Nature Podcast

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Adam Rutherford: Coming up, optimism in the face of a crowded planet from economist Jeffrey Sachs.

Jeffrey Sachs: I actually feel the enlightenment vision that science that can be deployed for the human betterment and human purposes to be even more true today than ever.

Kerri Smith: And ice, ice baby!

Geoff Brumfiel: It's an unusually warm day in Cambridge, and if I'm completely honest about it that's one of the reasons I'm standing in the British Antarctic Survey's freezer. The other is a little sliver of ice, barely a millimetre thick.

Kerri Smith: This is the Nature podcast. I'm Kerri Smith.

Adam Rutherford: And I'm Adam Rutherford. First this week, while much is known about the vertebrate eye with its squashy lens, and the light-sensitive units that make up the compound insect eye, another class of eye remains rather more mysterious. That type belongs to the cephalopods including squid, octopus, and cuttlefish. The paper in this weeks' Nature reveals the way that these eyes process visual signal differs from how vertebrate and compound eyes do it. I've got developmental biologist and pharyngula blogger, PZ Myers, on the phone. He is also a major cephalopod enthusiast. Hi PZ! Nature 453, 363–367 (15 May 2008)

PZ Myers: Hello!

Adam Rutherford: So, let's get a little bit of background. Although they look similar, squid eyes are qualitatively different from vertebrate eyes. Can you tell us how?

PZ Myers: Oh! It's in many different ways. The general structure is the same. You know, you've got a spherical ball with a lens at one end and it focuses images on a retina, but the retina of cephalopods is inverted relative to ours, it's got a different, sort of, layering.

Adam Rutherford: So, the arrangement of the lens is different from vertebrates as well as the retina.

PZ Myers: Yeah! There is differences in gross structuring, you know, how the lens is shifted around, also little things like, you know, we have a discrete optic nerve that comes off the back of the eye and they just have a whole little network of neurons coming off and later merging into a single optic nerve. So, they look kind of similar on the outside, but when you start poking around, pulling them up, looking at them in structure and in detail, they are very different.

Adam Rutherford: And the inversion of the cephalopod retina, so they have the photoreceptors closest to the light source, which is the opposite way around from our own eyes, in some ways, that makes more sense design wise.

PZ Myers: It makes more sense optically. You know, if you've got a structure that has the goal of capturing light, you want the light sensors facing the light. You could argue that physiologically there are other things that make it all right for our eyes to be inverted, things like being able to embed the photoreceptors in the retinal pigmented epithelium and so forth and making them more readily available to nutrient flow from the blood system, but optically, yeah, our eyes are a mess.

Adam Rutherford: So, in this new paper by Murakami and Kouyama reveals another rather unusual characteristic in the key protein in photoreceptors that begins the process of phototransduction that is how photons get converted into electrical signals in the brain. So can you tell us about what they've found?

PZ Myers: What we have is a little cascade of events that occur to turn a photon into a change in membrane potential and the first event is the absorption of photon by retina with molecules embedded in a big protein called opsin. They have a different opsin than we have. Well we actually have the same kind of opsin that they do, but we don't use it in our photoreception, we use it detecting circadian rhythms. So, anyway they have this opsin of a particular kind and then what happens is the opsin is going to undergo a conformational change and has to nudge another protein, a G-protein, and a G-protein then does the work of going around and activating these other enzymes that leads to the change in membrane potential. I kind of like to compare it to somebody standing on a hill, that's our opsin and you see something and you don't have a lot of strength, but what you can do is you can may be push on one little boulder and the boulder then is comparable to the G-protein and then the G-protein or the boulder will go tumbling down the hill, it will knock over other rocks and get an avalanche going. We have an opsin that is specialized to activate one kind of G-protein. Cephalopods have an opsin that they use that is specialized to activate a different kind of G-protein and this has consequences in where the avalanche will occur, both of them cause the avalanche all right, but they have different consequences downstream. So, for instance in us, one end result is that when light strikes our photoreceptors, we close the sodium channel and that means we actually have a decrease in activity in our photoreceptors whereas in cephalopods, they open a channel that causes an increase in current and it causes a depolarisation of the membrane.

