Robyn Williams: The Science Show this week has an average IQ of about 500. As many Nobel Prize winners as you're likely to hear in one exuberant inspiring collection. But add to them the young people who went to meet them in Germany, to be guided and enthused. The truly amazing thing about these ever so distinguished Nobelists is that they are as keen to learn from the youngsters as the ingénues were to hear from the mentors themselves. Our guide in Germany is Science Show producer, David Fisher.

David Fisher: It's an island on Lake Constance in Germany's south. There are ancient buildings, cobblestones and tourists eating ice-cream and admiring the Alps. And it's here for one week each year that young scientists from all over the world get unparalleled access to the scientists they've only ever read about - those who've been rewarded for their outstanding achievement with a Nobel Prize. The Lindau Meeting of Nobel Laureates began as a gesture of post-war reconciliation and has grown into an event researchers yearn to attend. It attracts more than 500 young researchers from over 80 countries. This year was the 61st meeting; the focus: physiology and medicine, looking at the challenges ahead for human health on a global scale. Today on The Science Show we'll speak to some of the Laureates and hopefully understand the excitement of the young researchers as they meet the scientists who inspire them. As if 23 Nobel Laureates weren't enough, this year's meeting kicked off with a name and a voice you will probably know.

Bill Gates: I'd admonish you to consider the needs of the poorest in the work that you do, because I think the advances there will be particularly important, and without your attention to them it's possible they will not take place. Thank you.

David Fisher: Bill Gates with his message for the 500 young researchers. He told the meeting that ten times more research funding goes into finding a cure for male baldness than finding a cure for malaria, and malaria kills 850,000 people a year. Peter Agre received the Nobel Prize in 2003 for his work on aquaporins, the proteins that regulate the movement of water molecules through cell membranes. He advises Bill and Melinda Gates in their work on malaria.

Peter Agre: There are more people infected with malaria now than ever before. We know how to handle it, but the fear is the resistance to the artemisinins, the current drugs of choice, may spread. They're being detected now, so there are concerns. I wouldn't be willing to admit defeat, although I would not celebrate victory. We're still in the thick of it.

David Fisher: When resistance happens, how long does it take to spread?

Peter Agre: The resistance to chloroquine, chloroquine the drug of choice from previous decades, emerged in South East Asia and within a decade it has moved over the entire planet, so that chloroquine is no longer useful.

David Fisher: I remember taking it.

Peter Agre: I took it as well. It was a good drug, but the resistance made it ineffective. It is, I should point out, still effective for treating Plasmodium vivax, the vivax form of malaria. So falciparum it's not useful, vivax it is useful.

David Fisher: A lot of money is coming into malaria research, particularly the Gates Foundation. What's your reaction to that concentrated amount of money on one problem?

Peter Agre: Certainly the Gates Foundation has been very generous. They put somewhere in the range of US$175 million into malaria every year. But they're funding specific projects, they're not funding all research. They've picked vaccine development as an area of focus and they also sponsor what they call Grand Challenges grants - one-time $100,000 grants to get started. This has had a beneficial effect, however science is not a matter of quick starts and quick kills; it's a marathon, and we need continuous long-term funding as well. And in different institutions different sources have been effective. Certainly in Australia the Walter and Eliza Hall Foundation has been enormously successful from both private endowment, from taxes. Our institution at Johns Hopkins has funds from the Michael Bloomberg Family Foundation. Mike Bloomberg, the Mayor of New York, was a graduate of Johns Hopkins and is exceedingly generous, very interested in public health. So money is coming in, it's being used wisely, but it's a difficult problem. We don't know how much it'll take. Right now it's still in question. We're very active in our pursuit of mechanisms to prevent malaria as well as treat and cure malaria.

David Fisher: I think the size of the problem is also shown by the timeline. Bill Gates here at the opening on Sunday said that they have an aim of 2025 to have a vaccine. Do you think it's wise to put a target date?

