to form and that's what they believed and so when the water would freeze then they had to celebrate and honor the ridge and do a purification ritual and they actually wrote down its direction and starting location and they used that to forecast harvest and rainfall for the coming year. Then there's also a group of Finnish Finnish merchants who began keeping records of another body of water of an area the Torn River that flows from the Arctic to the Baltic Sea between between Sweden and Finland and starting in 1693 Olaf Albom a merchant started keeping records and then other merchants kept records and basically the finding of this is that when they started keeping records hundreds of years ago these areas were experiencing warming and where the annual freeze date was changing and moving forward in the year but very slowly about 0.19 days earlier per decade 0.19 days earlier per decade alright and then the records show starting in the industrial revolution the change of the freeze date jumped to about 4.6 days per decade so this is hundreds of years of meticulous data keeping from what they're calling it's citizen science but these are people who were keeping records for business reasons for religious spiritual reasons and we have very accurate records going back hundreds of years that pretty much it's like oh that confirms and corroborates the industrial revolution is part of what's heating everything up the question is how many of these things do we need because we're taking cores we're figuring out all sorts of other measurements hopefully bringing in the element of humans actually being there and writing things down yes we'll really start to solidify things hopefully it's sort of like again this sort of goes back to the interview we're at the point where we can already tell by just doing genomic testing of our environment what's going on now it's time to be working on the solution it is it's time that's what we need to be doing we don't need to argue about this stuff anymore let's try and fix things people let's be fix it fix it fix it and you know what we do when we talk about the climate stuff and it's like oh it's you know it can get really kind of depressing and sometimes you think about like oh we're gonna die from we don't have antibiotics this is a problem that's a problem this is and you can look at all the negative but actually today with some of these medical breakthroughs and talking about how rapidly the technology like CRISPR Cas9 and those developments on that front are helping us come up with treatments and therapies we're really going to be helping ourselves a lot faster than we used to be able to so there's a lot of positive stuff going on in the world as well and so I want to be able to focus on that focus on what we can do and as you always say Justin the moment in which you can do is now yeah and we need to take the decision away from people that want to make it difficult and we can make the decision we just need to work together start doing that I want more solar I want more water I want more wind I want all these good things good things I want good things I want structure I want pretty happy healthy happy clean world let's do it and I also would like to take this moment to thank our Patreon sponsors because we have reached the end of our show thank you to Paul Disney Kevin Perichan, Keith Corsale, Steve DeBell Melissa Mosley, Jesse Moreno Patrick O'Keefe, Jason Snyderman Rudy Garcia, Gerald Sorrell's grade Goothman, Alex Wilson, Dave Naver Jason Dozier, Matthew Litwin, Eric Knapp Jason Roberts, Patrick Cohn, Chris Clark Richard Onimus, John Ratnaswamy, Byron Lee EO, Bob Calder, Jared Lysette Ulysses Adkins, Brian Condren Jake Jones, Mark Masaros Trainer 84, Edvardus Rymkus Brian Hedrick, Cassie Lester, Sarah Chavis Sheila, Shane and Tara Ginsberg, Marshall Clark Charlene Henry, Don Cumberidge, Gary Garcia Randy Mazzucca Ed Dyer, Tony Steele, Dave Freidel Craig Landon, Daryl Lambert, David Wiley Robert Aston, Debra Smith Mitch Neves, Flying Out John Crocker, Richard Porter, Christopher Dreyer Andrew Dolinger, Sylvan Wesby Artyom, Pixel Fly, Shu Wada Steven B. Dave Wilkinson, Steve Mishinsky Rodney Lewis, Braxton Howard, Phil Nadeau Rick Ramis, Salged Sam, Matt Sutter Emma Grenier, Phillip Shane Stefan Insom, Michael George Russell Jensen, Mountain Sloth Jim Drapeau, Tara Payne, John Maloney Jason Oldes, James No Wiles, Paul West Alec Doty, Illuma Llama, Joe Wheeler Dougal Campbell, Craig Porter, Adam Mishcon Aaron Luthon, Marjorie Paul Stanton David Simerly, Tyler Harrison Ben Rothig, Colombo Ahmed and Gary Swinsberg I love seeing that list get longer Thank you for all your support on Patreon And if you're interested in supporting us you can find information at patreon.com Remember that you can also help us out just by