 This is TWIS, this week in Science episode number 582 recorded on Wednesday, August 31st, 2016. Hitchhiker's Guide to the Genome. Hey everyone, I'm Dr. Kiki and I'm here with the TWIS team once again to fill your heads with a signal, breezy whiskers, and someone else's genome, but first. Disclaimer, disclaimer, disclaimer. The wonderful thing about being alive is that it's happening now. Yes, yes, yes, it's that great, great Gramps and Nana. They had lovely lives, but no matter how you look at it, they are long since departed, and even that which passed through the belly of the worm has long turned to dust, but not you. Oh no, you are alive now in the moment in which you can do. And what wonderful, life-living things you can do. It almost doesn't matter what you're doing. Being alive is an amazing thing all by itself. Certainly we can rate quality of life, good, better, best days, versus the occasional worst day ever. But always remember to step outside of your day-to-day, push, pull ups and downs and focus, even if just for a few fleeting moments on the wonder it is to be alive here and in the now. And while every moment may not be as incredible as the one that passed before, having another moment with which to do something is always the best place to be. And what better way to spend the next moments of your incredible existence than with This Week in Science, coming up next. 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? Science to you Kiki and Blair. Hey Carl, we have a guest. Carl, welcome. Hello. Welcome everyone once again to another episode of This Week in Science. Tonight we have tons of news yet again. It happens every week. A week full of science. We sift through it and bring it to you. I have new stories tonight about solar system objects, a toxo cancer treatment and an interview, right Justin? You're going to love this story and we all have an interview with science writer, Carl Zimmer. Justin, what did you bring for the show? Oh, what do I have? Let's see, I have got blood thirsty brains, monkeys with human guts, the oldest living European and the oldest dead earthling ever. Nice, that's quite a range there. And Blair, what did you bring for the animal corner? Oh, I have so much alliteration. Are you ready for this? I have wind seeking whiskers. I have counting cuttlefish and I have morphing marsupials. I think is my favorite of the alliterations there. I also like marsupials. Go figure. So tonight starting out the show, we are going to jump directly into our interview with Carl Zimmer who is a science writer of a multitude of books and articles with a history. He has a history of digging into interesting subjects like parasites, evolution and most recently his own genome. His own genes. Working with Stat News, he has released a series episodically about his investigations into the human genome. And the star of this series is his own genome as it's potent, prodded, digitized and analyzed to tell Carl who he really is and why. Welcome to the show Carl. You prepared to get those answers. Yeah. I have to go dig them up. I'm sure they're around here somewhere. So heading into this whole story that you dug into your own personal genome and you've been covering genomes and genomic science for years. What is it that finally inspired you to get your genome sequenced and then go to scientists and say, hey, help me read this? It just sort of came up. I got this chance to go to a meeting where this was an option. It was a meeting about genomes and they said for this extra charge, we'll sequence your genome and interpret it for you. And I thought, oh, it's interesting, although I didn't want them to just interpret it for me. I wanted to get that raw data myself and then try to dig deeper with the help of scientists. So I went to the meeting, got my genome sequenced, and then it was off to the races. And so in the beginning of your story for Stat News, you talk a little bit about the difference between what the initial company did where they said, okay, we'll sequence it for you and we'll analyze it for you and we'll give you that analysis. And then you went to get the actual sequence itself. And can you talk a little bit about what the difference is between what the company gave you and then what you really wanted? Well, a company can sequence your DNA and they can put it together, interpret the difference, try to look for things that you might be concerned about, a mutation that causes disease or something like that, and then they can give you a report. They can say, well, this is what it's about. Or they could give you a little computer file where they store lots of the little variants that you have here and there sprinkled in your genome. So you don't really have your genome. And that actually requires you to literally just get a hard drive with all the raw data that actually comes off of those machines. When they sequence your genome, it's not like it just comes spilling out in perfect text. Basically, they just shoot out billions of fragments and then try to figure out how to put them together and fix mistakes and all the rest of it. And so that's what I wanted. I wanted to start there. And so that took a few extra steps and actually a few months to really get my hands on it. And so let me just put it like in a perspective of, because I've done the NAT Geo1, I've done the 23 in me. And yeah, so they're giving me comparables to other people who are in the group who have also done this. It's mostly ancestry and they're not going into too much depth of health or anything like that. But they may not have done my entire genome. They may have only looked for specific regions or specific things that they were interested in looking at and comparing to everything else. So I don't even know that they have my entire genome on file with these. So what you did was though, you skipped that thing that said, ah, don't tell me the categories that you want to look at that you've already got answers for or figured out some sort of correlation to, give me everything, let me take it to experts in different fields of science and have them drill down specifically on stuff that I'm interested or just stuff that they happen to be working on. Yeah, that's right. You know, so if you go to a company like 23 in me, they're going to use special kinds of sequencing where they're able to zero in on certain parts of the genome that are going to tell them a lot. So they might want to tell you about your ancestry. So there are certain little variants that differ a lot between people from place to place and they can give you clues about where your ancestors came from. But all told, they're probably only giving you information based on maybe a tenth of one percent of your genome, something along that order. So it's not, so you don't have your genome, they haven't sequenced your genome. They have basically done a really good informative scan of your DNA and they've learned some things about you. And that's kind of how genetics was going until recently, but you know, we're starting to step up to a point where you can get the whole thing. And it took me some finagling to get my hands on this, and you know. They don't normally give it to you. No, they won't give it to you. In the hands of most people, this is absolutely useless information. This is a huge amount of useless data that they're going to mine with some specific interest. But they're not used to somebody saying, just, I just want the raw data of all of it and then I'll figure out what to do with it. Nobody else is doing this, is coming to them with this. Yeah, it's a real gray zone because, you know, the company that did this particular sequencing, it's Illumina, they're the big company with the big DNA sequencers. And they're doing these meetings basically as a way to sort of get people on board about genome sequencing because that's their business. I totally, I see that for what it is, that's fine. But in order to sequence people's genomes, they are being very careful making just a medical test. So you actually have to get a doctor to sign for it. It's a medical test. And you know, like you don't actually, it's actually hard for you to get hold of your own medical test. They're all these legal issues. And 23Me got into a lot of hot water with the FDA by using the genome to basically return a whole lot of extra medical information and the FDA told them to stop. So people like Illumina are being super careful. And so, you know, so the genome sequence, like they would not just give it to me. I mean, I actually had to go through a very kind of strange roundabout way to get it. I mean, basically a scientist who was helping me out said, OK, what I can do for you is I can enroll you in a study that's looking at what happens when people get their genome sequenced. And, you know, we'll get you, we'll have a special little, you know, extra part of it that says that you're going to get your whole genome and we'll see what happens. So I guess I'm like a guinea pig or something, you know, I mean, I was, that's how I was able to get this, this, all this raw data was through this, this, this, basically this trick. But I think this is going to change in the future. I think more people are going to be getting their hands on all that, you know, 3.2 billion base pairs of information. How many terabytes? And you said it was a hard drive. So, like, how big was your, so my, so, so, I mean, you know, so that's it. And it's, I believe it's, I believe all told it's like 70 gigabytes, which is, which is a lot more that you might think than what you need to record 3 billion or so base pairs. I mean, that's a lot more bytes. And the reason for that is that actually it's, it's like over a billion fragments of DNA, each about 300 bases long. And that's what comes off the machine. So these machines read your DNA, they spit out the sequence of all these short fragments, what are called reads, and then it's this colossal jigsaw puzzle challenge to put them all together to figure out, well, what is your genome actually. And so it was this raw data that they would then take to experts at places like Harvard or Cornell and say, you want to play a jigsaw puzzle? That's amazing. And so do they, I mean, when they go to play at the jigsaw puzzle, do they have just computer algorithms or is it also that their algorithms go this matches with this tendency of genes to be located in this, on this chromosome and this span of nucleotides looks like this gene, so we'll put it over here. Yeah, I mean, that was, that was actually was, you know, one of the most fun, you know, kind of nerdy parts of this was just like, like how do these people, this is what's called bioinformatics where basically you're taking the information of biology and trying to make sense of it. How do you figure this out? And how do you do this in a reasonable amount of time? If they were to take each one of those 300 bases and kind of glide along like an existing genome sequence to try to find a location where it matched, it would have taken years, maybe centuries, who knows, it would have taken just a colossal amount of time. But there are all these like really mathematical shortcuts they can use to basically zero in really quickly and just drop them into place in a reasonable amount of time. But then they, you know, there are mistakes that get into this, you know, the chemistry goes wrong here and there. So they then have to do other tricks to figure out, well, where are the mistakes? What can we trust as being accurate? What's not accurate? Can we figure out what something really is, even if there is a mistake there? And it's this amazing, amazing sort of cryptography that they do to then give you your genome sequence and it's not perfect. That's something that people have to remember is like, you know, if you take it to two different people, the same hard drive to two different people, they'll give you two different genome sequences. They'll mostly be similar, but there'll be some big differences. And you know, if those differences just so happen to be like in a gene that's involved, I don't know, like in cancer, you know, that's going to be a serious concern. So those are some of the issues why it's actually not so easy to get your hand on the raw data of your genome. Yeah, it's a little bit of knowledge or if the knowledge isn't actually as accurate as we hope for it to be. So someone in the chat room is asking about the cost of genome analysis and how an entire genome, I mean it took, what, 13 years for the human genome project to complete and it was a massively expensive multi-institutional project. Now we're down to institutions like Illumina that