IRA FLATOW, HOST:
This is SCIENCE FRIDAY; I'm Ira Flatow. The 2012 Nobel Prizes were announced this week in Stockholm, and groundbreaking research on stem cells, cloning, cell receptors and quantum optics, yeah, claimed the honors this year. The physics prize was awarded to French physicist Serge Haroche and American David Wineland of the National Institute of Standards and Technology and the University of Colorado.
The two scientists won for their work in quantum optics, investigating how atoms interact with particles of light, and their research on these bizarre quantum effects could give rise to super-precise clocks and powerful quantum computers. Here to help us understand more about this wacky world of quantum optics is Seth Lloyd, professor of mechanical engineering at MIT in Cambridge. Welcome to SCIENCE FRIDAY.
SETH LLOYD: Howdy, Ira.
FLATOW: Let's start with what they won for. I mean, they won for being able to make a very precise, at least Wineland did, quantum clock. Would that be correct?
LLOYD: Well, so they won for using light to interact with matter and with atoms and having the light behave in a quantum mechanical fashion and the atoms behave in a quantum mechanical fashion. I kind of think of them as some kind of like, you know, atom wranglers, you know, herding those photons and those atoms around and getting them to strut their quantum stuff in the right way.
FLATOW: And so you could actually make use of those atoms?
LLOYD: Exactly, so, you know, people have been addressing atoms with light for a long time, like the laser, the previous conversation that you were having, lasers and laser diodes. You know, people have been making atoms and light interact forever. But they have had a hard time getting them to work together in larger and larger numbers.
And I'd say that Serge Haroche and Dave Wineland are, you know, master atomic wranglers, wrangling those atoms and light and getting those dogies, those quantum dogies along the trail to build better clocks, more sensitive detectors, all kinds of funky new stuff.
FLATOW: And so by being great quantum cowboys, how can they test the laws of quantum mechanics using techniques that they did?
LLOYD: Well, so an example where they got a lot of quanta to behave in a very, particularly funky way is - comes from famous quantum mystery, and a quantum example that Erwin Schrödinger came up with in the 1930s. And he noted that well, you know, it's OK for an atom or a particle of light in quantum mechanics to be two places at once, you know, to be here and to be there simultaneously.
Yeah, it's kind of hard to imagine, but, you know, it's just an atom after all, it's very tiny. But if you could somehow couple this to something bigger in the world so that atom over here set off a train of events that ended up breaking a vial of poison and killing a nice cuddly cat, whereas atom over there left the cat alone, then you could create a funky quantum state of cat alive and cat dead at the same time - the so-called Schrödinger's cat paradox.
And, well, I mean, let's suffice it to say that if the SPCA had their way, they wouldn't let this happen.
(LAUGHTER)
LLOYD: But both Wineland and Haroche managed to get not full cats, but basically herds of photons, particles of light, and herds of phonons to behave in this way. So the whole herd of photons was, you know, over here and over there simultaneously, or the phonons were over here and over there, simultaneously.
They called these things Schrödinger's kittens. But they are - you know, though they're not, you know, full-blown cats alive and dead at the same time, they are still pretty macroscopic things in the quantum sense, being here and there simultaneously.
FLATOW: And so what is the connection, the practical use that they turned these into ultra-precise clocks?
LLOYD: So it turns out that these kinds of Schrödinger's cats and Schrödinger's kittens are exquisitely sensitive to their surroundings. So Haroche pointed out that, you know, if you're interacting with the environment that having a Schrödinger's kitten, where you have a whole herd of photons over here and there simultaneously, that, you know, it interacts N times faster or more powerfully with the environment, where N is the number of photons, than it would if it were just some ordinary, you know, non-funky quantum state.
And Dave Wineland and his colleagues at NIST use this same effect to construct atomic clocks that were exquisitely sensitive to time. So somehow having a Schrödinger's cat state of atoms in an atomic clock makes that state able to chop up time into much more precise bins than it could if you had just an ordinary classical kind of state.
FLATOW: These are not the kind of clocks we're going to have on our mantelpieces, I imagine.
LLOYD: Well, ironically many of us have them in our pockets, because this is the basis for GPS. So if you have a smartphone that uses GPS, by gum, you actually really have, effectively, an atomic clock in your pocket because the GPS system takes signals from atomic clocks at NIST, the National Institute for Standards and Technology in Boulder, and these clocks - atomic clocks hurdling through space and broadcasts them to your GPS receiver to tell you where you are in space and time, to an accuracy of a meter or so in space and to the accuracy of a billionth of a second in time.
So, you know, I mean, you've actually got one already.
FLATOW: All right, I'm glad to hear that. We can all be part of the Nobel party this week, then.
(LAUGHTER)
LLOYD: Exactly. At least if there's a proper app for it.
(LAUGHTER)
FLATOW: All right, Seth, thanks for taking time to talk with us today.
LLOYD: Thank you very much, Ira.
FLATOW: Seth Lloyd is professor of mechanical engineering at the Massachusetts Institute of Technology in Cambridge.