telling people about TWIS It's so easy And on next week's show I'm working on getting another really awesome interview but we will be back no matter what broadcasting live online at 8pm Pacific time on twis.org You can watch and join our chat room live But if you can't make it don't worry about that because you can find our past episodes at twis.org and also twis.org And oh, I just realized next Wednesday is May the 4th May the 4th be with you Thank you everybody for enjoying the show TWIS is also available as a podcast Just google this week in Science in your iTunes directory or if you have a mobile type device the number 4 droid is app is in the android marketplace or simply this week in Science and anything Apple Market Placy For more information on anything you've heard here today show notes will be available on our website that's at www.twis.org where you can also make comments and start conversations with the hosts as well as other listeners Yes, or you can contact us directly email kirsten at kirsten at thisweekinScience.com or at player at twisminion at gmail.com or player at playerbaz at twis.org Just be sure to put twis somewhere in your subject line or your email will be spam filtered into oblivion You can also hit us up on the twitter where we are at twiscience at drkiki at jacksonfly and at playersmanagerie We love your feedback if there's a topic you'd like us to cover then for an interview a haiku that comes during the night please let us know We'll be back here next week and we hope you'll join us again for more great science news And if you've learned anything from the show remember It's all in your head 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 for all the warming with a wave of my hand and all it'll cost you is a couple of grand This week science is coming your way So everybody listen to what I say I use the scientific method for all that it's worth my opinion all of It's this week in science This week in science This week in science This week in science This week in science This week in 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 yet understand that we're not trying to threaten your philosophy we're just trying to save the world from jeopardy and this week in science is coming your way So everybody listen to everything we say and if you use our methods better roll than a die we may rid the world of toxoplasma got the eye cause it's this week in science This week in science This week in science This week in science This week in science This week in science Science I've got a long list of items I want to address from stopping global hunger to dredging Loch Ness I'm trying to promote more rational thought 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 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 This week in science This week in science This week in science This week in science For the after show we are here for the after show time Yay Hey, Steve Everett got the Google Music Player podcast update a few days ago. Yes, we are in there. We are in the Google Podcast Directory, so soon maybe I'll see whether or not people are starting to listen to us through Google podcasts. But you use pocketcasts, okay? Pocketcast is a good one. Interesting. That was fun. That was fun. That was a good show. Good interview. Are you happy? Did Jackson Laboratory? Oh, yeah, I think that was splendid. I got to ask, I didn't get to answer one of my questions, but I did get answers to most of them. I still wanted to know more about the process of the how when you start, even with the two knocked out genes or whatever they are, how you get your final lab-ready specimen, that process is fascinating. Because it turns out, even if you've knocked out sort of what she called the founding, I think she called it the founding. Yeah, the founding generation. Founding generation. You still have to continue to test the mice after that, because they don't all, even if you've knocked it out in both parents, it finds a way back in somehow. Yeah. Yeah, or there could be mutations. There could be mutations in places along the way. Yeah, you don't want, yeah. Oh, yeah. One fun interview. Super fun. And I was feeling guiltier and guiltier as it went on, because I know we're doing this late at night, but she's three hours later. She was like, I was like, OK, you go now. It's almost midnight where you are. Good night. Starting to feel. I was like, this was supposed to be a 20-minute interview, and we're just. We took up the hour. Oh my gosh. But I'm very, very generous with her time. Very generous. So OK. What is this? I'm looking through the Zazzle Store right now, so that I'm doing. Through our Zazzle Store? Yeah. Oh, I need to go to their Zazzle Store. I need like a Jackson Labs shirt. That would be cool. Yeah, you should. I'm looking