have machines that can sequence very rapidly. What is the cost and how did the technology change to, did you find out anything about how the technology changed to allow it to become cheaper? Well, part of the solution is to sequence DNA in this fashion where you basically smash it up into tiny little pieces, make lots of copies of them and then sequence them all really fast. It's a relatively cheap chemistry to do that. The shotgun analysis, right? It's certainly building on that. And so then what you then need to do is you need to put it all back together and you need to do it quickly. And so because we have these powerful computers and these great algorithms to assemble these genomes back together, you can afford to use this kind of cheap method. And there are other methods that might actually be even cheaper and even more accurate coming down the pike. But just everything is just in the whole field is just crashing economically. It's crashing much faster than in the computer world. Moore's Law is really famous, how you get this doubling of computer power and so on. Forget about it. DNA just blows past that. And so we're getting, so Illumina Charge, it was like $2,800 I believe to sequence my genome. But now there are companies that have come on board just recently that are promising $1,000 or less. And then it's probably going to get down, I don't see why it won't get down to say $500 pretty soon. It's getting way cheaper than like an MRI or something like that. And it's your whole genome. But again, now you've got it, what do you do with it? Right? So you've got this raw data that in the hands of anybody else is utterly useless. Where did you take it? What questions did you try to pursue with it or how did you go about finding a direction to even start this drill down? Well there are people who I've met reporting on genomics, people who are really ready to engage the public about what their work is like and what the implications are and so on. People who are game for just having some fun. And so I kind of had my mental list of these people and I just started getting in touch with them and saying like guess what, I've got my genome. You want to play? And it was amazing. People just jumped in left and right because they just thought well this is interesting because these are people who analyze thousands of genomes at once all the time but they never actually meet somebody on the other end of one of those genomes. And so I was handing them my genome and saying okay, help me make sense of this. And so I had a couple places where the whole lab just jumped into it and sort of broke up the job into different parts. And then they went off and did their computing for like a week. Basically their computer is just humming away for like a week or two and then they would say okay we're ready, you can come back and we can talk about what we found. So there was a lot of enthusiasm I think because the scientists are realizing that what they're doing is going to really connect with the public very quickly and they want to figure out how to talk about all these issues. Right. And you're a science journalist too. So I mean part of this of course is that most of the work that they're doing, nobody's really hearing about it. And so here's somebody who they know they can show what they can do to and who's going to illuminate the rest of the world. Well, I mean one example was, I mean just one really straight forward example is that there's a scientist named Adam Seeple who's at Cold Spring Harbor Labs and I had written about some of his research last year for the New York Times. He has developed new ways to detect Neanderthal DNA in living people's genomes. And it's a very sensitive method and it can actually find parts that other people may miss. So I got back in touch with him and said like hey, would you mind looking in my genome for, is that Neanderthal DNA? I want to see you do what you do on my own genome. And so instead of just going to 23andMe and finding out oh you're 2% Neanderthal, whatever, I want a list. I want a list of the genes. I want to know like how, you know, where, I want to see where my Neanderthal DNA is in my genome. And he said yeah, that sounds like fun, let's do it. That's great. So more than just the 2.2, what is it? There's just, not everyone, but a large portion of people, yeah, have that 2.3% Neanderthal. I claim Neanderthal very strongly. You know, everybody outside of Africa has probably, you know, roughly 2% Neanderthal DNA. The range kind of shifts around based on, you know, the latest research. But you know, maybe 1.5 to 2.5%, you know, I've seen numbers like that. I, Cepo said to me like well, it's at least 2%, it could be more. But really it's... It's an important DNA from Neanderthals to really, you know, let's even, yeah. Yeah, because you know, how many times did our ancestors have sex with Neanderthals? That's a big question. It's definitely more than once. It could be the latest research I saw, I was going over. It's at least four times that humans, no, five, I'll take that back. There are five times at least that they can pinpoint and say like, yeah, here's one, here's one, here's one, here's one. There are probably a lot more. And yeah, when we look at more Neanderthal DNA, we may be able to match more of those interbreedings. And in the article, big surprise to you, not just Neanderthal, but Denisovan. Yeah. Wow. That's exotic. That's exotic? Yeah. So Denisovans, I should explain, Denisovans are this extinct kind of human, probably kind of like Neanderthals. But they were discovered when about around 2010, scientists had found this pinkie bone in a cave in Siberia. There was like a whole lot of Neanderthal and human bones mixed in there over thousands of years. So they find this pinkie bone and they can't tell what it is and it turns out it's packed with DNA. And they're like, oh, great. And they're expecting, well, maybe we'll get a human genome or a Neanderthal genome. Whoa. Like it's neither. It's something else, something else. And really that's, I mean, aside from a couple molars, this is all we got. So it's very weird. We don't really kind of know. You can't look at a Denisovan skeleton. You can just look at the whole genome. And they seem to have interbred with people in New Guinea, in Australia, in parts of the Pacific have several percent Denisovan DNA in them. Europeans don't. And our first evidence of this isn't Siberia, too, right? So this is also telling a huge story of a group we didn't know existed, spread out over a very large area. Right. So if you've got Siberia there, so you know Denisovans were there, and it looks like they must have interbred down in Southeast Asia, you're kind of looking at all of East Asia maybe with Denisovan territory, which is incredible. We really need to go find some Denisovan fossils because apparently they were everywhere for tens of thousands of years. And they probably had a massive influence on humans. And there was probably a lot of gene flow even though they faded out, their subspecies faded out. Yeah. Definitely. I mean, we have lost pieces of that Denisovan DNA and the Neanderthal DNA. We have fragments left over. And you know, in some cases we got rid of them because they were just kind of toxic. You know, it wasn't really, we were less likely to survive and have kids with this other kind of DNA in our genome. On the other hand, it looks as if some Denisovan and Neanderthal genes are actually pretty good to have. You know, they may help you fight more diseases, for example. Yeah. And then there's the other idea that there are some that might negatively, Neanderthal genes, not necessarily Denisovan, but the Neanderthal genes might negatively influence the immune system and lead to autoimmune disorders. That's one hypothesis that's been lofted out there. Did that come up in your conversation at all? Yeah, yeah. I mean, these sort of, yeah, these kind of medical implications came up when I talked to a scientist at Vanderbilt. So at Vanderbilt they have this amazing set of electronic health records that are linked to the DNA of volunteers, their patients who are part of the Vanderbilt system who have agreed to let doctors study their DNA and their electronic health records. And so you can do incredible things. You can like say like, okay, let's look for all the people in our biobank that have this mutation and let's see if they share some disease at some unusual rate. And you can just discover new links that way. So Tony Capra, the scientist I talked to, he said, hmm, well, let me just look at, see, you know, what kind of Neanderthal variants these patients have. And let's see if they're linked with any diseases. And he found several where it seems like these Neanderthal variants slightly raise your risk of certain diseases. And so I asked him, I said, hey, take a look at mine, what do you see? It turns out that I have one variant that can increase your risk of nosebleeds. Interesting. Do you think you have more nosebleeds than the average person? I haven't been counting. So you know, but like these are small risks. So who knows? Like maybe, you know, in my life I've had, you know, 11 nosebleeds and you've only had 10. You know, it's like you're getting down into kind of subtle signals there, but the hope is that by digging deeper and looking for more of these things, that there really will be some insights into how Neanderthals are affecting our health. Sort of my, so 23Me does all of these surveys and they'll ask you questions like, is your ear lobe attached or detached? Is your nose shaped like this or like that? And so what it's sort of doing is grabbing and trying to find connections between the large swaths of data that can sort of drill down on things. And I'm sort of almost picturing a day where we, we walk into a doctor's office and it's almost like going into a homeopathic medicine doctor today, right? They're like, oh, well I can tell by your ear lobes and the corners of your mouth that you suffer more nosebleeds than most people. Oh my gosh, how do you know, right? Like we might find these other crazy correlations, but what we need is, and for instance, your single, if you were the only genome that we had, the only data we had to work with, it would be completely useless. What we need is more and more people in the system and with as extreme amount of profile data as possible, everything from knowing whether the person has an attached or detached ear lobe, to knowing the shape of the nose, to knowing, you know, a health history, a mental history, all of these things, we need all of that information in there to sort of be able to pinpoint what genes are actually affecting things because a lot of what, if you were to pick out a gene and say, I want to know what that particular gene does, I don't care if it fits in it, I just want to drill down and find out what that does, it may, you know, be a slight increase in eyebrow hair or something, you know, it might be something really that wasn't as exciting as the disease or as a proclivity. Yeah, I mean, interpreting my genome in so far as I can in this series is only possible thanks to all the other people who have been willing to have their DNA looked at, like you said, and there are a lot of things that I can't know about my genome, you know, a lot of variants I have where people just sort of say, I don't know, I mean, could be bad, could be good, I don't know what this means that you have this mutation, I just can't tell you. The hope with these things like the precision medicine initiative that Obama put forward or other programs, there's something called the Million Veteran Program where there are just these huge numbers of people that are going to be brought together and their DNA is going to be sequenced and there's going to be some of this, you know, medical data or what's sometimes called phenotype data that's going to be collected, like what do you like, and then people are going to try to look for links. Now, I will say that, you know, I've definitely talked to people who are doctors who are intensely skeptical that this will lead to anything that's actually going to make a difference in how people's medical care plays out, you know. I mean, if you find things that really just just tell you a little bit about noise or if you discover something that's just too complex to interpret, then we're just going to have to go with regular medicine, unfortunately. And it could turn out that the entire data set is largely useless if we're missing information on the gut bacteria. That could actually be such a bigger influence on health compared to our own gene system that's, you know, or