Continuing on our look at the newest Nobel Prize winners, this year's prize in medicine is shared by British scientist John Gurdon and Japanese scientist Shinya - Shinya Yamanaka. This groundbreaking research has changed our understanding of how cells and organisms develop. In 1962, Gurdon became the first person to clone an animal, after he produced tadpoles from the cells of a mature frog.
Yamanaka expanded these findings a couple of decades later, by pinpointing how adult cells could be converted back to primitive stem cells. And here to clue us in on the cloning and the work by Gurdon and Yamanaka is David Scadden. He is co-director of the Harvard Stem Cell Institute at Harvard. He's joining us today from Cambridge. Welcome to the program.
DAVID SCADDEN: Thank you very much.
FLATOW: Interesting stuff and deserving, David?
SCADDEN: Oh absolutely. I think this really turned the sense - the identity of cells on its head, actually.
FLATOW: Well, tell us why.
SCADDEN: Well, you know, cells in general are thought to go from a very unspecialized state, like a stem cell, to become a more highly specialized cell like the cell that might be the liver cell or skin cell or brain cell that we think of as sort of the business end of an organ.
And that was thought to be something that happened in kind of one direction, that cells got more mature and more specialized, just to some extent, like we do as people. And so it had an intuitive logic to it. And what Gurdon showed, and then finally Yamanaka showed anyone, actually any laboratory essentially in biology can do any day of the week, is that you can actually reverse that. You can rewind and get cells to go all the way back to becoming a very primitive cell type with essentially unlimited capability.
FLATOW: Were people kind of skeptical of Gurdon's work when it happened?
SCADDEN: Well, you know, it's interesting. Gurdon was looking at a very different kind of question. Gurdon was working in the late '50s, and the structure of DNA had just been defined in the '50s, and people couldn't measure more than just the rough amount of DNA.
It was known that it was probably the stuff that was the language of life, but how it actually got communicated into the way a cell functioned wasn't clear. And so it was thought that maybe during the specialization process of a cell that perhaps parts of the DNA changed. Maybe some of them got kicked out, maybe some of them got replicated, and so Gurdon said, well, maybe I can test that by taking the nucleus, which he knew contained the DNA, and putting it into an unfertilized egg and seeing now whether the DNA that had previously told the intestinal cell of the frog to be an intestinal cell, to see if it could turn into something else.
And the egg educated it to go all the way back and actually become anything, and it became a whole frog.
FLATOW: Wow, and we really never talked about much of this, or heard much about this, until the cloning of Dolly by Ian Wilmut.
SCADDEN: Exactly.
FLATOW: Yeah.
SCADDEN: So decades later, in part, because, I think, of the nature of the question being asked, and I think Gurdon himself didn't really think of it as much in the terms of it being a cloning process as a demonstration that DNA is stable. And he published it in a fairly obscure journal. He was a young guy and, I think, you know, kind of fell off the map. It was something that was interesting, in frogs, for developmental biologists, but it didn't really have clear implications for people.
FLATOW: Mm-hmm. And so how did Gurdon and Yamanaka's work influence the research being done by you and your colleagues at Harvard Stem Cell Institute?
SCADDEN: Well, what Yamanaka showed was that that process of essentially rewinding the history of a cell was something that could be reduced to a fairly straightforward practice. And by that I mean we can actually grow a cell from any one of us, that you can put on a plate. It grows in a petri dish. And you can actually buy a kit that you add these components, and suddenly the cell will reverse its state, and it'll turn back into something that could be anything.
So, you know, in its most optimistic way of thinking about this, you can envision that this then would become a tool kit for any one of us to have cells in the freezer that our immune system would recognize as our own and could be, potentially, used to replenish cells that got damaged in disease or just by age.
FLATOW: Yeah, interesting. One last question for you. If cloning a mammal was such a huge breakthrough, was Ian Wilmut, who cloned Dolly, you think, passed over for a Nobel?
SCADDEN: Well, you know, Ian Wilmut's contribution was huge, but in reality, I think that his was an extension of Gurdon's early work. And Yamanaka really carried that forward to a much more practical dimension. So, you know, it was almost impossible to do much more with the nuclear transfer. And certainly what Wilmut had done could not be done, to date at least, in a human.
FLATOW: Yeah, yeah.
SCADDEN: But what it could be done with Yamanaka is that we could do this for anybody, and we could do it now and create disease models. It's been a huge explosion, from Yamanaka's first experience to what we do in a laboratory today.
FLATOW: Well, congratulations to them.
SCADDEN: To them. Absolutely. To all of us, we hope.
FLATOW: All of you, yes. You know, on the shoulders of giants, as they say.
SCADDEN: Exactly. And hopefully to the benefit of all mankind.
FLATOW: All right, David. Thank you very much.
SCADDEN: Thank you, Ira. Take care.
FLATOW: David Scadden is a co-director of the Harvard Stem Cell Institute at Harvard in Cambridge.
Finally, in our Nobel roundup, the chemistry prize, this year's prize is shared by Robert Lefkowitz at Duke University Medical Center and Brian Kobilka at the Stanford University School of Medicine. The two scientists discovered how our bodies sense our environment and communicate that information to our cells.