at the tie in here. We have a tie? Yeah. Kiki, I think, tried a whole bunch of stuff. What? Didn't you? It looks like you tried a bunch of different products. Well, I didn't have the energy to do each one individually, and there was like this button to just select all their product, and that's what I did. That's what happened. It was easier to select all and then delete the ones that really didn't work than to do it the other way around and selectively pick. So I don't know if I overdid it. No, I think it's fun. I'm looking at the toad necktie. You can have a toad necktie from Blair's Animal Corner. That's pretty awesome. So Ed from Kineticit, yes, the smell matching date site. Dating site, I saw that. I read that article earlier. We had other stuff for the show tonight. But yeah, an interesting story that Ed found where some New York artist and a researcher got together and they created a dating site where for $25 you'd get a t-shirt that you'd wear around for three days and then send back to them. And then you would be sent a number of samples and basically sniff the samples. And it's a bunch of samples that have been cut out of the armpit area of other people's shirts. And then you'd sniff the samples and decide whether or not you liked them. And then you would pick like your top three or four and then be set up on dates by this. And if the other people match you in liking the way you smell. So it was a very interesting thing. Mommy, how did you eat, Daddy? He was stinky. You smelled just right. Yeah. So it's, I don't know, very, it's an interesting. Excuse me, I've got the eyes. It's 10 o'clock. I hit a wall. Oh, wait. Yeah. I'm like, whoa. I yawned and then I completely forgot what I said. Yes, so I don't know if anybody out of it, people went on dates in the article that was written about it that Ed found. But it doesn't sound as though anybody found true love. Yeah. Although the author of the article said that one of the people she met, although it wasn't a perfect match for her, she thought that the guy would really get along with one of her friends. So she set up the guy with one of her friends. That's funny. Yeah. But they're going to do another, it's like an experiment art project that they're doing. So they'll be doing it again later. Yeah. Fascinating. I don't know. I'm glad I don't have to worry about that right now. Yeah, well, I'm intrigued. It is intriguing. Yeah. OK, I have to figure this. So you guys, there is this scavenger hunt end of July to beginning of August that I think would be really fun to do. Great, let's do it. It's called Gishwes, the greatest international scavenger hunt the world has ever seen. Great. Sounds amazing. Are you serious? No, I'm serious. Tell me more. OK. I'm tired. I'm sorry. I'm tired too. I'm totally dead serious. I want to hear more. I'm tired too, but yeah, I'll tell you. So Gishwes, I'm going to put it up here. Gishwes is Gishwes.com. Gishwes, Gishwes, Gishwes. Is that a seal kangaroo? Yeah, that looks like a seal kangaroo. Great. And so it takes place over a period of time, and you can sign up as a team, I think. And if, yeah, you can build your own team or they'll put you with a team. I was thinking it would be fun to like, I don't know, put together a team if people are interested in doing it. But the idea is that it's creative and artistic, and it's also helping in the community and doing stuff. So for example, from previous years, one of the scavenger hunt items was a VW entirely covered in shaving cream with two children in front of it. And so basically, you do this thing and then take a picture of it, and you have to send your picture in. A sock puppet show at a children's hospital, an evening gown made entirely of materials found in your bathroom, have a tin can phone call while surfing, a wheelchair superhero, senior citizens mud wrestling, you as your favorite dessert, a fully dressed bed in a Walmart parking lot, donate blood with a friend, you as your favorite statue, T-Kini, scuba in a ballet class, hug a veteran, watermelon cocktail wear, none on a rope swing. What are helium pants? Service men or service women holding up a sunbather, keep someone company going through kidney dialysis, amaze us with smoke and mirrors, last year's mascot out of natural items, buy a homeless person their favorite lunch, popcorn child monster, kitchen battle wear, host a diaper drive for a shelter, have a party in a dumpster, climb a mountain with a friend. These are all some of the past year's scavenger hunt items. And it just sounds like a really amazing, amazing thing to be a part of. How big are the teams supposed to be? OK, so let's see if I can. Q&A. This is where I'll find the Q&A. OK, so it's from July 30th to August 6th. I think it costs to register the registration fees, like $19, I think, at