Nature Podcast

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Kerri Smith: This week, we batten down the hatches against hurricanes.

Mark Saunders: As sea temperatures warm you would expect to get more hurricanes forming and hurricanes become more intense too.

Kerri Smith: And earthquakes.

Thorne Lay: This one is particularly unusual because the two large events are so large, they are both great earthquakes larger the magnitude 8.

Adam Rutherford: The destruction and disaster doesn't stop there, as we zoom in on the flu virus only to find two teams disagreeing on why the drugs don't work.

Christopher Miller: The two structures have totally different and as far as I can see irreconcilable pictures of how that drug is inhibiting the channel.

Kerri Smith: But it's not all doom and gloom, our podium speaker gives us some food for thought on how to advance scientific progress and its not longer hours in the lab.

Nick Bostrom: No contribution would be more generally applicable than one that improves the performance of the human brain.

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

Adam Rutherford: And I'm Adam Rutherford. We have got particularly a jam packed show for you this week, so without further ado we will begin with the tale of two giant earthquakes. Here's Charlotte Stoddart.

Charlotte Stoddart: A year ago a little known archipelago between northern Japan and the Kamchatka peninsula in Russia shuddered from the force of not one but two massive earthquakes. The Kuril Islands forms part of the Pacific ring of fire and earthquake and volcano prone region along the edge of the Pacific plate. Normally a large quake is followed by several smaller aftershocks, but very occasionally one of the aftershocks is as large as the main event and in this case the two shocks were not only massive in magnitude but also ruptured different faults. Thorne Lay from University of California at Santa Cruz has been looking at data from the doublet. He and his colleagues used the seismic waves generated by the earthquakes to understand how the first quake triggered the second. I called Thorne to find out more about this rare earthquake doublet. Nature 451, 561–565 (31 January 2008)

Thorne Lay: Perhaps 1% of the time you might have an earthquake sequence that's characterized as a doublet, but this one is particularly unusual because the two large events are so large, they are both great earthquakes larger than magnitude 8.

Charlotte Stoddart: So what exactly happened? Did the first earthquake somehow trigger the second one?

Thorne Lay: Essentially that's what happens. This particular pair of earthquakes involves a region where the Pacific plate, a thick slab of rocks, is sinking down into the mantle. As it sinks it's rubbing against an adjacent plate which is along the Kuril islands, North of Japan, and the rubbing between the two plates produced a bigger earthquake in November of 2006, but in this particular case after that earthquake occurred on the boundary between the two plates, the second grade earthquake happened two months later out within the pacific plate. Essentially the plate fractured in response to the sudden slip between the other two plates.

Charlotte Stoddart: So to be clear then the first earthquake happened in between two plates and the second earthquake happened within the Pacific plate, and so what kind of damage did this pair of massive earthquakes cause? Did they set of tsunami like the infamous Sumatra earthquake in 2004?

Thorne Lay: The area where these earthquakes occurred is fortunately has very low population, so there wasn't a lot of damage and the earthquakes generated modest size tsunamis that spread around the pacific. The November 2006 event did cause a tsunami that produced damage in California actually, but it was not a devastating event. The more interesting aspect of these earthquakes is their interaction.

Charlotte Stoddart: And does understanding their interaction help us with the notoriously difficult job of predicting earthquakes.

Thorne Lay: Well, in a general sense by studying how earthquakes interact and how a doublet occurs, we are able to understand how the release of stress from one event can induce the slip on a different form. So triggering is an aspect of earthquake prediction by telling us how the stressors go from one fault to another.

Charlotte Stoddart: I understand that the second of these two massive earthquakes, the one which was within the pacific plate, was quite an unusual kind of earthquake.

Thorne Lay: That's right, you can think of the Pacific plate as a big thick slab of rock about a 100 kilometres in depth and for it to sink, you basically have to bend that slab and the bending produces stress within the plate. This second of these large doublet events involved breaking up the plate that is part of the process of it bending and sinking.

Charlotte Stoddart: So what's the use of studying an earthquake like this? What can we learn?

Thorne Lay: Well there are several aspects. The most important from the doublet is that it demonstrated that very large earthquakes can happen out where the plate has being bent not just on the boundary between the two plates. The earthquake can generate the second event, cause much stronger shaking than the somewhat larger initial event and that's because when you're breaking the plate, the fresh break of the rock releases more high frequency seismic vibrations and that can cause more structural damage. Because these events are infrequent, we have had limited understanding of what seismic hazard they pose around the margins of the Pacific. There have only been a few such events, when they have occurred off shore populated areas like in Japan, they have been very devastatingly damaging.

