Justin: Disclaimer! Disclaimer! Disclaimer! There are by current estimates 70 sextillion stars in a known universe. That’s a seven followed by 22 zeroes, which means that if you collected every grain of sand from every beach on planet Earth you would still fall critically short in constructing a solar model of the universe.
And since this stellar magnitude maybe mentally incomprehensible like the following hour of programming, it therefore does not necessarily represent the views or opinions of University of California at Davis, KDVS or it’s sponsors.
And while pondering the scale of the universe may put some intimidating perspective on the day to day lives of the average earthling, you are not an average earthling. Yes, our earth may be comparable to a bit of dust and a grain of sand on the edges of the oceans of space but in all of the universe, there’s only one you.
Multiple magnitudes of galaxies may come and go but still, there can be only one you, which makes you a very rare properly of the universe indeed. So pull up a beach chair and together, let’s sun ourselves in the light of our mutually incomprehensible uniqueness as we improve our mental sandbox by listening to This Week in Science, coming up next.
Justin: Good morning, Kirsten.
Kirsten: Good morning, Justin. You’re back.
Justin: I’m back.
Justin: And you’re back.
Kirsten: I’m back.
Kirsten: I am.
Justin: Been working at the kinks on a time machine?
Kirsten: I’m back every Tuesday.
Justin: Went back to the protozoic era there for a little bit. When I came back everybody was gone. So I had to go back and tried to undo what I’d done and – well, thankfully, thankfully you’re back. You don’t have a Nobel Prize anymore, sorry about that.
Justin: But, I mean you’re here.
Kirsten: I have a Nobel Prize?
Justin: Yes, you’re doing really good.
Kirsten: Darn it.
Justin: Yes. I couldn’t get everything the way back it was exactly.
Kirsten: You have to go back again.
Justin: And you’re a redhead, red looks good on you. Good job.
Kirsten: Thanks, I think. Okay. Welcome everyone to This Week in Science. It’s Kirsten and Justin on the air for the next hour talking about Science news.
Justin: Science news. There’s a ton of it this week. It’s awesome.
Kirsten: There is a ton of it. Yes, it’s very exciting. There’s a story actually that I wanted to start off with but I have to bring it up on the computer screen so it’s related to genetic engineering of embryos. So it’s a story out of the New York Times. So, Justin why don’t you give a story and…
Justin: Okay. Hey, I hate to do this to folks but right off the top, I’m going to give you a pop quiz. Pop quiz, here we go, ready? Get your number 2 pencils out and prepare to show your work.
Subject is molecular biochemistry in genetics a.k.a. Biology, I mean it’s all Biology now, right? Question is, what do you get when you combine the DNA of a reptile, a bird, and a mammal?
You have five seconds to complete your answers. Extra credit will be given for diddles in the margin that relate to the subject matter in some way. And time is up. Put your pencils down. The answer to the question? The redheaded student sitting right up front. Yes, young lady?
Kirsten: I wasn’t paying any attention.
Justin: Okay. Yes, it’s a furry, venomous, otter-footed, beaver-tailed, egg-laying, lactating duck-billed platypus. As if the multi-species genetic trademark infringements weren’t enough, the platypus also has picked up another mutability owing away, electrosensory receptors in it’s bill that allow it to hunt with its eyes closed in the dark by tracking electrical fields generated by the muscular contractions of its prey.
A platypus can do that. I had no idea. That’s like sharks can do that.
Kirsten: Yes, that’s something that some fish and sharks are in the fish family but some sharks and some fish have that electrosensory perception.
Justin: So we are going to throw like fish into the platypus mix, I mean that’s a wild – that’s a pretty intense…
Kirsten: Yes, I think what they use it for it says there they sieve stuff like grab stuff…
Kirsten: …off the bottom of the waterways where they’re living and you know, they can use it to find little things that are…
Justin: In the mud.
Kirsten: …living in the mud, in the grass that they can actually see. I heard their eyesight is actually pretty bad as well.
Justin: They’ve got these tiny, beady eyes. This…
Kirsten: But they use it. They use – they…
Justin: Oh, yes.
Kirsten: …sense this – their bill as their sight is pretty much…
Justin: And they have venom in one of their claws.
Kirsten: Yes, like a shrew.
Justin: So intense, will they – this makes perfect sense. They sequenced the DNA of the platypus, which just makes so much sense, I mean you start your eye like you want to look at the chimp because it’s very closely related to the human being.
Kirsten: Mm hmm.
Justin: You want to get the mouse done because we do so much research on the mouse that it would be very helpful to have that whole model.
Kirsten: Right, and it’s also…
Justin: So those who…
Kirsten: …it’s also fairly – and a lot of diseases and things are very similar…
Kirsten: …that befall the mouse are very similar to those that affect humans, yes.
Justin: So those are definitely the first two you wanted…
Kirsten: Drosophila because they’re, you know, fairly simple and they have a wrap…
Justin: I don’t know what a drosophila is but I agree with you…
Kirsten: A fruit fly.
Justin: …completely. Oh, and fruit flies actually have a similar gene for aging that – in human so that – they just…
Kirsten: It’s an old
Kirsten: Right. That it’s of an old, old gene.
Kirsten: It’s been around for a while.
Justin: So there’s some stuff that makes sense but the platypus that, I mean I didn’t think of it before otherwise, I’d be saying, “Why haven’t they done the platypus?”
Kirsten: Let’s do the platypus because the platypus seems…
Kirsten: …kind of confused.
Justin: Yes. It’s such a combobulation of these features that we see in other creatures. So they did it. They went out and they decoded the platypus. And the information that’s coming out of this is some of which you’d expect to find and it’s different too, I mean the platypus does have a lot of the DNA that is typical of reptiles and avians and mammals all in the same system.