the lowest, per person for registration. So you'll be a team of 15 people. During registration, you can either invite friends to build a team, or they can join you into another amazing team. When we post the list on July 30th, your team would divvy up and accomplish the tasks over the course of a week. Yeah, so 15 people on a team, and then you divvy up the list and do it. And then you get points for every item you accomplish. And then for the winning team, I mean, there are hundreds of teams, hundreds of people that do this. The winning team gets to go to Iceland this year. Oh, that would be fine. Right, that'd be cool. Yeah. So anyway. So wait, I'm sorry. Did you say if there was a maximum number of people? And a team? 15 people. 15. Yeah. Good night, Ray. So Catrim, who can surf? Yeah. Right. Wait, but does that mean that everybody doing the things in the pictures has to be part of the team, or do I just have to capture it on camera? Oh, interesting. No, I don't think, no, no. So you just have to capture it on camera. Really? I don't think, because those little kids are not part of the VW, aren't part of a team. So you set it up, and you do it, and then you're one of the people on the team, and you submit it. Oh my god, three people made the same joke at the same time in the chat room. I can surf on the web. Is that good? You guys are hilarious. So funny. Ed, the team does not have to be in the same place. The team can be all over. And that's, I guess, a lot of people just sign up individually, and then get placed on a team. And then that way, it's kind of like a make friends around the world kind of thing also. So you can just meet people. We could have San Francisco, Davis, and Portland. I say we just get every person from a different city. Right? And then all of their friends can help. Who's in Venice Beach? Who's around about Malibu? I have a friend here. I have a very concerned surfing. Well, the surfing was last year. They probably won't do that. OK, gotcha. So this is, OK, this is the old bus. Yeah, so previous, I don't know if they have previous year's things up. But yeah, just the whole idea behind it is just really, I think, really cool. Yeah, anyway. Yeah, I'm down. When does it start? I think it's interesting. So registration closes. When does registration close? Why don't you tell me when registration closes? I don't know when registration closes. When does registration close? You said that the winning team gets a trip to Iceland. Live in Iceland, right? Wouldn't that be fun? So how do they determine the winners based on the quality of the missions or just who gets the most? It could be the most. Most points. We'll just think of it logically. Different items are worth different amounts of points, and then it's a points-based thing. But then if there's a tie, it might come in quality. Right. OK, we could do this. Why doesn't it tell me when I have to register? Tell me what it's called again. Gishwas. G-I-S-H-W-H-E-S. Found it. Oh, you know who's down in LA? Tom Merritt. I'm going to get Tom Merritt to play this with me. Come on. Yeah, I think that would be a great, fantastic resource. Right. Oh, that would be good. Scott down there, too. Yes, Scott Lewis. Keep it down, I'm sure. He would be so into this. Yes. All right, so let's round up the posse. Oh, it starts July 30th. We've got to get on this. It's only seven days. It's only a week. Yeah, so it's basically like they give you a giant list, and then we divvy up the list. And different people have to do different things, but you have a week to get it done. And then you have to take nice pictures of what you find or what you do. And then you send them in. I don't know. I think it would be a lot of fun. There it is. Thank you, April 30th to register. Wait, what? Wait, wait. Oh, crap. That's Saturday. Wait, no. That's Tranks. Podcast Awards. Podcast Awards. What? Oh. It's another thing we have to remember. We've got three days to enter. I better do that. OK. Thank you, Tranks. Thanks, Tranks. Thank you very much. I was going to miss it again. These are things I miss. Things that are not on my radar at all. All I'm doing is I'm doing my show. And then there's all these fluffy, fluffy bits out there. And I'm like, I'm not paying attention to fluffy, fluffy bits. I just want to do my show. Yeah, fluffy. Fluffy, fluffy bits. OK, so I will register. I put it. I have opened that window. And I will register, right? Host $10 registration fee. That's not bad. Let's see. What else was I going to talk about that was really interesting to me this week? Oh, oh, oh, oh. OK. Question for the community, because I think it would be, where did he get, where'd that email go? I got a lot of emails this week. Put a start. Start emails. That's where I put things. Nicolay, Nicolay. Nicolay said he's