Charlotte Stoddart: So can this help us perhaps with designing buildings that are going to sit on places that are likely to see this kind of earthquake?

Thorne Lay: Well indeed, we can build buildings if we know what levels of shaking they are likely to experience in their lifetime. So what we would want to do with this study why this earthquake occur, where it did look for regions around the world that have similar plate configuration or plate structure and evaluate whether they have the potential to have such large events out in the bending region of the slab and then design accordingly, build up building codes that are going to withstand the shaking from such large events. One of our co-authors, professors Kanamori, was recently in Malaysia, where he was been asked about the hazard from such events, because they've designed their buildings with consideration of the typical interplate thrusting or earthquakes between plates, but not allowing for the stronger shaking from these plate bending and breaking events.

Kerri Smith: Thorne Lay of UCSC. Coming up shortly, how to use DNA to build structures from scratch; but first the pesky flu virus. Influenza is traditionally fought using drugs called Amantadines. But resistance to these drugs now stands at 90%. How the drugs work is not well understood, but getting to grips with the mechanism could help design drugs that the virus can't outsmart. Two papers from different teams, one at Harvard Medical School in Boston and the other at the University of Pennsylvania address this by looking at the structure of the channels that the drugs works on. They agree on the channel's overall structure, but disagree on some other pretty fundamental aspects as I learned from Chris Miller who studies these channels at Brandeis University in Massachusetts. He has written a news and views article on the two papers and started by giving me the rationale behind this work. Nature 451, 532–533 (31 January 2008)

Christopher Miller: Why would you bother putting all the effort into trying to get these high-resolution structures of this protein that is found in the envelope of the flu virus? That's a good question I mean why go do this? First of all, in the general menagerie of ion channel proteins, these proteins that live in cell membranes of all kinds, this is the first ion channel that has been crystallized or has had a structure determined. That is a proton-specific ion channel. The other motivation is that this is a very ostensibly a very simple protein, it is very small compared to most other membrane proteins that have been studied. So there is a lot of hope that may be this is a more easily manipulable ion channel, a sort of minimalistic ion channel that might be just simpler to understand. And then a third reason of course is the kind of connection to medical relevance especially with all the bird flu hysteria that we've heard about over the last couple of years. This is an essential protein for infectivity and the life cycle of the influenza virus. What has the virus have been doing, to make itself immune to these drugs? And actually these structures are directly addressing that question.

Kerri Smith: So as you say then this minimalist or this very simple ion channel is not only useful for basic science but also for the applied research that goes along with it being the flu virus. These papers have both looked in detail at the structure of this M2 channel and do they both broadly agree on what it looks like?

Christopher Miller: There is broad agreement on the basic architecture of this channel protein. Both groups, one of which uses X-ray Crystallography, one of which uses Nuclear Magnetic Resonance spectroscopy, they both agree on these basics that channel is formed by a bundle of 4 of these identical transmembrane peptides. It kind of looks like an ice-cream cone upside down. And the other aspect of it is that the two groups have apparently determined structures of two different conformational states of this channel. The channel can open and close, so it has two different shapes. Essentially there is a door in there that plugs up the centre of the pore, that's the close state and one shape in which that door has kind of swung open, so now protons can leak through the centre of the pore and the two groups have apparently determined structures, one of which is the open state that is the X-ray Crystallography structure and one of which is the closed state that is the NMR structure.

Kerri Smith: They've just taken different snapshots of the same channel doing different things.

Christopher Miller: That's apparently the case, yes.

Kerri Smith: Okay, so that need not worry us in terms of their disagreement there because they've just got these two as you say conformational shapes, but is there anything in these papers that they have found to be different?

Christopher Miller: Yeah, despite this kind of general agreement these papers are certainly going to generate a lot of controversy and that has to do with their very very different views on how this antiviral drug Amantadine actually blocks this channel. The antiviral drug, as I remind you, works just by inhibiting the channel activity and the two structures have totally different and as far as I can see, irreconcilable pictures of how that drug is inhibiting the channel and moreover of why the natural mutations that the virus has made on this protein to make the protein resistant to drug, how those mutations work and why they make that thing resistant to drug? So that's where the big controversy is going to be about. It's no so much the structures themselves, but the interpretation of the mechanisms by which the drug, the antiviral drug inhibits this thing.