What they didn’t expect is that the DNA has a much, much stronger relationships to birds and reptiles than it does to mammals…
Justin: …I mean it’s furry, it lactates…
Justin: …it’s got, you know…
Kirsten: The marsupial…
Justin: ..some features of…
Kirsten: …nature kind of…
Justin: But the duck bill is kind of hard to avoid and you know, their egg laying and the (unintelligible), I mean there’s other feet but it’s much more…
Kirsten: So it’s…
Justin: …reptilian and avian…
Kirsten: Than it is mammalian.
Justin: …than it is mammalian. And the…
Justin: And that the picture is of a – the platypus comes from a line of creatures that were basically the predecessor of the mammal, I mean it comes – it’s more closely related to the split. And in a way, it’s a living missing link to that time because it hasn’t altered that much over the years.
Kirsten: Right. And it…
Justin: It’s like a prehistoric creature, really.
Kirsten: And it survived very well.
Kirsten: You know, it’s found a niche in the environment. That’s about it, yes.
Justin: It’s found a niche, I mean it’s very endangered right now but that…
Kirsten: Right. But, I mean considering the traits and how ancient and how far back everything goes it, you know, survived a long time. There are a lot of species that have not made it as long.
Justin: It should be one of those creatures that you look at in a fossil record and go, “Wow! That was an interesting stuff” only it’s still here, you know? It’s actually with us. And…
Kirsten: Yes. Yes, everybody is always looking for the missing link in the fossil record…
Kirsten: …but just…
Justin: It’s actually…
Kirsten: … “Just look at the platypus.”
Justin: …we’ve got pictures; I mean we got pictures now we have a full sequence DNA of it…
Justin: And they’re thinking for one it’s going to help show a lot of the evolutionary history of mammals…
Justin: …because it is so related to an early offshoot from the bird and reptile clan. And the other one is I think it’s actually going to have some huge import for disease research because…
Kirsten: Aha, that’s interesting.
Justin: …it’s going to – it’s a real world way of tracking back where a lot of genetic disease – differences show up in mammals by seeing one that sort of has the earlier record of the whole thing. So it’s going to be…
Kirsten: Right. Kind of a comparison, right, going back to…
Kirsten: ..some earlier form that is common to everything.
Justin: You may see the roots of a lot of the genes and…
Kirsten: So and Scott Sigler’s old – not old book but his book that we interviewed him on last year, Ancestor…?
Kirsten: …when researchers were looking for, you know, the common genetic link.
Kirsten: And it’s a very similar idea. The common genetic link way back when that could be able to be used to create organs that would never be rejected because it has a common link to humans as well as other animals. So they could grow a cow with these organs and we could transplant the cow organ although it’d be huge for a cow into a human…
Justin: Or a small cow. We’d have to shrink the cows first.
Kirsten: Pygmy cows. You know, and in his book it went horribly awry.
Justin: Well, (yes).
Kirsten: You know, the sci-fi horror thing but – now, it’s an interesting idea to be able to look at a platypus as that potential initial ancestor that we can use. We can use the platypus to our own needs and the platypus will never fight back, poor little platypus.
Justin: Well no I think it’s good news for platypus. If we get some good research out of this that means that there’s going to be a lot of platypus breeding going on – serious effort.
Kirsten: It maybe but I mean then the platypus will just end up in laboratories as opposed to in the wild and surviving.
Justin: You know, but this is all a debate like, you know, people who don’t like to eat cows. I think it works out good for cows because really, look how many cows there are on planet Earth…
Kirsten: And they were…
Justin: If the cows were that big and unedible…
Kirsten: And they would…
Justin: …there would be very few cows. They’d be a nuisance.
Kirsten: And the cows are at least they’re big and seriously, I don’t think cows could even give birth without humans around to pull the calf out, I mean seriously…
Kirsten: …I think cows would…
Justin: That’s pretty well debatable out but…
Kirsten: Cows would just die off…
Kirsten: …if people weren’t around to keep raising them.
Justin: No, if they weren’t getting milked in and it’s like the domestic animals got it good. Their genes are continuing to go on year after year and they’re multiplying because they have found a niche.
Kirsten: Have been domesticated and what else?
Justin: Well, domesticated or found a good niche within the biosphere. It’s all – they were food before just there weren’t as many of them and not as many have got eaten but that’s…
Kirsten: That’s enough story. It’s another day. Genetic engineering of embryos – there’s a story in the New York Times from May 13th; I guess that’s today, Saturday?
Justin: That’s – yes. I think that is happening right now.
Kirsten: Is today May 13th? And researchers at Cornell University – last year actually, they presented at a conference some research results that they – to use an unviable, abnormal embryo and inserted genes for a fluorescent protein into the embryo of a human egg and sperm combination, you know?
Justin: Mm hmm.
Kirsten: And they used typical viral insertion techniques not any new techniques. There’s nothing brand new about it. But suddenly there’s a firestorm around it as a British newspaper reported on this research in doing a review of this kind of embryonic research that’s going on in the UK and around the world and what kind of studies are actually happening.
And so, now people are kind of getting up and arms saying that we shouldn’t be doing any genetic engineering studies or research on human embryos because it could lead to the kind of eugenics…
Justin: Yes, it…
Kirsten: …and designer babies because they’re saying that these techniques could be used on normal embryos and people could insert genes, or change the genes for height or intelligence or whatever else.
Justin: That had nothing to do with what the Science was that was taking place.
Justin: it’s so completely unrelated to that that it’s just…
Justin: …absolutely absurd.
Kirsten: Right. And additionally, they’re just saying that the research should not have taken place in the first place; that it should have gone through stricter review and should never have happened.
However, the research was privately funded and it did pass a review board. And so, it’s not like, “Oh, how did the researchers get this to happen?” They actually put their idea in front of a review board that looked at it and decided that it was okay. They’re not – they weren’t developing…
Justin: This is a non-viable embryo.
Justin: This is something that was not going to turn into a person. And what they did to it is they added genes to it to see that if they harvested the stem cells if those genes that they add it to would be apparent in those stem cells.