The Nobel winners deciphered how certain cell receptors react to outside signals. And that research, of course, has helped drug companies develop more targeted drugs, making them more effective and with fewer side effects. Here to talk about it is David Agus. He is director of the USC Center for Applied Molecular Medicine at USC in LA. Welcome to SCIENCE FRIDAY.
DR. DAVID AGUS: Thank you so much. Great to be here.
FLATOW: A deserved Nobel Prize?
AGUS: Oh, yeah. I mean, this was a fundamental discovery that affected how we think about our humankind and also drug development.
FLATOW: Tell us about that.
AGUS: You know, what this was was a sensor. So we knew before that there were proteins in the body that tell cells what to do, but we didn't know how it worked. So Lefkowitz and his team did something very clever. They took these proteins, and they attached radiation to it, iodine radiation. And they traced them to the cells, and they pulled back, and they got the receptors, which are these sensors.
And these sensors are involved in both how the eyes work, and how the nose works in smelling, and how tastes work. And about 40 to 50 percent of all drugs now target this class of receptors.
FLATOW: Mm-hmm. This is SCIENCE FRIDAY from NPR, talking with David Agus. How long ago was this done?
AGUS: This was done about 25 years ago.
FLATOW: And, you know, because that's all we talk about today, you know? It's such a basic discovery that - as you say, that's what we talk about all the time as if we knew about it forever.
AGUS: Yeah, we knew they existed. But actually pulling them down and showing what they were and then, most importantly, showing their structure and that they were druggable, we can make something that could turn them on or turn them off.
FLATOW: Hmm. And the receptors, are they located right on the cell itself?
AGUS: Yeah. They're right on the cell, and then these proteins bind them. They change the shape of those receptors, and that change in shape sends a signal down to the nucleus, telling the cell what to do.
FLATOW: And what made them - what was the light bulb that went off in their head to be able to actually make, you know, to make this discovery?
AGUS: I think it was the fact that we had used - or science had used radiation, iodine, attached to other things before. And so it was taking a methodology from one field and attaching it to this new one. We all knew these proteins were there. Then somebody looked inside the cell and couldn't find them, so that implied that there had to be something on the cell's surface. So they went about with very clever methodology and showed that it existed.
FLATOW: Is this something like knowing that there is a DNA molecule structure, but you don't know what it looks like until you discover it, but this happens with receptors in this case?
AGUS: Oh, exactly. Back in the '50s, there were all these clues about DNA and about its periodicity, all kinds of things. And then Crick and Watson put it together and built the double helix.
FLATOW: And these folks did it with the receptors.
AGUS: They did it with a particular kind of receptor called G protein-coupled receptors, GPCRs, that turn out to be really the foundation of much of drug development in this country.
FLATOW: Give us a little idea how the receptor works with the drug. How do they latch on?
AGUS: So these drugs - and they're very common drugs that you and I all use - are anything from Benadryl for allergy. They're the Zantac and Tagamet for your stomach. They're drugs for motion sickness, drugs for blood pressure and heart rate. And what happens is, is that molecules in the body, these signaling molecules, they - these receptors sense something.
So these (unintelligible) bind there, and these drugs, they block it, and so they cover the receptors. So you can't get in there to turn it off, or they act like they're the molecule and get into that key - in a sense, like a lock and key - and turn it on.
FLATOW: So it really is, it's sort of a jigsaw puzzle.
AGUS: No question about it. It's just the change in shape. I mean, the whole body is about small changes in shape.
FLATOW: You know, when I hear about this, when I've heard about it for years, I'm just fascinated by the ability of the molecules to find the receptors. How do they find the receptors to lock on to them?
AGUS: You know, it's what we call contextual, right? The cell has to be in the right place. That molecule has to be there. And the body is so good at segmenting things and getting things to the right place, because these molecules, if they got to the wrong place, they could turn on the wrong system. You know, things like adrenaline, when you and I get excited. If too much of it went to the brain, we would go crazy. So the body built in a barrier for the brain and keeps it in certain spots so that we respond appropriately.
FLATOW: And how does - so how does this discovery influence your work, quickly?
AGUS: Well, I'm a cancer doctor. So, you know, to me, it's identifying what's going on in a cancer, what is that on switch. So many of these on switches are this kind of protein, and we can now develop something to block it and turn it off. So it allows us to do targeted therapy, which is really going to be future of cancer therapy.
FLATOW: Yeah. And it may be different for every single person.
AGUS: No question about it. And technology now, gene sequencing, which is going to be hundreds of dollars to sequence a cancer, will allow us to target in an individual what's going on in them.
FLATOW: Wow. Individualized medicine.
AGUS: Yup.
FLATOW: All right. Thank you, Dr. Agus, for taking time to be with us today.
AGUS: Thank you.
FLATOW: David Agus, director of the USC Center for Applied Molecular Medicine at USC in Los Angeles. We're going to take a break. When we come back, we're going to switch gears and talk about the Mars rover Curiosity. Strange doings going on there on Mars. Bright shiny object in the soil. If you want to know about it, just stay with us. We'll be right back after this break.
I'm Ira Flatow. This is SCIENCE FRIDAY from NPR. Transcript provided by NPR, Copyright NPR.