Adam Rutherford: So they've demonstrated – you just explained how squid rhodopsin is structurally different and functionally different from vertebra opsins and this new structures increases our understanding of the mechanisms by which phototransduction happens in squid retina. What does it mean for understanding how a squid actually sees?

PZ Myers: Well, what it is doing is it is giving us a clear picture of signal transduction mechanisms that are going on there. This is all very remote from things like perception, how the squid can actually, you know, visualize something in its environment, but I think what is particularly interesting is its also telling us how squid eyes have diverged from vertebrate eyes over 600 million years of evolution that here's this novel feature in their proteins that is specifically for this one particular function and we can get a clear picture of the differences between our kinds of eyes.

Adam Rutherford: PZ Myers who blogs at Coming up later in the show, we'll be finding out which anti-flu weapons we will be needing in our arsenal should there be a pandemic. These outbreaks are just one of the problems made worse by large numbers of people sharing a small amount of space, something that our next guest has been writing about.

Kerri Smith: That's right. Economist Jeffrey Sachs dropped into the pod this week to talk about his new book, 'Commonwealth: Economics for a Crowded Planet' with Chief News and Features Editor, Oliver Morton

Oliver Morton: I think one of the striking things, Jeff that you say very early on in the book is that the great crisis point is that we have a unified global economy and a divided global society and well as the big question is how can we use the first of those things to fix the second?

Jeffrey Sachs: I think the key is better understanding of the unique situation we find ourselves in. The world is now so crowded. The extent of resource use is so remarkable and unprecedented that we are putting pressures on the physical environment and on each other in ways that have never occurred before at this scale. Of course, the point of the book is to say if we don't understand the mechanisms of what we are doing and then address them, the consequences will be dire, at the same time, the very technological prowess that allows us to have the 70 trillion dollar world economy also allows us to find correctives to the problems that we are creating and so I believe that there is a way out that is not dire. This is not an end of the world book, it's only a warning that we have to change course.

Oliver Morton: It is noticeable that in the period from I suppose the early 1980s onwards, research and development in both agriculture and some of them, I think will come onto energy stagnated quite dramatically. Why do you think that was and do you think we will have a realistic chance now of turning that around.

Jeffrey Sachs: I think that there is stagnation in two senses. One is the overall levels of funding tended to go down, but perhaps even more pertinently funding of government fell precipitously, so the public sector funding went down. Why is this? Well there were temporal issues like the temporary decline of oil prices; it seems like a long time ago, but in the 1980s and early 1990s oil prices were low. People said, "Let's go back to fossil fuels" and they forgot all about the overall global need to develop alternative energy resources, so that was very short sighted. There also was a very mistaken privatization of science that took place in these applied areas, where it was said, let the private sector do it, let private sector run ahead on agro-biotechnology, let the private sector invest in energy, we don't really need government to do it, and this is a huge mistake.

Oliver Morton: There is some feeling in some circles that there is a real conflict between the two of the different agendas that you are pursuing. The climate change agenda and the development agenda. How do you respond to that feeling that as people get richer historically, the climate change problem gets worse?

Jeffrey Sachs: If we have continued rapid growth of the world's economy, which we want from a development point of view, I work every day for that. If we have that with our current technologies, we cannot meet the climate change challenge. So, in my view the essence of the climate change challenge is how to combine the very legitimate desire for economic development with the imperative of reduced emissions. I believe we don't have right now the technologies to do that. Just to take the African context, its absolutely a direct arithmetic point that a small part of the Sahara receives enough insulation to actually power Africa to a very large extent by solar power without any emissions essentially, yet this won't happen without a significant technological effort for the simple reason that solar power right now, whether its photovoltaics or its concentrated solar thermal power is perhaps four times more expensive than a carbon-based approach.