Justin: That was it. That’s the study.
Kirsten: It’s stem cell research…
Kirsten: …to learn more about how stem cells work and to determine whether or not stem cells are going to continue to be a viable avenue of research for therapeutic cloning, the idea that maybe you can use your own cells to eventually grow yourself an organ if you have some kind of a fatal disease that deteriorates in your body or if you have had an accident.
Justin: And growing an organ too. We’re not talking about growing an organ in a clone of you, in another human being…
Kirsten: No, we’re talking about just an organ.
Justin: …that you can slaughter to harvest the organ.
Kirsten: Just an organ. An organ…
Justin: That’s not in the Science anywhere. That’s not it.
Justin: And they’re not talking about cloning human beings. The cloning process as it stands right now, I mean to come up with a Dolly or to come up with any of these, you know, the Afghan lab that got the clone or what have you? They go through so – I mean it’s hundreds of unviable creatures are created in this that die…
Justin: …you know, before they’re born or shortly thereafter. There’s no Science in the world that’s going to be doing that with human babies. You’re not going to role a dice and see what comes out and how long they live. It just doesn’t – that’s not on the tape – nobody is doing that. Nobody is doing that.
Kirsten: Nobody is thinking about doing it either. But the argument is that maybe somebody will think of doing it and maybe somebody will start to create designer babies and give parents the option to do that using these same research techniques.
An argument also is that this is something that – basically, we use these techniques in adult humans currently to insert genes as part of research that inserts genes into adult humans to change muscle tissue or heart tissue or even nervous tissue. And to see if by changing a gene in a living human, then some kind of impairment can be corrected.
And this research seems to be going along very well. There have been a few kinks in the road but it’s, you know, we’re learning a lot about how genes work.
And the issue is that in adult humans, these gene changes don’t end up in the reproductive cells, whereas if you do the same exact technique in a blastocyst, a cluster, a clump of cells, you’re actually changing the cells themselves when they’re right before the stem cell is staged. So, those changes could possibly enter into the reproductive tissues and become inheritable changes. And if you have…
Kirsten: …something that you’re changing that becomes a heritable change, then if that embryo is viable and is allowed to grown, then those changes could eventually go on to their offspring and what not?
And so, people are thinking down the road and trying to see what we humans would potentially use these techniques for. And so, they’re saying that research like this just shouldn’t happen…
Kirsten: …because of the potential of misuse…
Kirsten: …or what could be considered by some to be immoral use of the techniques in the future. And so, I don’t know. I personally think why stunt our growth as humans and our ability to save ourselves and help ourselves medically by thinking of all the terrible things that we could do with the technology, I mean it’s like never giving somebody a car because they COULD get into an accident.
It’s like never allowing…
Justin: I’m happy about that policy.
Kirsten: …never – I know, never allowing a child to like leave the house or leave your sight because they COULD do something wrong when you’re not watching them. Or they could, you know, we have…
Kirsten: …to allow for the possible mistakes to take place but we also have to allow for people to be good and independent and do things, in the right way. We can’t just stop ourselves because…
Justin: Why is it I think that it’s the pro-intelligent design crowd that’s against the intelligent designing of human beings? Why do I get the idea that that’s like the same crowd?
Kirsten: No, I don’t think it’s just that same crowd though. I think there are a lot of…
Justin: (Unintelligible) a human.
Kirsten: No, there are a lot of, I mean that’s probably part of it. That’s probably one part of it but there are many people out there who do not agree that messing with the genes are…
Justin: Because we’re perfect!
Justin: We are perfect. We’re disease free and super bright. Okay, well (unintelligible)…
Kirsten: Moving on.
Justin: Oh, gosh. New study confirms that fact we are all as fat as we can be – all the time. Yes, yes folks. Be as fit, full bodied or bone skinny. Research has now proven for the first time that the number of fat cells in the human body doesn’t change along time or with weight fluctuations. It’s the amount of mass within each fat cell that is responsible for your added gravity.
Kirsten: My gravity. It’s gravity.
Justin: The study used some carbon dating techniques to help determine the turnover rate of fat cells. And it tracked the number of those cells in the human body in different individuals, their different age ranges and body weight fluctuations.
As it turns out, the number of fat cells in the body is determined right around the time you’re leaving the teenage years. There’s fluctuations before that but by the time you’re a teenager that’s pretty much the number of fat cells you’re going to have for the rest of your life. And it maintains that even keel throughout your life.
So what they found is there’s about a 10% annual turnover rate for fat cells. You know, 10% of them die off and they’re replaced by another 10% pretty much on a yearly basis regardless again of your body type.
And this rate of change in this level does not change with the onset of obesity nor does it fluctuate with your dieting. No extreme dieting that you can do that’s going to change the number of fat cells. What you’re doing is your pulling the lipids out. You know, you’re burning that energy that’s stored up in there.
Kirsten: Right. But there was a research that just came out last week that said that as you age and diet and whatever else that fat cells do die whereas in the past, it was thought that fat cells never died and they kept living. And – so, fat cells do die.
Justin: Well, they die but they’re replaced at the rate that they die.
Justin: That’s, I mean it’s an even keel.
Kirsten: They would have – so it’s an even…
Justin: The actual number doesn’t fluctuate. It stays very, very – right. And what’s even amazing is if you go in for the…
Kirsten: How did they figure this out?
Justin: Carbon-14 is what they used. And it was because there was I guess it can track the age of cells or they can recognize them with it. It’s – I don’t how exactly they used it. But they used carbon-14 in the cells to monitor which cells are which and what levels they were in.
Justin: Mm hmm. So basically, the one thing you can do to remove fat cells is the surgical weight loss.
Kirsten: That’s right. Suck them out.
Justin: It will actually take the fat cells out, which does reduce the number of fat cells in the body but that number rebounds as quickly as two years.