it's a combination of the two and it's going to take getting both completely understood and analyzed to actually see the connection and then be able to make any kind of prognostication or on future health. Well, you know, when you're getting into the microbiome, I mean, then you're talking about, you know, you're talking about DNA. If you add up all the thousands of species inside of us, you're talking about DNA that dwarfs one person's genome. You know, I mean, in your body that you have, I forget the figure. It's like 10 or 100 times more genes in microbes than human genes. I mean, you're just mostly a big catalog of microbial genes. And, yeah, exactly. And what exactly they're all doing and how mine are different than yours and what that really means. Then you get into like just explosive complexity that I don't think we're going to really figure out anytime soon. That could be your next stat series, though. You know, go with the microbiome sequencing and a bigger hard drive. Well, I don't know. I mean, I have gone so far as to get my belly button sequenced. Yes, you did, right. But all I found out there was that I have something like 50 or 55 species of bacteria living in my belly button, some of which are totally new to science or some of which have only been found deep in the Pacific Ocean before. And that's a really interesting question. How did that one get there? Yeah, last time I went swimming, I guess. But, yeah, it's not exactly, you know, news you can use. I mean, like, what does it mean to me to have these particular species? Nobody can tell me and I can't tell readers. So, you know, I mean, all the stuff I find very exciting. But as a journalist, I'm always trying to like balance the excitement with not making people get the impression that this is the, you know, key to immortality and the answer to all our questions and so on and so forth. But you also have to say something. You can't have an article that starts and ends with, it's really complicated. I'll get back to you once it's all figured out. It wouldn't really be following the process. No, and it, I mean, you know, what is nice is that we are in a sort of a cool spot where I can actually go to a bunch of scientists and say, tell me about what you see here. And we can like discover really interesting things. I mean, I can discover genes that I have that actually protect me from diseases instead of making me vulnerable to them. I mean, we tend not to think of beneficial mutations. But we probably all carry a few and I found at least one that I have. So what's your, what is your superpower? So my superpower comes from a gene called IL23B, which makes a protein that sits on top of cells and is involved in the immune system. And because of the mutation that I have, I am protected from certain autoimmune diseases like Crohn's disease or psoriasis or certain other diseases. And so I am less likely just based on this particular mutation to get those diseases. And actually, where this really starts to matter is when scientists can actually look at these mutations in, you know, a mutant like me or like you and say, huh, like, why is it that this mutation in this protein leads to this protection of this disease? And once you start looking at the pathway, then some interesting things happen because then you can say, oh, I get it. It has to do with this signaling chain. And this mutation blocked the chain so that things don't get out of control. So the immune system doesn't kind of get into this feedback loop and just started attacking everything like crazy. And if we can replicate it, we have a treatment. Yeah. And actually like Novartis and other big pharma companies have actually literally done that with this actual mutation in this gene. And you know, these drugs are just coming online now. There's one that's already out and there's one that's probably going to be coming out of trial soon. And they seem to work. They seem to be really helping people with these terrible autoimmune diseases. And it came about by looking at people who had these mutations. And so these mutations, they're basically these single nucleotide polymorphisms or are they, you know, are they other crossover event mutation? What are the events that you're talking about? Well, you know, there are these all these different kinds of mutations, like you said. And so in some cases, like this particular case, it really only took, you know, a mutation of one base like changing one letter in a gene to basically really change how it worked. There are other kinds of mutations though. And these are actually mutations that you can't really see if you just go to like 23m or something like that. But they could be really important. So we have lots of mutations that basically chop out a big chunk of DNA. So it's just gone. You might just like not have a gene. Or you might have a duplicate of a big stretch of DNA. So you might have, you know, a gene that sort of repeats part of itself. Or you might have an entirely new copy of that gene. So instead of walking around with one of these genes, you have two. And so once you start to get into what are these called copy number variations, things get very interesting because there are diseases that are being linked to copy number variation like autism and schizophrenia and some other diseases. So we really do need to understand these. But it turns out to be very hard to see them with the kind of sequencing that we do. You need extra special tricks to see those. And so I got to watch how scientists uncover those kinds of mutations. And in finding out one of the deletion mutations, you're lacking a big chunk of DNA. You're just missing a big chunk of DNA. What's missing? Yeah, it's a 122,000 bases long. It's just gone. It's just not there. I don't have it. And I've been pretty good health. And so obviously, it didn't take down a totally essential gene. But there could have been really useful things in there. But maybe I have like back up somewhere else in the genome so that I could afford to lose that. But I have literally over 700,000 other places where a little bit of my DNA has been cut out or been inserted in or something like that. Hundreds and hundreds of thousands of these little copy number variations. So it's a major part of how my genome is different from other people's genomes. And so we need to sort of understand that in addition to those single letter changes. In looking at the accuracy of this testing and how it's being, right now these companies are working to perfect it and make it something that can be certified by the FDA. And Ed from Connecticut in the chat room is saying that reminded me that there's prenatal testing that's done, DNA testing. I went through it myself. And you have a bit of testing to basically figure out whether and what kind of risk your child has for certain diseases. A lot of it, and then you go through the counseling afterwards. And it's a lot of statistics. And I think parents get really overwhelmed with the system as it is. Do you think that the improved accuracy of the genomic testing itself, the sequencing, the testing, will be able to help parents any more than what we currently have? Well, I mean, if you had gotten a false positive, that would have been a really hard experience. If your doctor had said, well, I'm sorry to tell you, but your child has a mutation for this terrible, terrible disease. So let's make plans about that. And then if you were to discover later on, like, oops, like, whoa, sorry. Actually, your child didn't have this mutation. Or maybe that mutation doesn't matter. Whoops, we didn't realize that. Those things are a big issue, especially as you move away from the really well-studied genes to the genes where we're not totally sure what they do. So yeah, that will have an effect. I mean, I had that experience literally within this process. I sat down with a clinical geneticist and I said, okay, look, I really want you to drill into a lot of genes and just show me, like, how you look for diseases. And we ended up, like, spending time on a gene called DSG2, which has been associated in published studies with a kind of a heart disease where basically your heart just goes into arrhythmia and you just die suddenly. So, but he was being very cool about it and calm. And I was kind of wondering why, because I was freaking out a little, but then he showed... Very cool and calm, bedside manner. Yeah, here's this thing, you know, and this is what it says here, you know, but he's not looking at me like, you know, you need to talk to your wife. He's saying, like, okay, now let me show you something else. And what he did was he actually went into a database called EXAC, which didn't even exist until a couple years ago. And he said, you know, it's got 60,000 people in it with all these different variants in there. And he said, guess what? Look, there are a surprising number of people with your mutation. And, you know, if... This is a very rare condition and, you know, like, it doesn't line up. I don't think that this actually matters. I don't... And looking at other evidence as well, he came to the conclusion that these reports, these published scientific reports, were wrong. And he was saying, like, don't worry about it. And that's kind of where the genetic literature, genetic science is at right now. So, you know, if we start flooding the zone with all our genomes with all of these ambiguous variants, this is going to be a big headache. And I don't think we're quite ready for that. From your story on STAT, what do you hope that you get that the readers... I mean, this is a big complicated... Everything that you're telling us, you know, there's your personal experience. And then there's also the overarching reality that this is really complex. But what is it that you hope that readers will take away with them? I hope that when they think about their genome, they don't just think about something that's going to make them terribly sick. When I was, like, getting... When I was sort of preparing for this, there were a lot of people saying, oh my God, oh, I can't believe you're doing this. You're going to find out something terrible. And, you know, I think I've gotten to this point in life where, you know, I have a heart attack, my doctor says I'm in decent shape. So, like, I don't think that's true. And I think that even, you know, when I got the report saying you don't have any mutations that we're really worried about, I didn't want to stop there. Because, like, genomes are not boring. They're just not. They're these amazing things that we all carry around with us, you know, these billions of letters, essentially, that make us who help to make us who we are, that we've inherited from, you know, billions of years of ancestors. So, and there's a lot too there. And we do know enough about genomes that you can dive in and learn something about it. The tools may not be available yet for everybody, but it's a really exciting time. And I wanted to convey the excitement, you know, of my own discovery, but also the excitement that these scientists are having at learning new things about all of our genomes. I think it is very exciting. And it's a really, really great series. I've read through it, and it's a great storytelling as you do. So, thank you so much for writing it. And if anybody wants to find this article, it's located on statnewsstatnews.com, and it's a feature called Game of Genomes, a story in three parts. It's fantastic. Carl, is there any other places people can find you or find out more information about this particular article series? Well, in addition to stat, if you go to Game of Genomes, the page for the series, there's also a link there to actually to all the raw data and analysis. We just decided just to think if you scroll all the way down on that page, you'll find it. So, Mark Gerstein at Yale, he and his colleagues just generated a ton of data, and they were like, well, we don't want to just throw this out. And I was like, great. So, they and others are actually using this data as part of their course where they teach bioinformatics. We put my genome up there. I've looked at it, so there's nothing too horrific in there that I know of. If anybody finds anything, please let me know. Just be an ongoing experiment then, right? You can be cloned. You're not just a science communicator to the general public now. You're now a tool of science to educate future scientists. That's quite a bridge to a travel there. Well, I have all this data. I'm a journalist, and so when I have data, I don't want to sit on it. And so this seems like the ultimate open access. But in addition to the raw data, everybody's analysis