Oliver Morton: Is having economists involved in that absolutely vital?

Jeffrey Sachs: I think it is and I'm grateful to have a seat at the table. I think the scientists often have said "we have solutions," the engineers say, "we have technologies," but they do not know how to get those technologies developed, demonstrated, diffused and as part of our broader societal life and economist started the other end, often which is about budgets scaling, market incentives and so forth but often know very little about the reach into basic mechanisms and technologies and so I do see there being an inherent good fit to essentially implement what I've summarized often as R, D, D and D that the challenge is Research, Development, Demonstration, and Diffusion of effective technologies.

Oliver Morton: For someone who works in what's sometimes perhaps clichedly referred to as the dismal science, you seem to manage to keep quite a remarkable level of optimism.

Jeffrey Sachs: I actually feel from the first days of my intellectual training and perhaps temperament that the enlightenment vision that science can be deployed for the human betterment and human purposes to be even more true today than ever. Of course there are grounds for worry and the book is filled with worries, but it also says that there are reasons for us and deeply evidence-based reasons to believe that solutions are out there and that we can choose to take them.

Kerri Smith: Reasons to be cheerful there, from Jeffrey Sachs. 'Commonwealth' is out now, published by Penguin, and you can listen to the full length interview in our Podcast Extra, that's on the same RSS feed as this show or on our web site at


Adam Rutherford: Now in contrast to Sachs' optimism, it falls to certain scientists to plan for the worst and where disease pandemics are concerned, we might need to change our contingency plans, as Charlotte Stoddart has been finding out.

Charlotte Stoddart: In 1918, the world experienced the most lethal outbreak of infectious disease ever recorded. The culprit was a particularly nasty strain of the flu virus, H1N1. Descendants H1N1 and its relative, the infamous H5N1 or avian flu virus, has the potential to mutate again and to cause another pandemic. To combat this threat, governments are stockpiling Tamiflu, one of two drugs that target the viral enzyme neuraminidase. But recently mutant viruses that are resistant to this drug have been appearing. To find out more, I went to meet John Skehel whose team at the National Institute of Medical Research in London have been looking into the molecular basis of the mutation. John first explained to me how Tamiflu works against non-mutant flu strains. Nature advance online publication (14 May 2008)

John Skehel: All viruses have proteins that recognize compounds of the cell surface. Well, it turns out that the receptor that influence the viruses use ubiquitous compounds of cell surface molecules, its sialic acid and as you can guess, neuraminidase is the enzyme which is the target of these drugs and its job is to remove all the sialic acid from the infected cell surface, so the newly made viruses instead of binding onto the cell that they've already infected are released and allowed to spread to infect other cells. So, basically what these antiviral drugs do is they block that process of release and in the presence of the drug, the newly made viruses remain stuck to the initially infected cell and the infection stops at that stage.

Charlotte Stoddart: With antivirals as with as antibiotics there is always the worry that your target germ will evolve resistance to your drug, but in the case of Tamiflu, researchers thought that any mutation that made viruses resistant to the drug would also prevent neuraminidase from doing its job properly and so stop the virus from spreading.

John Skehel: If the mutation influences part of the enzyme active site, then automatically, as a consequence of that it has been proposed that the enzyme is less active and as a consequence, the virus containing that mutant enzyme will be less viable. People have thought if you get a mutation, which causes drug resistance, okay that's one consequence of the mutation, but the other consequence may well be that the activity of the neuraminidase is impaired and they were taking some sort of encouragement from that.

Charlotte Stoddart: Unfortunately it turns out that these mutant viruses are viable. Last year, researchers in Memphis, Tennessee reported that mutant H5N1 viruses could be just as pathogenic as their non-mutant cousins as John explained.

John Skehel: In the H5N1 viruses, they found that this mutation didn't jeopardize virus infectivity very much at all and in fact what was worse, what they observed was that in mice, the resistant viruses were just as pathogenic, so that was against what had been hoped for.