Kerri Smith: And so this is just going to take more studies along similar lines with similar techniques.

Christopher Miller: I would think that the next step on this is, is for the structural biologists to try to overcome one of the soft spots, let's just stay, of both of these studies. Both of these studies show a structure, not of the full length protein, but rather of truncated versions of this protein. So you could criticize these and say "well look, may be this disagreement has something to do with the fact that we are only seeing part of the story" and I would say the other side of it is that the people who study the function of this protein, the electrophysiologists who look at proton transport across membranes, they may be now motivated to look more closely at some of the detailed mechanistic issues of how these drugs actually bind to the channel; that's now a question that has been very sharply posed by these structures and might motivate the electrophysiologists to look again at that kind of question.

Adam Rutherford: Chris Miller there. Another study that's likely to stir up some debate, takes a look at what newborn cells in the adult brain actually do. Kerri has been looking into this.

Kerri Smith: I have. The function of these adult stem cells in the brain has been a bit of a puzzle. They're thought to be involved in learning, memory, and fear behaviours, but it's been a headache to prove because it is difficult to selectively take them out of the brain in adulthood and removing them earlier in life means the brain doesn't develop normally at all. A team from the Salk Institute in La Jolla, California have devised a neat little method that allows them to take out these new neurons leaving the developing brain and other parts of the adult brain untouched. What they found was the opposite of what they were expecting. Co-author Ron Evans told me more about the study. Nature advance online publication (30 January 2008)

Ronald Evans: What we describe in the paper is the first genetic and functional evidence that neurogenesis that occurs in adult mammalian brain throughout life not only participates in allowing new neurons into our circuits that will provide the first evidence that these neurons are functional and play an important role in the classic process of learning and memory.

Kerri Smith: And to investigate the role of these cells then you've deleted a protein in the adult brain in mice, the protein called TLX and that is essential for making these neural stem cells, so what happened when you took that out?

Ronald Evans: So we devised a technique where we could inducibly remove this regulatory gene called the TLX and in that part of the nervous system it is uniquely expressed in the adult neural stem cells and when we used our inducible knock out approach, well, we noticed a few things. First the animals appear to be normal, they walk around, they have normal behaviour, everything seems completely unaffected except when we give them learning tasks, when we knock out the TLX gene in the adults, while they can still learn, they learn much less efficiently so the brain is able to capture a certain amount of the information, process it, but efficient learning appeared to be severely compromised.

Kerri Smith: So this quite specific component of learning is affected then, but their locomotion, their movement, and other things like that are seemingly untouched by these neurons not being there. Why do you think these neurons are only used for these specific functions?

Ronald Evans: Well we know that the hippocampus itself is mostly dedicated to spatial learning and memory, that's its role and particularly important in the process of consolidation of new memories and new experiences and there has been a great puzzle in the field of neuroscience as to whether new learning and new experiences are facilitated by new cells entering a circuit or whether the pre-existing wired circuit is sufficient for an efficient learning of new information and what our study suggests is that in fact new learning and new experience is tremendously facilitated by new neurons.

Kerri Smith: So these cells that are being generated are only essential for these processes or if you like, of learning that are carried on through life, so you need new cells for new memories, but for locomotion and things like that, they seem to be not be necessary.

Ronald Evans: Well, other processes such as locomotion, the animals are 100% normal. There is no loss of locomotion or coordination and there is no gain.

Kerri Smith: These mice that you developed then had the TLX gene taken out in the adult brain only. Do you think the same thing or a similar thing would happen if you took TLX out earlier in life?

Ronald Evans: Well, we've done that and the interesting thing about TLX is that earlier you go, of course the more neurogenesis there is because the brain itself has to form and TLX plays an important role in the embryo in the formation of the forebrain that is the structures that process complex information and environmental stimuli, so it plays a different role during embryogenesis. We had to eliminate that role to ask, what is it doing once you have a normal brain.

Kerri Smith: So do you think the field would be quite surprised then by this new paper?

Ronald Evans: Our conclusion which is different than that of the current dogma, in fact we got pretty much exactly the opposite results is that adult neuro stem cells in the hippocampus are important, but important for learning and memory and not important for fear conditioning. I am pretty sure that the field will be very surprised by the paper. I think that it will be very welcomed in general because people were desperately searching for clear evidence of the function of this cell population.

Kerri Smith: Finally then, how will you be able to use these new results?