is in there too. And that's interesting if you really want to drill down and say, okay, well, how did they figure out what my ancestry was? How did they work out exactly what my Neanderthal genes were? And so some of the scientists have said, okay, here you go. Here are my slides, here are my spreadsheets. Here's an explanation for what I did. You know, it's technical. It's not, you know, it doesn't have, you know, friendly science writing, but it's interesting. And for the people who really want more, there it is. Awesome. That's great. And I'm sure there are a lot of people out there who are really interested in this sort of thing. So how fantastic. Thank you so much for joining us tonight to share your story. And I hope more people read your, read your articles and peruse your supplementary data. Like genome reading before bed. That's right. That's right. Scan through a few genes before turning in. Yeah. Yeah. But if anyone finds something strange or mysterious or if anybody clones me, just, you know, shoot me an email. Let me know. So I know, I know when the door, I hear the doorbell that who's coming. Yeah. We'll have Carl's clone on the show next year. I don't know. The clone will be, the clone will be too young, very likely to be on the show next year. That is the result of that, that research he was guinea pig in. It found that 100% of people who received their whole genome become really successful scientists. If there's ever a shortage, we know where to turn to. Well, all you need to do is zero in on, you know, the gene for, you know, fast typing or whatever. And then I'm sure you can, you can assemble a journalist that way. My DNA is where it's remembering where you placed your keys and people's names. There you go. Thank you so much, Carl. Hey, thank you. Thanks for having me. It was really great to have you on the show again and to see you again. Have a wonderful night. All right. Thanks a lot. Take care. You too. Thank you. Bye. And that was the famed, the wonderful Carl Zimmer who has given his genome to science. And we brought him on the first half of the show so that we wouldn't keep him as late as it is now. Exactly. Which means he got out of here no earlier, but we got a lot more Carl out of it. So good deal all the way around. But now we're at the break. This is only the halfway point in the show. There's more show to come. We've got science stories ready to go in the second half. So join us, won't you, after this brief series of music or messages? I'm not really sure what happens in the break. You wouldn't know. This is This Week in Science. I'm going to give a few messages and then we'll be right back. More stories to come. Hey, everyone. I just want to say thank you for listening to Twist. Thank you for being a part of our twist journey, the week after week adventure that we take into the world of science and which is really the world around us. This Week in Science is supported by listeners like you in multiple ways. One way is through merchandise sales and you can find our merchandise if you head over to twist.org. Twist.org has a link where you will be able to find our zazzle store and our zazzle store. The link is in the main header bar. You can head over to the zazzle store. You'll be able to find all of our products, mugs, aprons, tote bags, hats, you know, necklaces, and it's all the twist swag. Twist logos and also artwork originally drawn by Blair for our Patreon sponsors but included in our 2016 Blair's Animal Corner Calendar. Blair is sporting a wonderful T-Rex cell phone cover. 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If you can help us out by giving a review on iTunes, telling your friends about twists, posting us our show on social media, just getting out there, helping us to get more YouTube subscribers, helping us to get more subscribers to the podcast, this is how it really ends up helping in the end. I would like to give a big thanks to people who are helping us right now, Brandon who is helping us to live stream this webcast to Facebook, to Fada who is helping out with some of our social media work and to Identity Four who records our audio every week. Thank you to these people for helping us out in these very important ways. This is a big, big deal. No matter which way you choose to support us, we thank you for your support. We really could not do this without you. And we're back with more This Week in Science. What you got Kiki? I have aliens? No, I don't have aliens. We don't have aliens, but we do have an interesting signal, that's for sure. People have been talking about a signal that was recorded by a Russian team but has been looked at now as being checked out by SETI. A star system 94 light years away is the point of origin we think for this signal. However, it could be a random terrestrial signal from our own planet that we haven't even figured out what it is yet. It could be something from a satellite. Or it could be from right here at home. It could be. So it's an amazing signal that it's a very striking signal. It's coming from the direction of HD 164595. And the astronomers were able to find this signal by using a radio telescope near the Caucasus Mountains. The radio telescope is called the Ratan 600. It's a ring that has a diameter of 577 meters that has a beam shape. So there's a beam shaped patch of sky that it is very sensitive to. And then it reported the signal at 2.7 centimeters equivalent to 11 gigahertz. This beam is about 20 arc seconds by 2 arc minutes. So it's a patch. It's elongated in the north-south direction according to Seth Shostak from SETI. So the patch where the signal seems to be coming from is in the narrow part of the beam based on HD 164695's coordinates. And so that's why people are assuming it's coming from that star system but they don't really know that for sure. So it was a weak signal because of the distance possibly. But it could also be weak because of dilution with other signals. Because the Russians were using a very wide bandwidth receiver. Could be. So we're talking a signal though. Talking a signal and they have no idea. And at this point the Russians are saying that it was probably a terrestrial signal. And so reported today by SETI they're saying that the Russian news agency is suggesting that the radio telescope found terrestrial interference. And so the Russians are saying the director of the Institute of Applied Astronomy at the Russian Academy of Sciences Alexander Epatov told the Russian news agency TASS that back at the Soviet period he had been part of a group of young astronomers at the special astrophysical observatory searching for signals from extraterrestrial civilizations. We indeed discovered an unusual signal. However an additional check showed that it was emanating from a Soviet military satellite which had not been entered into any of the catalogs of celestial bodies. Because it's secret. Right. And so as noted in the accompanying write up according to SETI we have been unable to find this signal using our allen telescope array. That would be consistent of course with it being terrestrial interference such as a military satellite. And what a bummer to find like a secret satellite. You're like look we found a signal and then it's well you know part of it there's you know if it were a secret satellite I mean the Soviet Union if it was a Soviet military satellite the Soviet Union is long gone and this signal was measured in May 2015. So yeah but I mean I'm talking about the first one but yeah this signal but there could still be secrets. Yeah so the the take-home message of all of this is that there is a signal that the Russians detected we don't know what it is yet. It's very likely not aliens but we don't know what it is. Not aliens yeah but the big thing is don't jump to conclusions because honestly we don't have the data out the allen telescope array has not been able to confirm this signal and oh they don't know what it is. They don't know. No clue. There we go. There we go. Not aliens. And then in another very interesting very interesting story this week researchers we've talked before about Carnegie Institute Scott Shepard and Chadwick Trujillo from Northern Arizona University who are looking for Planet X and looking for the evidence of gravitational forces on extreme trans-Neptunian objects. So basically objects outside the orbit of Neptune and how are they affected by very how are they clustered and do they seem to be affected by a large larger than Earth size planet way way out outside of Neptune. And they've been looking into this and so they've been looking for extreme trans-Neptunian objects and they just reported in a paper that's been accepted at the astronomical journal that they have discovered several and they are entering them into the journal they're entering them into the directory of objects that have been discovered in our solar system and they say they've found an object they have one that is they've submitted to the Minor Planet Center for designation called 2014 SR 349 and it has orbital characteristics to the previously known extreme bodies whose positions and movements initially led this duo to propose the influence of Planet X. So kind of matching orbital dynamics which is cool. Another object 2013 FT28 has other characteristics that are similar to the other extreme objects they found but they have one of its parameters an angle of the longitude of perihelion perihelion is different from the others so they're looking at clustering and how all of these eccentricity inclination perihelion all these things match up in these trans-Neptunian objects to kind of determine what's out there they have they've discovered a distant Oort cloud object 2014 FE 72 and it's got an orbit entirely beyond Neptune it's so far away from the sun that it they think it's probably being influenced by forces of gravity from beyond our solar system like other stars and the galactic tide i didn't know there was a galactic tide but i knew about the galactic wind yeah i didn't know that the tide went along with it but i guess you know wind affects tide so there should yeah it's two it's like there was something else i was reading about if there is a big ninth planet that's doing one of these like super far orbits it might mess up our predictions for what will happen when the sun collapses and that it may actually draw in some of these these super long orbiting planetoids into the inner solar system and they might ping pong or billiard ball about with some of the planets we know and love that would otherwise just sort of be stuck orbiting this collapse collapsed expanded and then collapsed the sun well it's not something we have to worry about right exactly by the time the sun is collapsing i hope we're not around anyway i think one of the oh yes i think i think one of the really interesting things about this story is the researchers themselves are kind of saying this is very similar to that um the period of time during which objects were really just being discovered for for our solar system so similar to mid 19th century says shepherd we're now in a similar situation as when alexis buvard noticed uranus's orbital motion was peculiar and that eventually led to the discovery of neptune so uranus aibs were observing it's very far away and they went oh it's not moving in a track that you would expect based on just normal orbital dynamics and so there's got to be something big out there and so that led them to look for neptune and this is kind of where these guys are and they're they're thinking they're like we've got the inner solar system planets but we don't know anything about what's really far out there like we're looking far far away but you know with a telescope you really see only what you're focused on and so we have to focus on certain parts of the solar system to be able to see them and to be able to determine what's out there and so we're just taking a closer look at that the far reaches of our soul our own solar system right now and it could really help us learn a lot about the dynamics involved in the work cloud and in the asteroid asteroid belt and in you know so many aspects of the planets and why they move the way they do and also you know what are they called now pluto like pluto like bodies I don't remember I don't know what are they called not pluto dwarf planets thank you yeah dwarf planets thanks Justin like that's not pluto anymore it's um the dwarf planets yeah so we're in a very interesting period of discovery right now which is very cool and we will be for all time to come at least yeah yeah all right Justin what you got I have a new study led by University of Minnesota that's