Kirsten: Really? So they kept…
Justin: The body will…
Kirsten: The body replaces them in.
Justin: Yes. So the body is monitoring how many cells you have. It’s like no, that’s how many you’re going to have PERIOD! That’s it. You’d – no, don’t argue with me.
So the bad news is you can’t get rid of fat cells. If you got them, they’re yours. The good news is you’re not going to get any more of them. That’s, you know, you’re not going to get more fat cells regardless of what you eat. You’re just going to make the ones you have now.
So the real nuisance story is it’s not how many fat cells you have that determines your size, it’s how fat the fat cells are that you have that counts. So, it’s not you, it’s your fat cells that are fat if you, you know, worry about such things.
I’m actually a little bit disappointed…
Kirsten: That’s a good and would have been, “Yes, I’m not dieting. My fat cells are dieting.”
Justin: Well, I’m not a lollipop by any means but I’m like I’m skinner than I would like to be.
Kirsten: You’re lean.
Justin: I’m more than lean. I would like, you know, I was like, gosh, you know, I wonder when my metabolism is going to kick down to a lower gear and I can, you know, get that…
Kirsten: Maybe never.
Justin: But if it does now I’m like even like maybe I don’t have enough cells to really, be nice and plump. Researchers’ collaborative effort that included Lawrence Livermore National Laboratory and Karolinska Institute in Sweden, Humboldt University in Berlin, Foundation of Research and Technology in Greece…
Kirsten: Wow! These are some good research institutes. This is big setting.
Justin: I’m (done). This isn’t one that that this is a makity-up story, Kirsten, “Well, what did they used to determine?” Don’t question me I’m not the scientist. It’s carbon-14 it’s the stuff that came up when we are blowing up all those above ground atomic bombs, okay?
It’s the little let’s say – let me draw you a picture of it, yes. That looks something like this.
Kirsten: Yes, you’re going to draw me a picture, right.
Justin: Yes, it’s exactly what it looks like. And that’s a radio, who cares? I’m going to be silently indignant while you do your next story.
Kirsten: Oh, my goodness. Researchers at HP, Hewlett-Packard. This is a story…
Justin: Never heard of that school. Is that accredited university laboratory? What is that?
Kirsten: It’s not a school. It’s…
Justin: HP – oh, I didn’t think so, okay.
Kirsten: It’s, you know, a company that does research and develops…
Justin: They make my printer.
Kirsten: They make your printer, that’s right. Anyway, I was sent – let me see if I can find the names of the people…
Justin: Speaking of which, look at this. This is like a half-page print.
Kirsten: (Kyle), (Kyle)…
Justin: It printed half on one page and one on the next.
Kirsten: And you got – you need to…
Justin: I may have to talk to these HP people.
Kirsten: You got to fix it.
Justin: They may need to do some more research.
Kirsten: (Kyle Himker), (Mike Sherman) and maybe a couple of other people but these guys sent me this memristors story because it’s actually, this is one of the – I think one of the big developments of the year.
So, in electronic circuits you have the resistor, the capacitor and an insulator. And there are these three types of circuit connectors within electronic circuits.
However, some 37 years ago, a researcher who was studying the problem – what was his name Leon Chua. In 1971, he was studying non-linear circuits. As an engineering student, he mathematically proposed that there should be a fourth type of element for circuits. Then he called it the memristors, which is a resistor that actually has memory of the charges that go through it and can change, based on the memory that it has.
Kirsten: You know, and thinking of it in memory is basically that it changes based on…
Justin: Mm hmm.
Kirsten: …experience with charge. And – yes, and it’s…
Justin: …something like nickel-head batteries maybe, mm hmm?
Kirsten: Maybe. So, for like 37 years, people have just kind of going along and nobody found the memristors and nobody is really been able to figure it out. And they’re like okay, so let’s assume that this should be this fourth type of circuit element but nobody has ever figured it out.
However, Stanley Williams, who was one of the researchers at HP Labs, he has said that they have figured it out. And HP Labs was studying some circuit design with some materials that they are developing and they realized that they had actually created memristors.
Kirsten: Yes. So based on their research, they have actually built these working memristors, the fourth basic circuit. And by having built it and then starting to understand how the memristors works it’s going to allow for faster computers, the ability for computers to start up and not have to boot from a disk.
Justin: Oh, I’d love that.
Kirsten: So right now, circuits don’t have any kind of memory. So, in a computer – when you turn a computer on it has to rebuilt it memory from a magnetic disk where the memory has been stored. So, when you turn the computer off, everything goes away except for the magnetic storage because magnetic storage doesn’t go away over a period of time that computers are turned off.
When you turn it back on, electrical signal goes into the magnetic boot disk and that helps rebuild the memory in the rest of the computer. And so, you have to go through the long boot process when you turn your…
Justin: It’s painstaking.
Kirsten: Right. And sometimes – and depending on your computer like I had a computer at one point that was dying and it took like 15 minutes to actually start my computer.
Kirsten: It could take forever. So it wastes energy and it also wastes you time. Could you imagine a computer that because of the memristor you don’t need to have the boot disk? The memory is maintained within the computer itself. You turn it on…
Justin: There it is.
Kirsten: … and it’s everything right there. So you have a computer that boots instantly.
Justin: It’d be awesome.
Kirsten: Right. So this is the kind of technology that can be developed now that these materials are starting to be understood. So, it’s really, I think in terms of technology- one of the biggest discoveries or inventions in recent history.
Justin: Yes, maybe this century.
Kirsten: And I honestly think so.
Justin: Maybe the biggest this century.
Kirsten: Yes. So it’s going to pave the way for I think new technologies that we haven’t even considered yet.
Justin: Mine actually – my computer takes longer to shutdown than it does even to start up. I don’t know what the…
Kirsten: Right. And the shutdown is, you know, making sure that everything is saved on to that magnetic disk…
Kirsten: …before it turns off so you don’t lose data while the computer is turned off. So, yes, I think that’s big, big story and thanks, you guys for sending it in because it’s HUGE!