a longtime twist listener. And he tells people about our podcast when he thinks that somebody might be interested. He has a couple of kids in third and first grades. And he's very excited to get them interested in science. But he has a company that he's starting called Womper, W-M-P-R dot C-O, WomperCo. And he's offered to help spread the word about the podcast. And it goes through, it's through Facebook. And I'm not exactly clear on how it works. But he says that we do some kind of like a survey or a campaign that can have like a question we want to ask. And then we ask a question. It allows people to put a comment. And then when they submit their survey, the ratings and the comment are posted on their Facebook wall. And so people have to allow the service to post on their Facebook wall. Womper stands for Word of Mouth Promotions and Rewards. Ooh, nice. Yeah, so it's basically using Facebook as and people's Facebook friend networks to spread the word about stuff. And not really like as an advertisement. But I'm just wondering. So yeah, he's offered to let us use his service. And I don't know if our listeners would be down for that. Oh yeah, you guys need to nominate us for the podcast awards. Oh yeah, I can register. We need to be nominated. Yeah, anyway, I don't know if people are. I just worry that if we were to sign up for it, my only concern is that it might be something easy for us to use as twists. But then are people going to be annoyed by the Facebook aspect of it? Or is that just not a real, people will be fine with it? I don't know. That's what I wonder. I don't think that if we tried to introduce advertising to television, anyone would go for that. It would interrupt the program that they're watching. I think that's where the media is now. And it's what it is. There's room. I think it's OK. All right, I'll email him back. And I will say, sure, let's go for it. Yeah, Strength Swamper does sound like a scam. You're probably right. But Facebook sounded like a scam initially, too. And it still may be. It still may be. Don't get me wrong. But that doesn't mean it's not useful. Yeah, I mean, it can't hurt to try. Yeah, I can try, see if people use it, see if it, yeah. A lot of people, a lot of identity and strengths are saying they don't use the Facebook. But if other people do answer the question, then maybe it'll be like, hey, maybe it'll perpetuate the love of twists around and about. Yeah, yeah, OK. We'll see. We will see. Yep. Yeah. Anyway, it's someone who listens to twists and wants to help us out. So that's cool. It's very cool. And then I'll get a Whamper shirt. Yeah, then you can have a Whamper shirt, too. I could not find a Jackson Lab shirt anywhere. No? I just want some. This is Jax, J-A-X with a big lab mouse. That'd be perfect. Well, I could draw you that. Yes, you could. We could put it up on our Zazzle. Zazzle, Zazzle. Yep. Zazzlego, Zazzlego. What is it called again? You just got a website. You got a website. The link is at your www.twist.org. That's T-W-I-S dot O-R-G. And you look for a giant button that says Shrag. I don't think I'm installing a Whomp server. No. No. No. W-O-N-P-R. No. Whamper, which I kind of like saying. Whamper. Whamper. Whamper. Whamper, whamper, whamper. It's like that sound that your computer makes when you click somewhere that you can't click. Whamper. Oh, it makes me think of drum and bass dance music. Whamper, whamper, whamper. Whamper, whamper, whamper. Whamper, whamper, whamper. Whamper, whamper, whamper. Whamper, whamper, whamper. So we didn't know I had these talents. Hang on. I did not know. Maybe that's not us. But maybe that's adjustable. We might have to go into our Zazzle store. For some reason, our banner behind us is like art supplies. Probably because I haven't put in a banner. Yeah. I probably just put some random thing in there. Probably. It's art supplies. I'm sure that I uploaded our picture. Oh, I need that hat again. I don't have my hat. Oh, there's a grocery tote. And it's a canvas looking. Yeah. Twist grocery, canvas bag. Oh, my goodness, I'm going to spend a fortune on this. Look at this. Wow. Yeah, you can get a tie with a TX on it. That would be really awesome. Oh, wait. No, I don't see it. There's six pages of things. Shooting Whamperats. Oh, when does registration end? Misha hasn't decided yet, but it will be after the summer solstice. OK, so registration will end after June 21st. So we still have some time to think about it. Everybody go home and think about it and see whether or not they could have the time and the energy to be involved in something like this. Yeah, I'll talk to Scott Lewis and see if he's interested. I think it would be really fun. I think we need to re-upload the Blair's Animal Corner Mouth Rats shirt. Why? There's a few things that are aligned