showing monkeys in zoos have human guts human gut bacteria anyhow and this is a fantastic finding maybe because it can shed light on one of the most tiresome and interesting questions plaguing modern man how does the modern human diet affect health and should we be eating more fiber so the typical monkey zoo diet doesn't contain cheeseburgers mega slurp sodas are heavily processed foods but captive monkeys do have lower plant fiber diets than free their free monkey counterparts and it's not just that the zookeepers don't feed them these things it's that maybe they just prefer something that's less leafy when they have an option for it yes they're not hungry all the time not starving to death it's just that they would rather eat a banana than chew on leaves because it's more efficient or whatever they're get that I have no idea what monkeys get better it is you Blair do you have any idea what monkeys get better I do yeah what do monkeys get better it depends on the species but there's usually some form of wet primate food that is fortified there is a dry primate biscuit and then a variety of fruits vegetables occasionally insects things of that nature for special treats they might get something like banana or grapes or applesauce lentils pasta and if you're a wild monkey you don't have access to that so what do you do you chew on lots and lots and lots of leaves yeah and as a result have a much higher fiber diet so and in the wild each primate species it says here has its own signature footprint of microbes and captivity however they were found to lose this distinctive microbe set and ended up being dominated by the same bacteria that dominate human guts and so then there's the question well how does this affect monkey health after all you know you they've evolved very well with a microbe that is doing specific things having specific outcomes with the specific diet and now their diet is different their microbes are different how is this going to affect their health and are there correlations to human health as humans have gone away from higher fiber diets and because there's also people who have been claiming or research has been showing that I can see Blair scanning through this story as quickly as she possibly can see what's going on and how does this affect human health is it the western diet affecting our health because it's lower in fiber oh yeah the results to switching from low fiber western diet may have the power to deplete most normal primate got microbes in favor of less diverse set of bacteria is sort of the analysis here this is published in the proceedings of national academy of sciences pna s the research there's studied two different species of highly endangered red shank duak what is how do you say d you are do you see red shank duke monkeys and they also studied the mantled howler monkey the author's in compared the captive primate microbes to the microbiomes of other wild counterparts and those of modern humans living in developed nations and in the united states not only did captive monkeys lose most of their natural wild gut bacteria but they vary consistently and this is across many zoos in different continents they all lost their diverse set in favor of the modern human gut this along with other analysis drop confounding factors like genetics geography antibiotic usage suggested a simple explanation for why captive primate guts look more like human guts on the inside and it was they weren't eating enough plants to test whether partial loss of plant derived dietary fiber result in partial loss of native gut microbes the authors collected fecal scamp samples from a semi captive population of monkeys who lived in the sanctuary they received about half the normal variety of plants eaten by wild monkeys interesting the lee it says these semi captive animals fell right in between those of the wild and the captive monkeys so that they say further supported their hypothesis fibers good yeah i have quite a few things i don't know i won't get to it because i have the same questions wild primates stool contained up to 40 percent plant DNA while captive primate stool contained almost none uh cody voice uh this is knights who's one of the researchers here we think the study underscores the link between fireber rich diets and gut microbe microbiome diversity so the main question i got maybe it's the same one you're leading to uh is this correlative yes the diet changes in zoo settings but so does proximity to a lot of humans and in case where they had semi captive monkeys i presume they had less contact and thus less exposure to humans because we know that we share uh our microbiome with our house cat or dog and that it's sort of as uh jizaya pointed out they sort of move closer together and i don't think you know necessarily like the fiber diet of the cat or the dog is being affected by the amount of plants and fiber that they eat compared to being in the wild so i have uh i would underscore this study thinking gosh there could be another explanation for this yeah there's there's a lot going on here so that's definitely one of the things and um you know primates in zoos and human primates we are primates uh we're very similar which is why for example when i was a primate zookeeper i would have to wear a mask if i had any sort of cold because i could give the monkeys or the monkeys could give me something because we are so similar so the idea that our gut did the monkeys ask when they had a cold yes yeah it's pretty much a little mask on it's adorable um so the fact that they're that i could transfer some microbes to them in the process of preparing the food in the process of them picking through the hair on my head while i'm cleaning their enclosure because we know our microbes are all over us and so being able to parse out the difference between those two things the the diet versus the proximity and then on top of that i'm really curious because even though all zoom monkeys diets are similar they're not the same so just like a human's diet in minnesota is different from a human's diet in california the the resources zoos pull from to feed their animals are different and then on top of that the nutritionist working at that zoo might have a different idea or those specific monkeys might have a high body score and they're trying to make them thinner or monkeys in another zoo might be thinner they're trying to make them thicker and so their diet is going to vary microbiomes human microbiomes differ between individuals also but the what what this is sort of standing is those types of bacteria that dominate humans from minnesota to california also dominate monkeys from california to istanbul you know so it's it's so and i would i would argue that it has nothing to do with with fiber the fiber because i guarantee you there are some zoos where monkeys are eating a pretty strict leaf based diet and there are other zoos where monkeys are less so for example here in san francisco we have such a temperate climate that a bunch of different leaf leafy plants grow all over the zoo year round and so zookeepers can walk around clip down native plants and feed those fresh clippings to the primates and those primates will choose those fresh clippings sometimes over the less fibrous food because it's fresh it's moist it's delicious and they will actually eat it it will eat some comprasma instead of a banana at times now i'll go one layer further in this and then i'll i'll and and and this the sub tangent thing and reference of referencing but the other thing that's sort of interesting about this i mean i i agree with you i think it's proximity all the thousands of humans walking around in the zoo are contributing just by inhaling and exhaling to have a cloud of microbes but it's also sort of interesting in taking into account a higher fiber diet is that this is material that makes it further down the gut further down the chain from stomach to to to leaving right and there's microbes that live further down that track that perhaps uh can can populate better if you have things that weren't digested in the first go round so this is another one of those things and like we were talking to Carl there's a whole more complicated field yeah of understanding what contributes to health be it uh human or well primate or other primate in this case then simply the amount of fiber intake and i think we both had that same reaction yeah well and looking at the monkeys that were in this study now i lost the study already but so the the dukes it looks like you call them are a type of langer those are primarily an herbivore monkey they're they don't eat a lot of things that aren't just plants um and then i lost what the other species was but if they were looking particularly at herbivorous monkeys or predominantly herbivorous monkeys that could be very different than ones that have a higher protein content in their diet already so is is another monkey that has a higher protein content are they going to have the same shift or do they have less of these fiber-based microbes already because they don't eat as much plants so we're both in agreement then this could just be correlative yeah yeah uh could be correlative but they did do a nice uh a nice study design where they fed the animals different differing differing groups of animals differing amounts of fiber and they looked at the resulting microbiome and so it is it's not causal it's definitely not a causal relationship but they have shown that there is there is something interesting about fiber in the diet and that's what ended on it was they had different levels of contact with the ones that got that i mean if it was just that they had changed the diet of captive monkeys but they used they went to the semi captive to show the variation and that's i think the part of the problem i had sorry what you need to do is go out into the wild and just throw a bunch of biscuits and bananas into a group of monkeys and then collect the feces later university of adelaide led project has overturned the theory of human evolution one specific kind of detail of it anyway that the evolution of human intelligence was simply related to the size of the brain there is uh still truth to this to a great extent but what their research showed is that it wasn't so much or just the size of the brain that mattered but the supply of blood to that brain international collaboration between australia yes they have scientists and south africa showed that the human brain evolved to become not only larger but more energetically costly and blood thirsty than previously believed ha ha sensationalism the research team calculated how blood flow flowing to the brain of human ancestors changed our time using the size of two holes the base of the skull that allow arteries to pass to the brain uh it says here brain size increased about 350 percent over human evolution but we found that blood flow to the brain increased an amazing 600 percent so you know size of the brain important yes but brain flow or blood flow to that brain seems now to be perhaps more important says professor emeritus roger seymour from the university of adelaide we believe this is possibly related to the brains need to satisfy increasingly energetic connections between nerve cells that allowed the evolution of complex thinking and learning to allow our brain to be so intelligent it must be constantly fed oxygen and nutrients from the blood the more metabolic metabolically active the brain is the more blood it requires so the supply arteries are larger the holes and fossil skulls are accurate gauges of arterial size and it's sort of interesting about this uh i think is it it says uh it says a lot about okay here's the here's the quote i really like about this ancient fossil skulls from africa reveal holes where the arteries supplying the brain pass through the size of the holes show blood flow increased from three million year old australopithecus to modern humans the intensity of brain activity was before now believed to have been taken to the grave with our ancestors meaning we couldn't really know just based on the size of a brain how active that brain was right uh sure the brain got bigger the skull got bigger that encapsulated it we can maybe assume or not assume that the activity going on in the brain was uh equally increasing but showing the increase in blood flow indicates a higher level of activity thinking processing cognitive ability increases and then in the level of intensity over time so this is like one of the more fascinating tidbits of information that's come across a long time in human evolution and that we may have some sort of a marker to say this is