Charlotte Stoddart: What's more, drug-resistant viruses have also been found in H1N1, the strain that was responsible for the Spanish flu pandemic almost one hundred years ago. Descendants of the Spanish flu virus have been circulating in the human population since the mid 1970's.

John J. Skehel: Well, the observations that were made about the H1N1 viruses this year is that a reasonably large percentage of them contain this mutation in their neuraminidase and as a consequence were resistant to Tamiflu.

Charlotte Stoddart: These findings together with the work that John and his team have done to explain the molecular basis of the drug resistance suggests that Tamiflu alone will not be an effective weapon against any future flu pandemic. So John is advising governments to augment their stockpiles of Tamiflu with the other neuraminidase inhibitor, Relenza, which their study shows, is still effective against mutant viruses, but better still says John.

John Skehel: What we would really like to have is some other compound, which targeted some other compound onto the virus, and then you could use these drugs in combinations like has been shown with HIV. With the use of combination of drugs, they decrease these frequencies of isolating resistant viruses. So, we advise the governments to certainly stockpile both neuraminidase inhibitors because that's what you've got, but support people who are in the business of trying to develop other drugs.

Charlotte Stoddart: Developing these other drugs could take another 5 to 10 years says John, but the threat of an H5N1 pandemic is certainly spearing on flu research and so it could have a more robust armoury of drugs available much sooner.

Kerri Smith: Charlotte Stoddart there. Scientists and politicians were hoping that the UK government will take their advice this week on new laws that would allow the creation of hybrid embryos for research. Mike Hopkin went to the UK parliament on Monday.

Phil Willis: At the end of the day, unless you find we allow all the research to develop we will not know the answer because we do not know where the next breakthrough will come and the reality is that this bill today is about whether science should progress or whether in fact we should limit science. My answer is quite simple, unless we allow science to progress and to challenge science, we will never know.Well done!! (claps)

Michael Hopkin: That was British politician Phil Willis speaking at an open air rally held in London this week to support new legislation governing work on human embryos and fertility. Although controversial, the new rules look set to be approved allowing the creation of human-animal hybrid embryos in UK labs, which could lead to new stem cell lines for the study of genetic diseases. The legislation also addresses the issues of time limits for abortions and whether all female couples can be allowed to have children via IVF. Another politician supporting the new bill is liberal democrat MP Evan Harris.

Evan Harris: Well, I was very keen to support this show of support from patients and patient groups, scientists and doctors because far too often when we are debating this sort of legislation, the only people outside parliament are the people that I think that are minority view, I should say a few, which I expect that are minority view which were against all embryo research, essentially all IVF and women's access to abortion full stop. The legislation is imperfect, but it's pretty good and I think that opposition MPs like me should still support for a government bill that is generally on the right footing and I'm delighted that patients and scientists have joined us today in that.

Michael Hopkin: The bill represents a broadening and updating of previous rules governing embryo research to accommodate new lab techniques.

Evan Harris: Well, firstly this isn't a very large extension of what was passed in 1990 when embryos were allowed to be created or spare embryos from IVF were used for research. In 2001, there were new regulations allowing such embryos to be used for stem cell research, thinking of the use of cells as potential cell therapy to replace cells that are no longer functioning appropriately in degenerative diseases. So that's all already legal and indeed some forms of animal-human hybrid are already permitted under 1990 act and 2001 regulations, but what this bill does is bring everything together and update the statute and there are certain areas we moved things on to, it will allow if there was ever a scientific cause for that – the use of true hybrids, the fusion of animal and human gametes up to the 14 cell stage just as with human embryos. It will allow for the first time the genetic modification of research embryos which was disallowed on a blanket ban in 1990; if those embryos are going to be destroyed at 14 days, so why should genetic experiments not be permitted?

Michael Hopkin: S.H. Cedar works in one of two UK labs that have already applied to do research under the new legislation. She and her colleagues at Kings College London want to create human-like stem cells by injecting human DNA into empty cow eggs creating a form of hybrid embryo.