Justin: And once you get your computer turned on and booted up, I have a got a great place for you to go because this is one of the greatest ideas in scientific research this century as well. It’s a video game that does actual Science.
Kirsten: Oh, I like.
Justin: So the video game is called Fold It! It’s a free puzzle game that allows users to fold three dimensional puzzles that are proteins for fun in Science. The ultimate high score being potentially a real-life Nobel Prize.
Justin: Some kind of…
Kirsten: A real-life Nobel Prize?
Justin: A real one. An earlier version of this was…
Kirsten: I want a video game and a Nobel Prize.
Justin: Heck, yes. The earlier version was that there was at home, a program that folds proteins with the unused processing the capacity of a personal computer so it run in the background kind of a SETI@home or an Einstein@home. It’s like folding, folding when you’re not using your computer.
Kirsten: Mm hmm.
Justin: But it hasn’t really been that, I guess successful. I haven’t gotten a lot of that yet. And so, they realized that they have all the computing power on planet Earth that’s still going to be a long time and then it’s up to the computer to decide how to do it.
So what they’re kind of hoping now is that the Fold It! game is being introduced as an attempt to tap into sort of a unique or intuitive ability of humans to work with these three-dimensional objects.
Kirsten: Mm hmm.
Justin: Our approach, our strategy in doing it is going to be much different than the computer models.
Kirsten: Right, where a computer model is going to systematically try this, try that, try this, try that, try this, try that, the human brain might intuitively see a pattern that…
Kirsten: …that isn’t apparent immediately.
Justin: Yes. And it’s…
Justin: The game teaches you what to do and it’s going to add difficulty along as you go sort of like any good puzzle video game kind of thing would do.
Kirsten: Mm hmm.
Justin: So away you go and your video gaming for a better tomorrow. And Science is really helping to discover individuals who do have a really innate intuitive three-dimensional protein folding skill. Some sort of like you figure it’s going to be some kid who…
Kirsten: Who folds origami all the time or something.
Justin: Oh, who doesn’t? And who just, you know, plays video games most of the time but gets into this…
Justin: …puzzle game and then suddenly he’s making these incredible patterns and designs that weren’t thought off before in terms of, you know, like how they go together fine. He might be able to actually…
Justin: …see it and then because if you get prodigies to the puzzle game, they’re going to contribute to Science because if they’re successful, if they come up with the…
Kirsten: Mm hmm.
Justin: …and the successful part comes later but right now it’s hard to judge what the successful model, right?
Kirsten: Right. It’s going to get some time to get there.
Justin: But if they’re successful, the computers will then be trained to mimic the human strategies and the process will then be accelerated.
So, what they’re looking to do is further down the road, challenge players to device their own proteins to lock into real world like a real world virus, like an HIV, something that can combine with an HIV protein and unfold it.
There’s also applications to anti-cancer or Alzheimer’s applications with the proteins and enzymes you can create as well as if you’re building your own protein, you might be able to create an enzyme that can be used to break down toxic waste or remove carbon from the air, I mean like there’s a lot of real world applications once they put in the models that you’re going up against.
Right now it’s the training phase. By the next few months – by fall, they’re going to put in like some viruses and stuff and see if people can take them down.
Justin: So the game – plus the game is going to compete with other research groups around the world because the top designs that come out of this will actually be synthesized in a real world lab and tested in Petri dishes.
Kirsten: Well, they have to, yes. The designs that come out have to be tested to see if they actually work.
Justin: Right. And what the people are saying, you know, if we people put this all together and fold it as we can go, I think it’s just fold.it, http\\fold.it. But they’re kind of building is like yes, if your design is the one that they create, based off the design you came up with, then, you know, you get the credit for the discovery. Hey, Nobel Prize is yours, right? You probably have to share it with the creators.
The game is called Fold It! new frontier in Science, a new discipline in Science – we got to come up with a name here, (videogamologist)? Videological gamemomadics? Or simply video it with a Nobel Prize – I kind of like that.
Kirsten: I like that one.
Justin: Nobel Prize and video it, (video), (video) – whatever you call it.
Justin: I’ve got to play a little bit offline because their server’s been down since it launched. I find it very addictive. And it is the mindless time sucking type of activity that you shouldn’t be avoiding except this one is actually in the name Science so go for it.
And I started a group – there’s a group there called minions of twist. So if you go and you sign up to the Fold It! and log in you can join a group that’s the minions of twist. And then when you’re doing your research, it also accounts to some sort of point total as a team all together. So it become a think tank, a brainiac think tank all unto our mini me self.
So go check that out.
Justin: Fold it, fold it, fold it.
Kirsten: It is fold – it’s http://fold.it.
Justin: Fold it.
Kirsten: Fold it. Looks fun.
Kirsten: Great. Well, we have to go to our break and we will be back in just a moment. Stay tuned for more in This Week in Science. Science news coming at you to the radio.
Justin: That song rocks. That’s so awesome.
Kirsten: That’s right. That’s (oka). (O-Science) off of the 2008 Science music compilation CD, which a number of people were able to pick up at the KDVS fund raiser that took place a couple of weeks ago. Thanks everyone for donating. I hope you enjoy your CDs when you get them.
Justin: Mm hmm.
Kirsten: Yes. It’s a great CD. And people have been emailing me, wondering if the CD is still available. It has been taken off of the market for the time being. I want to make sure that the people who donated for the fund raiser that they will special, you know?
They get the CD first and they get to have it for…
Justin: I just got mine today.
Kirsten: …they get to have it for a while because…
Justin: I haven’t even heard the whole thing yet.
Justin: I just got it at the beginning of this. I haven’t been able…
Kirsten: That’s right.
Justin: …to listen to it yet. And all I’ve heard is what’s been bumpered on air.