Ronald Evans: Well one of the things that this begin to suggest is that since we now know that there is continuing proliferation in the adult brain, we can began to think of ways in which we might be able to use pharmacologic processes to help stimulate that process, increase neurogenesis which we know naturally declines with age, and particularly use stem cells to potentially go into diseases of learning and memory and think about ways to correct it because at least what we an say is that new stem cells entering into the circuit do contribute in a positive way.

Kerri Smith: Ron Evans of the Salk Institute in La Jolla, California.

Adam Rutherford: Better memory through stem cells is an extreme form of cognitive enhancement a subject that seems to repel and attract in equal measure. At the end of last year we had Cambridge University's Barbara Sahakian on the show talking about the use of brain boosting drugs among healthy individuals. Nature received some spirited responses to her article and we've given over the Podium this week to one of them. Here is Nick Bostrom at the University of Oxford's Future of Humanity Institute explaining how to speed up scientific progress. Nature 451, 520 (31 January 2008)

Nick Bostrom: There are three ways to contribute to scientific progress. The direct way is to conduct a good scientific study and publish the results. The indirect way is to help others make a direct contribution. Journal Editors, University Administrators, and Philanthropists of fund research contribute to scientific progress in this second way. A third approach is to marry the first two and make a scientific advance that itself expedites scientific advances. The full significance of this third way is commonly overlooked. It is of course widely appreciated that certain academic contributions lay the theoretical or empirical foundations for further work. One reason why a great scientist such as Einstein is celebrated is that his discoveries have enabled thousands of other scientists to tackle problems that they could not have solved without relativity's theory. Yet even this deep and beautiful theory is in one sense very narrow. While relativity is of great help in Cosmology and some other parts of Physics, it is of little use to a Geneticist, a Palaeontologist or a Neuroscientist. General relativity is therefore significant, but not a vast contribution to the scientific enterprise as a whole. Some findings have wider applicability, the scientific method itself. The idea of creating hypothesis and subjecting them to stringent empirical tests is one such. Many of the basic research in statistics also have a very wide applicability and some scientific instruments such as the thermometer, the microscope, and the computer have proved enormously useful over a wide range of domains. Institutional innovations such as the peer-reviewed journals should also be counted. Those who seek the advancement of human knowledge should focus more on these kinds of indirect contribution as superficial contribution that facilitates work across a wide range of domains can be worth much more than relatively profound contribution limited to one narrow field, just as a lake can contain a lot more of water than a well even if the well is deeper. No contribution would be more generally applicable than the one that improves the performance of the human brain. Much more effort ought to be devoted to the development of techniques for cognitive enhancement, be they drugs to improve concentration, mental energy and memory or nutritional enrichments of infant formula to optimize brain development. Society invests vast resources in education in an attempt to improve student's cognitive abilities? Why does it spend so little on studying the biology of maximizing the performance of the Human Nervous System? Imagine a researcher invented an inexpensive drug which was completely safe and which improved all around cognitive performance by just 1%. The gain would hardly be noticeable in a single individual, but if the 10 million scientists in the world all benefited from the drug the inventor would increase the rate of scientific progress by roughly the same amount as adding 100,000 new scientists. Each year, the invention would amount to an indirect contribution equal to 100,000 times what the average scientist contributes. Even an Einstein or a Darwin at their peak of their powers could not make such a great impact, meanwhile others too could benefit from being able to think better including engineers school children, accountants, and politicians. This example illustrates the enormous potential of improving human cognition by even a tiny amount. Those who are serious about seeking the advancement of human knowledge and understanding need to crunch the numbers. Better academic institutions, methodologies, instrumentation, and especially cognitive enhancement are the fast tracks to scientific progress.

Adam Rutherford: Nick Bostrom there and you can read his and others thoughts on cognitive enhancement in this week's issue. That address is


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Kerri Smith: Next Katharine Sanderson finds some multitalented DNA strands being used as blueprints and construction worker, not to build life but to construct crystals out of nanoparticles.