where the increase in blood flow to the brain got to the point where we could be like a little bit neurotic about whether or not we go chase mastodons because that's really dangerous or maybe we should just try to like go pick clams by the ocean because that seems safer like this is like when we started you know really using our brains for a higher cognitive thinking that's tied to the blood flow that's awesome i need more blood flow let's get this blood flow and do you know what time it is i think i do i think i do it's that it's that point each week in which uh we turn the entire show over to blair and start playing some music that we then kind of dance do for a second and then she started you don't need to keep talking like that i was waiting it's time for blair's animal corner yeah that's what it was except for giant what you got blair oh to start i have some really good news oh which is actually related to genomes uh Tasmanian devils they may be adorable but they are the most vicious and largest carnivorous marsupial and the biggest problem that Tasmanian devils have today is devil facial tumor disease dftd which is a nearly 100 fatal and transmissible cancer it was first detected 20 years ago in 1996 and it has killed about 80 percent of the devils in Tasmania the only place in the world where they live they are talked about it a lot on the show and just how awful it is and devastating to this population yeah yeah and so we've talked before on the show mostly about vaccine plans and so far so good but definitely it's something that would have to work aggressively in order for us to save the species if it's 80 gone the really good news is that in this case uh natural selection has worked in the devil's favor and it appears as though so they are starting to evolve a way out of this problem so um looking at two small genomic regions in the dna samples from three different sites where they caught devils they found significant changes in response to the strong selection imposed by the facial tumor disease five of seven genes in those two regions were related to cancer or immune function in other mammals which made them think that these specific regions were related to the facial tumor disease and that they are in fact evolving resistance so if they can determine the specific functionality of the genomic regions that they found then they can start to identify devils that are immune help capture them for breeding efforts and then they will have a fortified group to reintroduce into the wild that will be immune to this facial tumor disease that's fascinating a few questions come to mind though number one they've already lost about 80 percent of their population so it's a massive population bottleneck they're going through absolutely yeah so what effect is that going to have on their survivability and fitness moving into the forward the future even if they do overcome the cancer um secondarily are you know we don't know if there are any other deleterious effects of these mutations because they're allowing them to allowing them to survive the cancer but we're not looking at other effects because the cancer is really the big thing that's killing these animals right now so are these is this population gonna benefit from this later or what's absolutely yeah and so now in the now though because this is actually great well this is also I think one of the first stories uh they're like this is like first year of at least my being on twist stories that we covered was was this facial tumor disease yeah and so it's it's not really it's not been halted but at least nature finds way right yeah so for the past 20 years scientists have been trying to fix this problem but it has been looked pretty grim and the my favorite example of a genetic bottleneck that has so far turned out okay is the elephant seal oh I think we're gonna say humans oh no sure the elephant seal their bottleneck was mostly due to humans and so the main reason that these elephant seals got away is that they had this kind of isolated population that we didn't know about and so that was their bottleneck there could still be any day some disease that wipes out all of the elephant seals because they all are so closely related now and that is something to be concerned about luckily it's been quite a few generations and it's looking okay and as you give it more time then the species will start start to diversify again hopefully because as you can see evolution moves fast it's only been 20 years that we've started to see this decline and Tasmanian devils are already we're seeing a change to this selective pressure so the best that we can hope for is that we can keep the species going long enough that they will then have a chance to kind of radiate out again to create some sort of stable base for their population and yeah go ahead oh it's just I was just gonna congratulate you on creating my quote of the week oh yeah it's how you started off this story natural selection works in the devil's favor yeah in this case it absolutely does and I do think it's important to your to mention that these guys are marsupials which means that it's what some people would call a more primitive type of mammal but really what it means is that their selection just kind of stopped in that space which when you're on an island there's a lot less selective pressures from from larger predators from all sorts of other changing things it's a smaller space so when a species finds a way to to keep going it they can just keep going that doesn't mean they've stopped evolving that doesn't mean that they're more primitive it means that they've found a comfortable spot the species has found a spot and so this is a new pressure that is now causing it to change in new ways and the fact that it's happening in just 20 years I think that's fantastic news for the devil I always think that's a strange thing to say too whether something's primitive or more primitive more evolved or less involved it's pretty silly um but people do like to lean on they do but I would I would I would say like that when I hear that the thing I think of is something like a whale or a dolphin or any sort of marine mammal like orca whatever oh but they're the opposite of primitive no no no but what I know I mean that's what I mean I mean I think of that is more evolved because all the effort to get you on land breathing air and then you went back to the ocean and reversed a bunch of stuff and traits and have vestigial organs to me that's like the most evolved thing is just the thing that changed the most to adapt to its environment yeah um so next I wanted to talk for just a moment about whiskers what are whiskers for okay oh it's to tell it a cat or a rat that is uh as something is is too small or for them to fit through it yeah it helps them feel so what I always talk about with kids is I explain when you get up in the middle of the night and you don't want to turn on the lights to wake up the rest of your house if you have to go find the bathroom you put your hand out to feel your way but if you're a quadrupedal animal you're on all four feet you can't stick a foot out to feel your way so that's what your whiskers are for they feel your way for you they feel obstacles in the way well a recent study from northwestern university has found that they have another use as well and that is to sense the movement of wind and this I love this experiment you know how I geek out about the design of experiments occasionally with animals so this experiment shot shot a rat so the rat was a given entry into an area and that area was shaped like a semicircle and there were five holes across that the the curved part of the semicircle then there was a fan at each hole and one of the fans not visible to the rat would be turned on and that airflow would be the signal to go into that hole and in that hole would be a treat so if there was if they couldn't sense the wind at all they would be right 20 of the time of course that's one in five but they were able to consistently get it right about 60 of the time that is plenty enough to indicate that they could sense the wind next what the scientists did is they cut off their whiskers now that does that sounds like a bummer but it's not painful it's whiskers are hair so it just felt like a haircut they didn't feel it at all and they grew back later but they're there they had a 20 drop in performance after they removed their whiskers so that's still better than just hair cut because i i mean we don't suddenly all of a sudden can't like make our way down a hallway because we got a haircut sure but you might be cold on your head or something like that it's it's it's for science so anyway uh they they had a 20 drop in their performance so it definitely affected them but they were still checking they were sensing other cues it was clear because it was still better than just chance um so they were definitely using more than one cue but they still chose to rely heavily on whiskers which suggests that those whiskers facilitate wind sensing even uh when the wild one wild rats are just exploring naturally they can sense the wind um and just to check that the rats were not just confused by getting their whiskers removed another group of rats were trained to run to a light source instead of the wind and then they had their whiskers trimmed and there was no difference in their performance after whisker removal when it had to do with light yeah so the whiskers they have a lot going on to them besides just feeling actual physical objects they can sense all sorts of things including the wind with their whiskers i feel the wind over me um and then real quick just since we are trying to wind down i'll give you my really fast cuttlefish story and that is that cuttlefish can count well not really cuttlefish can tell amounts so they can tell relative amounts so experiments uh this experiment from national singhua university in taiwan offered cut young cuttlefish choices for a meal a dead shrimp or a live one a large shrimp or a small one or two different quantities and then looked at how the cuttlefish responded the cuttlefish preferred the live shrimp over the dead ones pretty much always but there was more nuance to their decisions they preferred large shrimp over smaller ones when they were hungry but chose the smaller ones when they were not hungry and when the cuttlefish were given quantity options they always picked the larger quantity option two versus one three versus two four versus three so they can definitely sense numbers and quantity and their choice of prey is dependent on how hungry they are or the quality of the prey state dependent valuation so newsflash cuttlefish are smart catfish are smart hey uh blare kiki uh if you were to guess the age of the oldest european what would you guess just throw out a number any uh 145 wow that's pretty old i don't know 130 those are decent guesses but if i were to tell you that the individual question here was a tree uh oh oh a thousand three thousand wow those are disparate actually uh in greece a pine tree growing in the highlands was dated to over a thousand years 1075 ish to be approximate the millennium old pine was discovered by scientists from stockholm university sweden university of mains germany and the university of arizona which i believe is still portion and part of the united states currently it is a remarkable find that this large complex and impressive organism has survived so long in such inhospitable environment in the land that has been civilized for over 3 000 years says swedish dendro chronologist paul krzak leader of the expedition that found the tree many years ago i read a thesis about a very interesting forest in greece in our research we tried to build long chronologies to construct climate histories so finding living trees of old age is one of our motivations one of the things they got to look for because they're going to do a core sample right to the age of the tree we need to take a core of wood from the outside to the center the core is one meter long and has 1075 annual rings says krzak scientists hope the annual variations in the tree rings from trees like this and those fallen centuries past get still preserved on the ground will provide an formative history of climactic and environmental conditions going back thousands of years considering where the tree was found it's venerable age the scientists have named the individual adonis after the great god of the and desire i am impressed in the context of western civilization all the human history that surrounded this tree all the empires the Byzantine the Ottoman maybe some mongols all the people living in