Kirsten: Bumpered, bumpa, bumpa. It’s a great CD this year.
Kirsten: It’s great. It was – all the bands that were involved, thank you so much for donating your songs. I know that people are going to enjoy them. I enjoy them. I do, I do, I do. And what else do we have to say? Oh, yes. If you have any questions, comments, et cetera, email me at Kirsten@thisweekinscience.com, Justin@thisweekinscience.com.
Justin: I’m the official complaints department.
Kirsten: Yes, that’s right. Yes, keep it to you.
Kirsten: If you have complaints, send them to Justin.
Justin: And you got to put the twist in the subject otherwise it goes immediately to the spamophere.
Kirsten: Yes. Put twist in the subject. It’s wonderful help for both me and Justin so that, I mean I have a filter that puts everything into a TWIS inbox so that I know – I just check that box if – when I’m…
Justin: That’s it.
Kirsten: …going to try and reply at – to twisted-related emails. Yes, so thanks everyone for listening. So far, we have more Science news for until the 9:30 in the morning. And – oh, what’s…
Justin: Wait, where is the guest?
Kirsten: We don’t have a guest here. It’s just us doing Science news but I have a story.
Justin: No, need to get more – need more…
Kirsten: So, antibiotics…
Justin: Sorry, oh yes.
Kirsten: …is something that we – it was a story sent in by (Ed Dire). Antibiotics, that’s something that we use when we’re ill, you get sinus infection, whatever. You know, bacterial infections are tough to kick on your own. Sometimes bacteria tend to get a little feisty and they try taking over.
Kirsten: And sometimes you have to knock them down with medications that are specially created to do battle with the bacteria. There is a third generation antibiotic drug that is called – oh, I cannot pronounce the name of this thing. It’s ceftriaxone is what it’s called.
And so, it’s used because it’s small enough to fit through the blood-brain barrier so it’s able to get into the brain and be able to combat bacterial infections that actually end up in the brain. So, spinal meningitis, other infections of that severity.
When you get a bacterial infection of the brain, it’s really hard to kick it. It’s hard – there are not a large number of drugs that can be used to fight something that gets into the brain because the blood-brain barrier is so, so tight it’s hard to get things into the brain without directly injecting stuff that you…
Justin: You drill.
Kirsten: Yes, drill. Just open it up, inject. Just drill it in there. Yes, you don’t want to do that. So, we have drugs that are able to get – slip through the little, teeny, tiny, tiny cracks in the barrier. We can actually help fight those infections.
So, this is one of those drugs. At Virginia Commonwealth University, researchers have been looking at this antibiotic and other effects that it has once it gets into the brain.
So, in addition to actually helping fight infections, it actually affects nerves in the brain that can get in there. And it could possibly be used to fight neurodegeneration…
Kirsten: …based on glutamate toxicity.
So, glutamate is one of the neurotransmitters used in the brain to send messages back and forth. And sometimes there’s a glutamate transport system and a system of – when glutamate gets released into the synapse, the space between nerve cells, sometimes things go awry and the garbage trucks that come along and clean up the left-over glutamate, you know, the unused glutamate that hasn’t been attached to receptors.
If that goes wrong, glutamate can build up to unhealthy levels. It causes what’s called glutamate toxicity and as a result, nerve cells end up dying because the glutamate makes things sick in there and the nerve cells die away.
Kirsten: And that have negative effects…
Justin: So let me…
Kirsten: …including Alzheimer’s disease, Huntington’s disease, epilepsy, stroke, dementia and malignant tumors.
Justin: Let me try an analogy here just on fly.
Justin: Okay, if you ever had the, you know, the rolling ball mouse and all of the sudden you’re trying to go and it’s just not as effective as it was. Your mouse is like it’s not very responsive. You open up the bottom and you pull all that gunk off of the rollers inside the…
Justin: …mouse, that’s kind of clearing out the neuro pathway there.
Kirsten: Sure. Sure, we’ll go with that.
Justin: That even…
Kirsten: Yes. So there are things that clean it out. And the glutamate transport gets messed up and you want to fix it sometimes but – and so, this antibiotic, ceftriaxone, gets in there and somehow it helps to combat the glutamate toxicity as well. And it seem – and so, the question they have been trying to figure out is how does it do it? What is it getting into?
And so, the team found that it affects a transcription factor called nuclear factor kappa B, NF-kappa B. And that regulates a lot of functions in the brain and other parts of the body. It’s a central molecule involved in regulation of genes that controls cell growth and survival.
Kirsten: And so, they’re able to identify this promoter region that regulates this transcription factor’s activity. And so, the glutamate actually – it affects the NF-kappa B site by mutation and it up regulates this transcription factor and glutamate clean up.
Justin: I’m going to switch analogies. I’m going to say…
Justin: …this is like a neuro colonic. This is now – so okay, Kirsten are you going to tell me what type of infection…
Kirsten: Yes, so the ceftriaxone…
Justin: …do I have to pretend to have to get this prescribed just so I can try it out?
Kirsten: I wouldn’t suggest…
Justin: What do I have to pretend I have got so I can – because it seems like, you know…
Kirsten: No, you’re…
Justin: …I’d like to go get a mental colonic.
Justin: I want to misuse the little bit of information I just got.
Kirsten: That would be horrible misuse.
Justin: Yes, but it would be, you know…
Kirsten: No, because – no, no, no just no. Not even – don’t. Read another story we’re going to move on.
Justin: Oh, lord. I think I want a just a placebo effect alone of thinking that I’d had a mental colonic for my feeling…
Kirsten: Do you feel better?
Justin: It might. It might really…
Kirsten: Okay, let me know how it works for you.
Justin: Okay. So this is great study on self-esteem. I don’t think I’d – did I do this story because this is an old story. This is from my plan B is in the back. I might have done this one already, if so, I apologize.
Well, high self-esteem is generally valued as a good quality. It is important to be happy and productive and I kind of argue with that.