Katharine Sanderson: DNA is the blueprint for life. It contains the information needed to build proteins, cells, and whole organisms, but two teams have now used DNA as a blueprint in a totally different way that has nothing to do with genes, cells or life. One of the teams is led by Chad Mirkin at Northwestern University. They have taken advantage of the fact that complementary strands of DNA bind to one another. They attached one end of the DNA strands to gold nanoparticles and at the other end finds and binds to other strands locking the nanoparticles into specific crystalline geometrical arrangements. I asked Chad Mirkin what led to his latest discovery. Nature 451, 553–556 (31 January 2008)

Chad Mirkin: Our strategy that we put forth a decade ago was to use DNA, the idea being that now with modern day gene machines, we can synthesize just about any sequence we would like, we can tag those sequences with small molecules that will chemically bind to nanoparticles of interest and we can learn how to coat the surfaces of these particles with specific sequences of DNA and that means we can program effectively their ability to assemble with other types of particles that have complementary DNA into discrete structures.

Katharine Sanderson: So what did you do in this paper then?

Chad Mirkin: We learned how to for the first time literally effect crystallization to use different types of DNA modified particles and get them to assemble into discrete structures and that is really fundamentally important because it is a major step towards literally learning how to program materials formation from the bottom up being able to build exactly what you want based upon the types of particles that we employ and the types of DNA that we use. So again the need saying here is, adding one reagent and simply by changing sequence, we can take one set of building blocks and drive it to two different crystalline states and presumably if we can learn how to modify the particles appropriately, we can make lots of different types of crystal structures and it opens up a whole new area of science.

Katharine Sanderson: So you are essentially just taking DNA, nothing to do with its other properties in biology, you are using it just as a tool?

Chad Mirkin: We are using the DNA in this case as a blueprint and as a construction worker to carry out the plans.

Katharine Sanderson: You mentioned briefly why you'd want to do this - from a chemist's point of view you wanted to be able to design your molecules, but then what? I mean what are they going to be used for eventually?

Chad Mirkin: Well that's a very good question, so you know all these types of materials are going to be used for anything, the answer is they already are, so building half of the work that we originally published in Nature in 1996, we've learned that these types of particles and materials formed from them have all sorts of interesting properties that depend upon their distances within larger structures; for example, they have a plasmon resonance which gives rise to a very intense colour, so gold nanoparticles that are dispersed are red in colour, nanoparticles that are assembled are blue in colour, and we've used that colour change and many of the other property changes associated with these assembly processes to create new types of detection systems for DNA and for nucleic acids in general. And some of those systems are now commercialized by a start-up company that we initiated about 8 years ago and FDA approved. And that's pretty exciting because those are some of the first major innovations, real innovations of nanoscience and nanotechnology, where, you know, we are not just doing something neat on the nano scale and interesting from a chemical standpoint or chemistry standpoint but we are really learning how to take advantage of these unusual properties associated with assembly processes to create very useful diagnostic tools, in fact some of the most sensitive and selective diagnostic tools out in the market today are for DNA and RNA detection.

Katharine Sanderson: So now that you've built up your crystalline nanoparticle network, what are you going to do with it?

Chad Mirkin: I think over the next couple of decades we are going to see a lot of work aimed at learning how to take particles and selectively put different ligands, in this case different DNA strands on different phases, at different vertices depending upon the shape of the particle, different edges that allow you to build directionality into the process that we are reporting in this Nature manuscript because if you can do that then really the sky is the limit. You can get the DNA to assemble these types of particles into any material you want, any crystalline state you want, diamond any sort of structure that you find interesting and useful for a given application or ones that you simply just want to study from a fundamental standpoint.

Katharine Sanderson: What's the most exciting part of this work for you?

Chad Mirkin: I think what is the most exciting about this paper is, it is a Turgor force demonstration of the power of DNA and its utility in inorganic material synthesis.

Adam Rutherford: Chad Mirkin talking to Katharine Sanderson. With the devastation of Hurricane Katrina still fresh in our minds, the destructive power of tropical cyclones is more apparent than ever. Hurricane activity in the Atlantic has increased at an unprecedented rate since 1980s. What's behind this frightening effect? Mark Saunders and Adam Lea at University College London have looked at these patterns and demonstrated a simple, but startling correlation between rising sea temperatures and increased cyclonic activity. I spoke to Mark and he told me how hurricane trends have been on the up from more than a decade. Nature 451, 557–560 (31 January 2008)

Mark Saunders: Hurricanes are intense tropical storms and historical record does show multi-decadal patterns in the number of hurricanes, but there's been a particularly marked increase since 1995 when levels ran about 50% above the long-term norm and this has generated a lot of interest and concern as to the cause and this is what our study is principally addressing.

Adam Rutherford: How does this increase correlate to land falling hurricanes, I presume, such as Katrina that caused such devastation in America?