this region so many things could have led to its demise fortunately the forest has been basically untouched for over a thousand years and it just looks like a tree it's just a tree and it's not like really in a foresty kind of area it looks like it's kind of a lone yeah it seems like a very lone tree uh and uh last story i've got of the night is probably the biggest i brought tonight australian scientists yes again australia does have scientists why does everybody seem confused when i say that uh only the only these ones weren't actually in australia they were in greenland studying an ancient seafloor that had been revealed by melting ice the ice had been doing pretty good job of preserving the ancient seafloor because what the australian scientists discovered there was amazing fossilized structures from a community of microbes that lived there stromalites which are microscopically detailed layered structures that can be produced by a community of microbes these stromalites were about half an inch to one and a half inches high but how old were they how ancient are we talking using a standard dating method of layers of vast from volcanoes tiny zircon with uranium and throw it all into a magic bag of understanding how things work and tada 3.7 billion years old which compared to a four billion ish year old earth makes these not only the oldest dead thing on the planet but also the earliest living thing we have ever detected according to study and uh yeah so this is this is uh and it's in the current edition of nature if anyone wants to look further into this but this this makes the first story about the that's coming from space this actually accelerates and the potential of planets out there that have life if it could have we're talking then what 300 thousand years or yeah no three million years three million years of the planet being here and and life is existing but then this is like in the hundreds of thousands of years after lava earth right i mean this is pretty darn quick after life where the planet was just this smoldering lava ball on the surface uh to microbes creating structures this accelerates greatly the pace at which life can exist on the planet hugely fascinating story yeah it's a big story and it's gonna it's i think there are going to be a lot of people talking about um the chemical evidence that they're that they're using i mean these kinds of discoveries it's there's not a living there's not a living organism left you know so you're looking at chemical evidence of past living organisms and that's what these stromatolites are and um you know there have been other ones found but um hotly debated within the scientific community so but it is a big idea about yeah how when where life actually got its start my final story for the night toxoplasma gondii is being yeah it's being rewritten scientists are uh genetically engineering toxoplasma gondii so that it doesn't replicate and it doesn't form cysts in the brain and so that it can potentially be used as a vaccine for cancer yeah so uh desperate leaps of things that they're doing at once yeah so uh t gondii is a kind of parasite that um tries to keep its host alive right you know keep uh it it manages moderates modulates the immune system of the host by secreting proteins that affect the immune system to decrease the immune system's effectiveness so that the immune system won't attack the t gondii and so that the t gondii can set up shop and survive but at the same time t gondii also doesn't want to overwhelm its host and doesn't want the host to die so it doesn't completely destroy the immune system so there's some interesting stuff going on there um and so these researchers pretty much thought they're like okay maybe we we can get t gondii to secrete its immune system modulating proteins and allow the survival of hosts that are um are that have cancer so they used a mouse model where these mice have highly aggressive ovarian cancer they vaccinated the mice with this non replicating non-cyst forming vaccine strain of t gondii and they found that um it reversed tumor associated immune suppression and activated potent anti-tumor immunity it also led to increased survival of these mice so basically vaccination with this um genetically engineered t gondii strain um led to better survival of of mice with cancer that's so right yeah and so this is this isn't the only place where researchers are looking into using parasites as potential uh potential vaccines for diseases there are other places where they're looking into this but it's a really neat idea of being able to take this take this um pathogen that affects uh human humans around the world but animals around the world and actually make it work for us instead and so this is uh first in a probably long series of studies and we'll see um how it can work to devise more effective therapies against solid tumors will be pretty cool pretty cool go t gondii go aren't we happy about aren't we happy we know about t gondii now more cat more cat more cat that's the bad kind we still need to get rid of people we still need to get rid of the cats uh no but you know what needs to be gotten rid of this show at the end of this show come on we are done with this show it is time for us to go but before we do that it's time for me to say thank you to our patreon sponsors i would like to say thank you to chris clark paul disney david friedel john ratna swami richard onamist byron lee eo jared lisa ulysses adkins kevin perichan andy keith corsell jake jones eric schwaub patrick kohn bob calder mark bizarre else a dire trainer e4 and martyrs room kiss by brian hedrick kassie lester sarah chavis layla marshal clark charlene henry don karmarachke larry garcia randy mezuka tony steele steve de bell haroon sarang melissa moseley alex wilson jason schneiderman rudy garcia greg geuthman david neighbor jason dozier matthew litman eric nap jason robert greg landon darryl lambart 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once again oh my goodness we'll be getting into september next wednesday september seventh we will be talking about the great red spot on jupiter with a scientist who's been doing some research on that great red spot i think that will be a lot of fun and i hope you all will be back to watch the live show broadcasting online at eight p.m pacific time on twist.org slash live you can watch and join our chat room but don't worry if you can't make it you can't find our you if you can you can't if you can what if you can't you can find our past episodes at twist.org slash youtube or just at twist.org thank you for enjoying the show twist is of course also available as a podcast just google this week in science in your iron tones directory or if you have a mobile type device you can look for twist number four droid app in the android marketplace and again anything apple market placey just google this weekend science for more information on anything that you've heard here today show notes will 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setting up shop got my banner up curled 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 the warming with a wave of my hand and all it'll cost you is a couple of weeks sciences coming your way so everybody listen to what i say i use the scientific method for all that it's worth and i'll broadcast my opinion all of this weekend science this weekend science this weekend science science science this weekend science this weekend science this weekend science science i've got one disclaimer and it shouldn't be news that what i say may not represent your views but i've done the calculations and i've got a plan if you listen to the science you may just then understand that we're not trying to threaten your philosophy we're just trying to save the world from jeopardy this weekend sciences coming away so everybody listen to everything we say and if you use our methods to roll and i die we may rid the world of toxoplasma god yes this weekend science this weekend science this weekend science this weekend science this weekend science this weekend science science science my laundry list of items i want to address from stopping global hunger to dredging Loch Ness i'm trying to promote more rational thought and i'll try to answer any question you've got the help can i ever see the changes i seek when i can only set up shop one week of science this weekend science this weekend science this weekend science science science this week this weekend science this weekend science this weekend science that was a two hour show i'm done let's release two different shows yeah next week off then you don't have to do a show So with that we, oh wait, you have an interview. I have an interview, which will be an awesome interview. I'm looking forward to it. It'll be great. And of course, as I was remembering to announce it, I forgot what our interviewer's name is, and it's Dr. James O'Donoghue. Dr. James O'Donoghue. You'll Twitter it later. I will Twitter it later. I also want to remind people again that we will be in Portland. I will be in Portland. Not this weekend. Next weekend, September 9th, 10th, 11th at the Mini Maker Faire in Portland doing a podcast booth. That'll be fun. Podcasting all weekend. Oh my goodness. I'll be at a zoo and aquarium conference instead. I wish I could be there. So much I have to do. How come that's the one weekend? That's the one weekend where things are happening. Both of the things. I need to find people in Portland to interview and do podcasts with. Podcasting is fun. Ta-da. But are you trying to reassure yourself right now? Yeah, exactly. It's fun, right? It's fun, I tell you, when I'm not this tired. I am in Portland almost every weekend. Ben Rosig, you're right. But at the Mini Maker Faire, the 10th and 11th. And then November 4th, Baltimore, the Baltimore Aquarium Live Show this weekend science in Baltimore. November 4th. Oh my goodness, that's coming up pretty soon. I know. It's like right now, when September hits, I realize how close the end of the year is. It's like in May, June, I was like, oh, summer. Such a long summer. It's awesome. And then the summer disappeared. And we're back again at the end of the year. And I find myself panicking a little bit. My child starts kindergarten tomorrow. Yeah, I was at we went through a massive preschool play date, preschool, can we go? Just preschool play date with all the different classes that are going to this preschool. And it was just a swarm of children climbing, swinging. It was at a park. Kids were just all playing like crazy this morning for hours. I was worn out, but the kids wanted to keep going. They were just like, no, I'm going to slide again, swing again, more playing. Children. On the 2016 calendar, tomorrow, species requiem day. That's right. So who's on the calendar? I haven't turned the page yet. I don't know. It's a surprise. Oh, wait. Not anymore. It's one species that's not around anymore. There are many more requiem for a species or several million or more. Ed from Connecticut. Another great show and guest. Yeah, good job, Kiki. That was another fantastic guest. I really do feel like we kind of condom a bit. What do you mean? Well, because by bringing him into the first half of the show, like normally we would have been. No, no, he would have been here till 1 in the morning. It is, he was there till midnight. Yeah, that's my point. We would have gotten through the first half of the show as quickly as possible to get to the second half. And then we probably would have hard outed him after about a half an hour or 20 minutes. No, it would have been 9.30. We probably would have gotten through the first half of the show. 45 to 50 minutes interview there. He was very gracious. It's always a good question. Yeah, I'm stretching. Stretching, stretching, stretching. Yes, Portland, science and beer. It's true. And I can't wait until to Portland. I've never been. I can't wait for you to come to Portland either. It'll be fine. How are you doing? No, she's not. She's going somewhere else. I'm going to Santiago. Santiago. I like Santiago. I don't think I need to talk about anything else right now. So OK, so my three-year-old has been looking through animal books. And she's I'm noticing she has a very advanced, I think, for a three-year-old ability to categorize these animals. Because she doesn't point to birds and say bird. She can tell the difference between like a parrot. That's parrot. That's toucan. For whatever reason, and as much as I've tried to suggest an alternative, macaw is pretty bird. But she's got it nailed down. Like whenever she sees a macaw, she's like, pretty bird. But parrot is parrot. Parakeet is