Kirsten: I like it.
Justin: More researchers are breaking down high self-esteem into a finer gradations and starting to understand where and when high self-esteem turns from being a good productive, motivating part of your psyche into something that’s actually negative.
Okay, so in fact, it’s now thought there are multiple forms of high self-esteem only some of which consistently rate to a positive psychological function.
Research by a psychology professor, Michael Kernis from the University of Georgia is added another text to support of the confident man — those with secure, high self-esteem and those who have fragile high self-esteem. So that I can kind of like already see where that goes.
I’m like already like I can see – because then it’s like there’s high self-esteem that’s conceited and delusional versus high self-esteem that’s can still be modest and humble, which I have find humility to be really annoying.
Kirsten: I am the best in the world.
Justin: Yes, like to me that…
Justin: …is keeping – no, that’s – actually I like that. It’s kind of the way I would be because like you keep humility humble, right? You don’t flaunt your humility in front of people. I don’t like people who flaunt their humility, that go out of their way to show that they can be humble. Like if you just did something that’s really awesome, you won the World…
Kirsten: Get back to the story.
Justin: …Cup or you’ve got the trophy and then you’re like, “Yes, you know, I just, you know, I guess I got lucky.” No, no, no, you accomplished something huge, like celebrate it. Don’t give me humility then because that really – that’s flaunting it, that’s not right.
Anyway, put back to the story. So there are many kinds of high self-esteem in the study. And we found that those in which it is fragile and shallow, it’s really no better than having low self-esteem according to Kernis I can never like it, who knows?
They should do phonetic spelling in everything when it comes to names. People with fragile high self-esteem compensate for their self-doubts by engaging in exaggerated tendencies to defend, protect and enhance their feelings of self-worth.
So, I say gosh…
Kirsten: They’re really, really trying to feel like they feel good about themselves and they have to like defend it and it’s not actually a true high self-esteem and that’s sends them…
Justin: Yes, because then if you’re having to go on…
Kirsten: Mm hmm.
Justin: …the attack to basically and some kinds of defending yourself is really attacking somebody else?
Kirsten: Yes, but maybe eventually the longer that you, you know, are good to yours, you know, keep bolstering your self-esteem, maybe eventually that becomes stronger and you don’t need to go on the attack anymore but yes.
Justin: See but that’s not where this is indicating…
Kirsten: No, (unintelligible).
Justin: …because at the other hand, individuals with a secure high self-esteem – I love the way they phrased this – appear to accept themselves warts and all.
Kirsten: Mm hmm.
Justin: I said that because I have so many visible warts that, you know, that makes sense to me to know.
Kirsten: You know, that’s kind of disgusting.
Justin: Hey, no. I accept my warts and all. Feeling that they feel less threatened are less likely to be really defensive or blaming others or providing excuses even when they speak about their past transgressions. They’re just so like, “Yes, I did that. That was – what was I thinking, huh?”
You know, like these findings support the view that the heightened defensiveness reactions show insecurity and fragility and less than optimal functioning rather than the healthy psychological outlook.
So, when folks are feeling good about themselves – when feeling good about yourself basically becomes the prime directive like you have the highest self-esteem so you can feel good about yourself and the heck all with everything else…?
Kirsten: Mm hmm.
Justin: …that’s, I mean I’ve me these people, they’re very delusional. They’re, I mean I could, you know, they will feel good…
Justin: …about themselves and have high self-esteem no matter what activity they are in, no matter what they’re doing.
Justin: And it’s like a really weird…
Kirsten: You have it questioning it.
Justin: Yes. And then if you, you know, if you say anything like, “Gosh, you know, the way you are beating that small child with the walking stick of that little, old lady,” you know, and then they come out and attack you like, “Well, you don’t know what it’s like to be me. You don’t understand…
Kirsten: Oh, no.
Justin: …when it comes up where you have to be the child with an old lady’s walking stick. You don’t get it.” So, okay, now feel good about yourself. So high – and basically…
Kirsten: Mercury, the planet…
Justin: Wait, wait , wait there’s the one – okay, we’ll get to Mercury. But the basic point of is you can be completely – it’s the same as having low self-esteem. They have the same patterns of really people who don’t feel good about themselves…
Justin: …all the time…
Justin: …even though they’re – I know that’s…
Kirsten: I got it.
Justin: You got it, you know.
Kirsten: The planet Mercury, the closest of the planets to the sun in our solar system is a little, tiny planet. It has a strange magnetic field that really I had a problem describing and understanding to this point.
Justin: Mm hmm.
Kirsten: You know, like Earth, we have our magnetic field, what we believe it comes from a core of iron in the center of our planet, magnetic material that’s been magnetized in, you know, switches around from every 20,000, 60,000 odd years.
Justin: Switches poles.
Kirsten: Switches poles, you know, hell, but it’s there. We have a magnetic field that are magneto sphere keeps us protected from a lot of that radiation that comes in from out of space. You know, it’s a wonderful thing to have. It keeps our atmosphere, you know.
However, Mercury has this magnetic field that moves around. And it’s very, very strange and it’s been hard to describe. But because it has a magnetic field, we believe that Mercury’s core is made mostly of iron. However, it’s been modeled that I think it also contains sulfur which lowers the melting point of the iron so that the core instead of being a solid core is actually molten so it’s constantly sloshing as the planet moves around in its orbit.
So, it got a sloshing core. And now, recently, Earth-based radar measurements of Mercury’s rotation revealed a slight rocking motion. And so, that’s why we’re thinking it’s partially molten.
And in the absence of this kind of any seismological data says graduate student Ben Cheng, the lead author of a paper that’s been published recently and was funded by the National Science Foundation, he says we know very little about its core. And so, the researchers used an apparatus to kind of model what was going on and to study the melting behavior of this iron-sulfur mixture.