funny, but we just we need to rotate some things and it's not a big deal. If you want to give me log in info, I can tool with it too. Yep. OK, I will do that. I'll be happy to do that and I can upload some edited ones or something else too. That would be good because that kind of stuff is the kind of stuff. I'm like, I really don't want to be spending my time doing this. Yeah, I'm happy to do that if you want to send me that stuff. I can work on that on my weekend. OK, so let's see. This week in science, cooking apron. Right, don't you want an apron? I do, I would be so proud. You want an apron. Let's see. I love the ceramic ornament, the T-Rex ornament. That's pretty cool. Twist editing, KDBS, and then we've got Zazzle. Some of the stickers, yeah, there's a lot of off. Yeah. Yeah, easily fixed. It just takes time. And so I can take some of that. OK. Let's see, oh, podcast awards, registration. How come I didn't see the T-Rex tie somewhere in all of this? Let's see, I see the, uh. It's in there. Twist YouTube. Description, I'm writing my list of things to do tomorrow. Oh yeah, I'm only showing 60 a page. There's apparently 344 items hanging on, oh gosh. Rough edit of that video. OK, yeah. Yeah, as you can tell, I just clicked all. That's fine. I can edit some things. I was like, let's just get something in there, like everything, oh, oh. Yeah, it's like the mouse has this black border area behind it that's funky up all the time. Yep, I'll edit it. Yeah, so I had originally sent Kiki the three animals, or four maybe, in different backgrounds, different sizes, so that we could see what we liked basically and what fit on the items. So now that we know that, I can pick the appropriate version of each of those things for the right item. But yeah, it's going to take time. And I'm going to have to rotate and resize and all this kind of stuff. Get on it, start tonight, and I can purchase something. What? Nope, this weekend. Yeah. It's more of a weekend project with a laptop, and you're having a beer. Exactly. There's the T-Rex tie, I see it now. Yeah, the T-Rex tie is good. Work through the night, says Saldiash. No. Yeah. It's a style tie. It's tempting. A romper, that would be good. It would be good to have a romper in the Zazzle store. Oh, yeah. Ooh. This is interesting. Strengths found an article. The Scientology leader's father is releasing a memoir next week, and they're threatening to sue him. Ooh, he's a squirrel. What is his memoir, tell? He's acting like a squirrel. I don't understand squirrel. That's what Scientologists call people who rat out things about Scientology. They call them squirrels. Some of this is also outdated. It's like, get your iPhone 4 case. Yeah, but if you click on that, there's a drop down, and you can pick your iPhone 6 case. That's how I got this. You need to get it sized right. Wait, let me see. Oh, wait, see, yours fits on there, and the other one's on here don't. Yeah, because I edited it separately. I did this separately. Yeah, you uploaded the picture yourself, right? Yes, exactly. Yes. Identity 4 still has an iPhone 4. Yeah, you can get your case at Zazzle, apparently, Identity 4. OK, of course, I already have my iPhone. Oh, nice. Yeah, T-Rex fights. This is a good one. Doctor Who box. Well, there was that episode where Doctor Who's box got jammed in a T-Rex's throat, right? Yeah, he spit it right out. Whoa, whoa. That's what they sounded like, right? Sure, not. I think they sounded like if you take a chicken fucking bark, bark, bark, and then slow it down. Mixed with a lion, too, I think. Maybe what we should do is take a chicken bark and slow it way down. I did. I did that for an episode of Jack's Feedback, actually. Oh. I think that sounded like perfect. Nice, very nice. All right, let's get out of here. All right, goodnight, everybody. Minions, see y'all next week. And some of you, perhaps, tomorrow night. Hopefully, we'll make it. Yes, head on over to the Minion Hangout, Twist Minion Hangout, tomorrow, Thursday. Is it at 7 PM, 8 PM? I think it starts about 9 PM Pacific time. 9 PM Pacific. It's a late night show. Oh, OK. And we'll be back next week. In the meantime, if you have any ideas or thoughts on these things that we've talked about, get in touch. Let us know what you think. Yeah, and if you look at a zazzle thing in the store that's broken, let Blair know about it. Yes. But please don't until Sunday. All right. And I'm going to work on Sunday. Sunday. And Ed says an 11 to 12 PM Eastern time start, which would be about 8 to 9 PM start time. So it's the scienceisland.org Science Island chat, if you head on over there. You guys, thank you so much for sticking around for the whole show. It was wonderful to see you in the chat room again and to know that you were here with us. We will see you next week or sooner.