S.H. Cedar: Well in the Kings Lab in general what we're interested in is regenerative medicine and so we are trying to look at human embryonic stem cells and derive them into, differentiate them into different lines so that they can make all the different type of cells in the body and we are looking at therapeutic applications.

Michael Hopkin: The new measures have been opposed by religious groups, particularly the Roman Catholic Church who oppose all work on human embryos. While speaking at the demonstration, I asked Dr. Cedar about her attitude to this opposition.

S.H. Cedar: The Catholics have one particular view of when the embryos are formed and when humans are formed and other religions have different ones, so it wouldn't fair to just go with one religious view.

Michael Hopkin: Despite the controversy Evan Harris believes that a yes vote will reflect the general public's attitude to this kind of research.

Evan Harris: But there is a split of public opinion. There is an Orthodox Catholic and sometimes other religious view that no embryo research should be permitted, that IVF shouldn't to be allowed because it involves the destruction of embryos, you know, that is their view it's a minority view and my view is even if wasn't the minority view the rights of patients to access the potential therapies coming from this research should not be denied because of the dogmatic religious view, however sincerely held by the individuals or religious leaders.

Kerri Smith: Evan Harris there, talking to Mike Hopkin. And there will be more on stem cells in Nature's special issue on the subject next week, so watch out for that in the mag and on the pod.


Adam Rutherford: Coming up in just a moment, find out why Geoff Brumfiel spends sometime languishing in a freezer this week, but before that as a new series of essays on music and science begins, Nature's Editor-in-Chief Phil Campbell takes to the podium to gives us a hint of what to expect. Nature 453, 160–162 (8 May 2008)

Phil Campbell: Laughter and hisses, that's how a London concert audience greeted the world premier of a revolutionary musical composition in 1912. Audiences of the day were regularly having their assumptions challenged by composers bent on redefining western music, but unlike other dissident masterpieces of that era Arnold Schoenberg's five orchestral pieces still come across to many as little more than noise. There are reasons for that as our weekly series of essays on science and music is currently making clear. But then noise has its treasures too. Schoenberg's compositions deliberately defied all of the prevailing standards of music. The five orchestral pieces, he said, were devoid of architecture or construction just an uninterrupted changing of colours, rhythms and moods, but he also insisted that they had an expressive purpose. The music seeks to express all that swells in us subconsciously like a dream. Indeed for today's sympathetic listener, the musical elements are distinctively recognizable and the emotional charge is tangible, yet the language is still a challenge. Even more traditional music defies all attempts to explain its function in terms of mathematical or cognitive naturalness, yet many essays in the series will highlight the universalities in music. For example, how our mothers lullaby and rocking during early childhood are thought to lay a foundation for human's oral and physical responsiveness. The articles are also celebrating music's diversity, the range of cultural conventions in such apparently fundamental elements as pitch scales and perceptions of rhythm. Drawing on musicology, statistics, cognitive and evolutionary biology and acoustics Nature's music essay series will help us understand one most of Schoenberg's music is more challenging than that of his contemporary and champion Gustav Mahler, let alone the scores of Johann Sebastian Bach. That said none of these disciplines has yet been able to answer the fundamental question why does music have such power over us? Nor can we explain how avant garde composers in the 1950s were able to take noise itself and make something new and true with it. Karlheinz Stockhausen's kontakte, for example pioneered much subsequent electronic music by presenting manipulated electronic noise amid the sounds of percussion and piano. Anyone who has performed it will tell you that the piece has an incomprehensible power, I have and indeed it does. The average listener isn't the least worried that musicologists and scientists cannot explain why we enjoy music. What matters is that its true bounties are recognized, explored, and analyzed and what matters above all is that the analysis strengthens rather than weakens Human Kinds' sense of wonder and that's all the more so as great composers make understanding music ever more challenging.