And so, in their experiments, they took an iron-sulfur sample and they compressed it to a particular pressure and heated it to a very specific temperature to try and mimic the conditions that are assumed to be at the center of Mercury.
And then, they like they cooled it off really fast and they sliced it and they analyzed it with a scanning electron microscope to see what was going on in the middle of this ball of iron and sulfur that they had just created.
So, they find that there’s a separate of the solid and the liquid phases and the sulfur content in each phase. And so, based on the experimental results, they’re able to figure out what’s going on. And they think that the iron atoms in the outer core condensed into these little flakes that then fall kind of like snow falling through the atmosphere of Earth but this is in the core of the planet that these flakes of iron fall from the outside to the inside of the planet.
And as it sinks and the lighter sulfur-rich liquid rises, convection currents are created that then power the molten core dynamics and produce a weak magnetic field on the planet Mercury.
Justin: Mm hmm.
Kirsten: It’s really cool. So based on these little experiment – no, you know, little there’s probably like heavy machinery involved in this but this experiment here on Earth…
Justin: Oh, yes because they got to recreate a whole planet for a model and that’s not easy.
Kirsten: Yes, so they’ve created this model for how Mercury’s magnetic field is produced.
Justin: Super cool.
Kirsten: It’s really cool work. Congratulations on that. And they work at the University of Illinois and Case Western Reserve University and it was published in Geophysical Research Letters if you’re interested in trying to find that paper.
Justin: Mm hmm.
Kirsten: Yes, it’s pretty cool stuff.
Justin: Well, I’m like out of story so this…
Kirsten: Well, I guess hot stuff actually, molten cores of iron.
Justin: There’s – I’ve got stories that I haven’t read yet. Apparently, we found a piece…
Kirsten: I have another.
Justin: …of missing matter like…
Justin: Like I don’t know. It’s like it’s a nine because this story doesn’t really – the story that I’ve got here only gives you like a history of the fact that there’s dark matter and we’re still missing 90% of the matter in the universe…
Justin: …but it doesn’t really give a great explanation of what this missing cosmic matter that we just discovered is. But it’s baryonic.
Justin: It’s something that has mass. And it apparently, spider webs between galaxies.
Justin: And it’s super, super hot.
Kirsten: That’s cool.
Justin: Yes, but other than I couldn’t gleam from this is – it’s like breaking…
Justin: …scientific news. I think it’s from the – oh, it’s at the Max Planck folks. Yes, the Max Plank Institute of extraterestial physics.
Kirsten: That’s fascinating.
Justin: Has found this missing mystery stuff that they thought existed that says, ultra thin gas that’s super, super hot and forms sort of a spider web network between galaxies and galaxy clusters.
Kirsten: Nice and new thing. Researcher studying E. coli at Princeton University in New Jersey has found that these bacteria can learn.
Kirsten: They have a form of memory that is similar kind of to Pavlovian conditioning and it occurs over generations.
So, as opposed to the way we learn when our single organism self, we learn from experiences and remember them and connect on them later.
Justin: Well, perhaps.
Kirsten: For some people or animals do, yes.
Kirsten: And so, this researcher – his team took – they used computer simulations first but they used live E. coli to see if they could show learning skills in the laboratory. And they took lab dishes of E. coli, so these Petri dishes that contain the bacteria at a particular temperature, 25 degrees Celsius and then they shifted them to 37 degrees Celsius, so made them a lot hotter.
And then when they shifted them to 30 degrees Celsius they removed 20% of the oxygen in the environment. And they did this over and over and over again over a hundreds of generations until they found…
Justin: So sort of teaching them if the temperature changes…
Kirsten: The oxygen is going to go down.
Justin: …your oxygen level is going to change too.
Justin: So be ready.
Kirsten: And they were mimicking what actually happens when a bacteria on food goes into your mouth and then ends up in your gut. So this is the same…
Kirsten: …so it’s going from environmental temperature to body temperature to low oxygen content in your gut. So it’s basically mimicking a natural phenomenon. And they found that these microbes changed – after hundreds of generations, they started changing their metabolic activity when they were put in that hotter temperature. So, they learn over hundreds this, you know, basic kind of learning but, you know, it’s at…
Justin: It’s good to know that but…
Kirsten: …instead of at the neural level in the sense of like organisms…
Kirsten: …it’s at the genetic – it’s like learning at the genetic level. Fascinating.
Kirsten: But we are done. We don’t have anymore time. We have to go away now. We’ll be back next Tuesday with more Science for you.
Justin: Fold it!
Kirsten: Fold it! And also, we are going to be – Justin and I are going to be at the BayCon convention…
Justin: Oh, yes.
Kirsten: …in Santa Clara in two weekends of a memorial…
Justin: It’s like a sci-fi…
Kirsten: It’s a sci-fi convention
Justin: We signed up for this thing. I thought we’re getting a press pass to go and check out this sci-fi convention.
Kirsten: Yes, we’re actually presenting.
Justin: I’m on my panels. I’m like supposed to explain how to survive a zombie attack…
Justin: …like apocalyptic zombie, a meteor or alien invasion attack. I’m supposed to teach you how to survive the aftermath. It’s going to be pretty straightforward. I’m just going to teach you how to loop. I’m going to take…
Justin: …but I don’t know how that happened because I have – I’m on there with like a navy seal and some sort of Science fiction writer and then…
Justin: …I feel like I have no idea why I’m there. Okay, so if…
Kirsten: Yes, but – so, we’re going to be at this BayCon conference. Come find us if you’re planning on heading up there. It’s BayCon.com, I think it’s…
Justin: San Francisco this coming weekend.
Kirsten: It – no, it’s a memorial day weekend.
Justin: Isn’t it this coming weekend? No, it’s the weekend after that.
Kirsten: Next weekend. So, yes.
Justin: I want to show up at the wrong time.
Kirsten: Yes, great. And that’s it for us.
Justin: If you learned anything from today’s show, please remember…
Kirsten: It’s all in your head.