parakeet. Toucan is toucan. And macaw is pretty bird. She should call it a herdy bird instead. And then I got, and then I confused her the other day because we saw a blue jay. And I called it, first I called it scrub jay. And then I said blue jay. And now she's like, and then she was drilling me like, well, which is it? Like, you can't have an answer. Yeah, get it together. You have to pick one, Papa, which is it? OK. Why does a fallen star miss loud Justin? I don't know. Who are you? Don't understand. Did Justin get quieter? OK, because this is a question. Am I quiet in this episode? Because I did turn down a little bit of the volume. Are you quiet or are you not loud? Because those are two different things. I miss loud just so apparently the lady hosts have their headphones turned up, their volumes turned up. Because I had to turn down my output, my mic, or my pickup on my mic because they said I was hot mic-ing. And I was pointing out that this is the same setting. Yeah. Thank you, Southeast. Justin is quiet in about every episode. I think the way that we are. That's funny. No, you are coming across louder than Blair. To me, you are coming across more loudly than Blair. For me tonight, it's been loud. So it's interesting that it. That's important to the audience. Which is, that's really. Yeah, according to the audience, I'm turned down too much. Which is really interesting because I did not turn your volume down on my end. I have a control. Well, I did at the beginning of the show because I was being told that I have hot mic. But I was pointing out that we all have volume controls on our headsets. Yeah, but I was talking, when I think you're too loud, it's because you're louder than Kiki. So because each of us have two voices that we're hearing. Yeah, and I compare against Blair. I compare against Blair. We got me listening to twists because I could overhear my brother listening all this years ago. Yeah, look, the chat room is spitting it out right there. Justin is quiet. Wow. Justin, don't look at it. No, no, I got to find a game on this thing and crank it up a bit. I think your headsets are just up a bit too much. No, because Kiki is not loud when I think you're loud. And I'm the loudest to identity for and everybody out there. So I'm the loudest. And so if, yeah, so I should be loud in your headsets. Let's redo, redo. Pop quiz, who has been the loudest in the episodes you've been listening to? Who wants to go to bed? Who is the quietest? Kiki is the loudest. So Kiki, sounds like you need to turn your volume down a little bit. And I need to crank mine up a little bit. And you need to turn down the headset just to touch. I feel like being trolled. I feel like this is just the chat room trying to mess with us right now. I feel like it's Google. No, our headsets don't play our own voices back to us. So you can't tell that you're louder. And though I seem louder compared to Blair, because that's the only two that you're registering, right? Yeah, identity four. The problem is that Justin is super quiet in my audio mix. Kiki is the loudest. But see FallonStar said, you burst your loudness. See, that's the problem. Because sometimes you get real excited. You leave way forward in your chair. Somebody to hear me. What we need, we need your microphone. We need to get you that boom mic on a thing on your head. So you get one of those umbrella hats, right? But instead, you rig it up with the boom mic. So the mic is always the same distance from your face. That's funny. That's possible. That's possible. So for myself, Hot Rod is saying that we need a UV meter, and we need to touch the red to be set properly. That would be great to have one that was fantastic. That's what's missing from Google. What I look at, yeah, they don't have a meter. But what I look at is there is a meter at the bottom of my screen. I can see little green dots telling me whether or not how loud I am. And I look and see how often I tap. If I'm all the way maxed out, then I'm too loud. And so I think I have actually a very good mix on my end. I'm not, the board that my mic is going into is barely even registering. But again, look at mine. OK, look at my little green dots. You think I'm being very loud right now, but I've only got a few of those little green dots compared to watch. You just talk normally and see how many green dots you put up. I would say your green dots are higher. I don't know. I can't. You've already got way more green dots than me and just those I can't. And I was being shouty. This is the problem. We have multiple volume controls. Some are headsets. It's the volume I have on the speakers that the headsets are connected to. You might have volume controls on your headset. But if you look, I'm getting those little two dots there. Why are you? But the thing that I don't understand. You're getting into four dots. I don't understand why you are louder to me than Blair is. I think Blair is right behind me. Went to the audience. Blair is in the middle. She's quieter than me, louder than you. Right. But if you're the loudest, it means you need to turn your headset down a little bit. Oh, I don't. Yes. Because if I'm too loud, listen, if I'm too loud and I'm not at the same volume as you. You're not listening to me. It's a headset problem. I am listening to you. It's not a headset problem. Ah, I think it is. It's not a headset problem. Charm, who do you agree with? Charm, who do you agree with? The fact that Google doesn't have a full mixer. Yeah, there's not a mixer. Through Google, that's the issue. And the other issue that I think no one is mentioning here is that your highest and your lowest frequencies go away when you have any issues with your hearing at all and your voice is lower than mine, and mine is middle. Whose voice is lower? Yours? No, mine's voice is lower. It's not about talking like this. OK, I'll talk higher from now on. Yeah, I mean, before I put the podcast out, I hit a normal. I normalize it, and I always have to turn the volume up when Justin talks, but this is the issue. Look, Ed from Connecticut, I agree with Justin. I'm not the only one saying this. No, and it's not always. It's only been for the last few pop. It's probably been for about the last month since you moved, because your audio used to be fine and something changed. It's been for like the last month. It's not, it has, it is a new thing. Well, I think this month, you said I was coming in way too hot, I needed to turn down. And it was, it was turned down a little bit. It wasn't maxed out where it used to be. That's why I'm saying it's the headset. That's why I'm saying, that's why I'm considering the idea, at least, that the volume control you have on listening to the two of us might be set higher than, say, mine. Because neither of you sound like that to me. But then, see Justin, I wouldn't sound a different level than you. That's the part where it doesn't make sense, is that you sound louder than me to Kiki, which if she was just overall the volume was too high, we would both be loud. If overall Blair was loud and you were loud, then yes, I would turn down my headphone volume, but it makes no difference if I turn down my headphone volume. I've tried that, you're louder than Blair, which is why I have told you to turn down. But everybody listening to the end product is saying the opposite. Why do we always have to argue the same points over and over again? I heard you already. I've heard you four times. Then how does it make sense? It doesn't make sense. It's something in Google. It's different. We don't have a mixer because Google takes the audio inputs and ends up doing something with them. It's not, yeah, I don't know, because you're hearing yourself on your end and you set yourself to a certain way. I don't hear myself at all on my end. That's my point. I don't hear it at all, and none of us do. None of us should be hearing ourselves, and that's what makes it difficult. That's why we need these people saying what the end product is to tell us where to put our settings. Turn up. Just turn way up. Go ahead. Turn way up. Just tap out the green. Turn it up. And my green still, it stays at the little two dots. Like I have a hard time getting into three dot territory. So you just turned up and I heard absolutely no difference. The other thing too is that when I say you're being too loud, Justin, it's because I adjust my sound to Kiki because Kiki is also running the sound board, so she has music. Really, we should be adjusting to Kiki's sound volume because she's running the music. Does that make sense? So you should be relatively the same volume as Kiki. You would think, but obviously that's not working to the end product. This is all I'm saying. I don't care about what we're hearing, not talking about that. Obviously that is really hard. It's a three-way telephone game, but what we need to be paying attention to is what the end users are hearing. That's the only thing that should count. Justin also fix it. And so a big part of it too, though, fix it. It's not my headphones. Right. So maybe, Justin, also, you could move the mic closer to yourself when you're reclined so that there's less fluctuation because even moving a couple inches closer to your mic, you get way louder. Yeah. Your microphone is very directional and it's not a room mic. And whiskey running it, I know I sound good, but I also just increased the gain like 10%. I just increased gain 10% on this. So I mean, I'm this far away from my mic or I'm this close to my mic, and I don't know that that's going to. It's a huge difference. Is that making a huge difference going from here to over here? It's a massive difference, Justin. You go from a sound volume of like a four or like a, you go volume level of four to like an eight when you go back to forward. I'm going to stick with the chat room agrees with me, so I no longer need to justify any points. All right. Well then, as long as I've got the minions on my side, I'm happy. I'm out of water. I went the whole show without water, which is probably why I'm cranky. I finally went and got, I usually drink a glass this big of water every time we do a show, and I didn't. I'm tired. Yeah. You need your face close to the microphone. Yeah. I'm not going to do this. Not that close. Just move you the mic closer to your reclining posture. I actually, Blair, I think you've got it. I think you did nail what I needed to do. I need a hat. Oh, the hat thing? I need a hat. Oh, Mike. That just maintains the same. Like a carrot for a donkey, but a microphone. You're at the show. Yeah. Because I do, I'm going to be moving around during the show with my Justin fluctuations. Which is probably why Google has decided that your volume fluctuates a lot and made you really quiet. Yeah, I know you're right. It probably took peak, Justin, and since that is the level of the side of your rights. Yeah. All right. Which is why you need to turn down your headset. That was, that was me pushing buttons. That wasn't a, that was stupid. You're not kidding. Well, you could. So something you could do is get a lav mic and wear a baseball hat and just ding. Or wear your soup. Cowboy hat. Can we get a cowboy hat? You could put a lav mic on your Superman glasses, right in the middle. What's a lav? Lavalier. A lavalier mic. I like it already. All right. Anyway, okay, you guys, I'm sorry I'm cranky and that I was fighting with Justin about this. I'll miss you guys next week. We'll miss you. Why? What? Where? When? How? You're not going to be here? Where's going to a zoo professional meeting? Professional zoo people. What? How's that term doing this? It's the Association of Zoos and Aquariums, their annual conference. It's a week long. I'm going. Nice. In San Diego. San Diego. Watch my Instagram and Twitter. So wait, so what is our show? So we're doing a Blair List show next week. Correct. But you're going to have a guest. I will have a guest. About Jupiter. Yeah, yeah, but are you going to be, that's not the same day where you're going to be at the live Portland thingy. No, no, that's the weekend. But I'll still be in San Diego. Gotcha, gotcha, gotcha. Okay, say good night, Blair. Good night, Blair. Say good night, Kiki. Oh, good night, Kiki. Good night, Justin. Good night, Minions. Thank you once again for hanging out with us. We enjoy your company, especially when you're agreeing with me somehow. Oh, get out of town. We like you even more than that. Goodness. Okay, everybody. Check out the Minion Hangout tomorrow night with Ed Dyer over at scienceisland.org. That could be super awesome. It really is. Yep, we'll see you again next week. Going to see you on the flip side. Bye, thanks for joining us again.