Adam Rutherford: Phil Campbell and we will be adding to the essay collection every week till July. Find those online at and listen out for our special Music and Science podcast in the next few weeks.

Kerri Smith: Finally this week, despite the hot weather here in London we are not talking about ice tea or ice cubes, but ice cores. Here is Geoff Brumfiel.

Geoff Brumfiel: It is an unusually warm day in Cambridge and if I am completely honest about it, that's one of the reasons, I am standing in the British Antarctic survey's freezer. The other is a little sliver of ice, barely a millimetre thick. It is crystal clear and filled with thousands of tiny bubbles. Eric Wolff, a scientist with this survey explains how they got there. Nature 453, 379–382 (15 May 2008)

Eric Wolff: You don't get any melting in the Antarctic, so the only way you get the solid ice is by the weight of the overlying ice building up on top and squashing the snow flakes together until eventually they form a solid matrix with bubbles in between.

Geoff Brumfiel: As it turns out all those bubbles are like little time capsules. The air inside them has been trapped for thousands of years and contains valuable information on Earth's ancient climate. A few years back, a team of European scientists set out to get samples from three kilometres beneath a place called Dome C in eastern Antarctica. It wasn't easy Wolff says.

Eric Wolff: It actually took about 4 years to get to the bed on this course, so there was a lot of effort, actually longer than that, because we got the drill stuck once, but we won't go into that too far.

Geoff Brumfiel: Two papers in this week's Nature showed the pay back from all that effort. They described atmospheric carbon dioxide and methane concentrations over the past 800 thousands years. It's the longest record ever extracted from a piece of ice, says Thomas Stocker at the University of Bern in Switzerland.

Thomas F. Stocker: We were able to show that the greenhouse gas concentrations both of methane and of CO2 assume very low values during certain times. What we also identified time periods, which look like fingerprints for abrupt climate change.

Geoff Brumfiel: This climate change was probably the result of huge glaciers that covered America and Europe. As the glaciers receded at the end of each ice age, they dumped enormous icebergs into the sea.

Thomas F. Stocker: These icebergs that were released into the Atlantic Ocean disrupted the circulation in the ocean and that brought upon very rapid cooling or very rapid warming.

Geoff Brumfiel: Because we seem to be in a warm period at the moment, these cycles have switched off, but understanding them could improve our grasp of present day climate change and climate change is at the heart of the second big result of the study. The core shows that greenhouse gas concentrations are now higher than they've been in hundreds of millennia says Eric Wolff.

Eric Wolff: We are way outside the normal range. Carbon dioxide over a 800 thousand years had a range between about 170 parts per million up to a maximum of 300 or right now its 385 and going up by 2 parts per million a year. Methane it's a similar story has now doubled what it was at any time before the industrial revolution.

Geoff Brumfiel: Now scientists would like to go still further back. Marine records indicate that just earlier than 800 thousand years ago, the entire climate cycle operated on a different time scale. Wolff says that finding all other samples won't be easy.

Eric Wolff: We don't even know where to go to get all that ice here. We just know that we didn't choose Dome C to be the very oldest on any particularly rational grounds, so that there must be older ice.

Geoff Brumfiel: The hunt is on and the British Antarctic survey and its partners are now planning to drill for ice that is at least 1.2 million years old.

Kerri Smith: Geoff Brumfiel there, who eventually managed to escape the confines of a Cambridge freezer to bring us that report, that's all for this week's show.

Adam Rutherford: And we round off with a sample from a Nature paper, the mating call of the female concave-eared torrent frog. Males of the species are known to attract females by calling to them, but a team of researchers led by Peter Narins of the University of California at Los Angeles, have now found that the gals get involved too. The sound you can hear from the ultrasonic calls they make processed so that we can hear them. Nature advance online publication 11 May 2008 I'm Adam Rutherford.

Kerri Smith: And I'm Kerri Smith. Thanks for listening.

[Sounds of Science: Sounds made by male and female concave-eared torrent frogs]


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