Mark Saunders: There is a link between numbers of Hurricanes in the sea and those that do strike the US and Caribbean and for the period since 1995 US land falling hurricane activity has also been about 40-50% above the long-term norm.

Adam Rutherford: And this 40% increase which is really quite staggering, you've correlated this with the rise in the sea surface temperature of the Atlantic. Can you tell us how you did this study?

Mark Saunders: We created a statistical model based on two environmental fields, one being local sea surface temperature in the Hurricane main development region, that's between the west coast of Africa and the Caribbean and an atmospheric wind field over the same region. And using these two variables for the months of August and September, which are the two main months when hurricanes occur, we replicated between 75 and 80% of the variability in numbers of hurricanes between 1965 and 2005 and then by removing the influence of the winds from this two environmental variable model, allowed us to assess the contribution from a sea surface temperature alone and we found it to have a large effect.

Adam Rutherford: Can you give us an indication of what the mechanism at work would actually be here, where the increase in sea temperature actually causes more hurricanes?

Mark Saunders: Warming sea temperatures impart more energy and moisture to the atmosphere, which are key ingredients for powering hurricanes when they form, so that it really makes reasonable sense that as sea temperatures warm, you'd expect to get more hurricanes forming and hurricanes become more intense too.

Adam Rutherford: And in your paper you very specifically don't attribute this correlation to global warming. Why are you so emphatic about that?

Mark Saunders: Well our analysis is based on using data from the last 40 years, so we are confident the link between sea surface warming and the changes in hurricane activity is about it for that period, but we don't know whether that same sensitivity will necessarily carry on in the future as sea surface temperatures warm. So I think our analysis as you said, does not identify whether greenhouse gas induced warming has contributed to the current increase in water temperature and thus to the increase in hurricane activity. What I think is important from our results is that climate models are able now to reproduce the observed link between hurricane activity and sea surface temperatures. So that then we can have confidence in their ability to better predict what hurricane activity will be in the future and how it will respond to climate change.

Adam Rutherford: And what predictions about hurricane activity does your model make? Can we expect this trend to continue?

Mark A. Saunders: I think based on our results if sea temperatures do carry on rising as most climate models expect them to and also if the wind's patterns stay fairly constant, then I think it balances the probability to suggest that hurricane activity will carry on increasing, but we need to have reliable projections, in particular for the winds because if they did start to change significantly in the future, that could counteract an heartening effect from warming sea temperatures.

Adam Rutherford: Mark Saunders from University College London. That's all from us this week.

Kerri Smith: For those of you with an artistic bent Nature and the Royal Institution of Great Britain are running a competition to occupy a space at the newly refurbished RI in London.

Adam Rutherford: It's called the Niche Prize the idea here is to create an arresting and inspiring image or installation that conveys a scientific idea. If you fancy your chances go to for guidelines and the entry form, but you better get your skates on, as the closing date is the 22nd of February.

Kerri Smith: This is the Nature Podcast, I'm Kerri Smith

Adam Rutherford: And I'm Adam Rutherford. Here's this weeks' sound of science, Tom Lehrer and the element song.

[Sound of Science]

There's antimony, arsenic, aluminum, selenium,And hydrogen and oxygen and nitrogen and rhenium,And nickel, neodymium, neptunium, germanium,And iron, americium, ruthenium, uranium,Europium, zirconium, lutetium, vanadium,And lanthanum and osmium and astatine and radium,And gold, protactinium and indium and gallium,And iodine and thorium and thulium and thallium.There's yttrium, ytterbium, actinium, rubidium,And boron, gadolinium, niobium, iridium,And strontium and silicon and silver and samarium,And bismuth, bromine, lithium, beryllium, and barium.There's holmium and helium and hafnium and erbium,And phosphorus and francium and fluorine and terbium,And manganese and mercury, molybdenum, magnesium,Dysprosium and scandium and cerium and caesium.And lead, praseodymium, and platinum, plutonium,Palladium, promethium, potassium, polonium,And tantalum, technetium, titanium, tellurium,And cadmium and calcium and chromium and curium.There's sulphur, californium, and fermium, berkelium,And also mendelevium, einsteinium, nobelium,And argon, krypton, neon, radon, xenon, zinc, and rhodium,And chlorine, carbon, cobalt, copper, tungsten, tin, and sodium.These are the only ones of which the news has come to Ha'vard,And there may be many others, but they haven't been discavard.


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