Peter Agre: Well, it would be imprudent for me to tell Bill Gates how to run his business. On the other hand, I am an advisor for the Malaria Group for the Gates Foundation, and some find target dates useful, incites energy, excitement. My own style is not to do that. This is not the Olympic 400 metre. It's something of unknown duration, and I'm a little more cautious. On the other hand I understand he's a bit younger than I am, he's impatient to see results. But he should be; that's his nature. I guess I'm a little bit more of a plodder. I want to make progress, but I don't want to create possibly an incorrect sense of urgency that we've got to get it this week, next week or it's finished. Bill Gates also has said we're in it for the long haul; 2025 for a vaccine is his estimate. It would be nice if a vaccine emerged in the next year. I don't think from what I've seen in the pipeline we're close. Others may disagree. A vaccine could be enormously useful, but this is not a simple virus or a bacterium; this is a complex parasite, and vaccines for parasites have not been successful generally. We know that the parasite can elicit an immune response. Individuals who've had malaria repeatedly become less seriously ill with subsequent infections, but they can still get infected. They're never totally immune. A vaccine to be useful has to be useful in most who receive it, and it should have a long-term effect. To get some partial immune protection wherein you'll get malaria a little less seriously but in six months you'll need to be vaccinated again, and by the way it costs $5,000, probably is not going to be an effective way of preventing the disease.

David Fisher: Peter Agre from the Johns Hopkins School of Public Health in Baltimore, Maryland. At the Lindau Meeting each of the Laureates presents a short lecture. Elizabeth Blackburn grew up in Hobart and is now at the University of California, having received the Nobel Prize in 2009 for her work on telomeres. These are structures at the ends of chromosomes which protect the chromosome and its genetic information. She co-discovered telomerase, the enzyme that replenishes telomeres. Here she's describing the difference between observations made in short-lived organisms and humans.

Elizabeth Blackburn: Well we certainly know that the underlying molecular machineries are going to be similar. We have telomerase, just as do Tetrahymenas and yeasts and so forth, but the important point is that the kinetics of all of this is now going to be played out over decades of life. So how does it all play out? So that's been the subject of research from many, many different labs in the last few decades. So a simple observation, very broad-brush, and there will be exceptions, is that in a general way telomerase is often limiting in adult human cells, and so they do in fact undergo some shortening. In various systems in the body one can see evidence that this is likely to be occurring, that the telomeres are progressively shortening and senescence is occurring. And one can see evidence for that in vivo, in people. Now the question was does that cellular phenomenon play out in our lifetimes? You know, does the candle burning down for the telomeres, so to speak, does that actually get reflected in human life courses or not? So that was the question that many, many labs have been collecting evidence for.

Elizabeth Blackburn: I'm Elizabeth Blackburn, I'm at the University of California, San Francisco, in California. Well telomeres are found in all of the cells that have nuclei accepting of red blood cells which don't have nuclei. Telomeres are the ends of chromosomes. All our cells pretty much except red blood cells have the genetic material in there. So telomeres cap the ends of chromosomes and protect the genetic information. And when they wear down, then the cells end up ceasing to divide or can become cancerous, more rarely, but dangerously. And so we happened to study immune system cells initially because they're a convenience sample, but actually they're very informative, because a lot of what the immune system is doing has real effects in cardiovascular disease development, in cancer development and now people think actually even in diabetes. So the immune system cells, although people very kindly have veins in their arms and let you have blood samples, are not only convenient, they're also very much a window into what's going on in your body as a whole system.

David Fisher: I was interested this morning, you mentioned stress.

Elizabeth Blackburn: Yes, well chronic psychological stress.

David Fisher: And also the influence of your very early upbringing. Could you just elaborate there?

Elizabeth Blackburn: Yes, well what's been studied recently is childhood trauma exposures or childhood maltreatment exposures, and interestingly one is finding quite persistent quantitative readouts of those kinds of events in middle aged adults, in which you see that telomere shortness is related to things that have happened a long time ago. So there's probably a lot of self-perpetuating physiology that starts getting set up and seems to persist into later life. And certainly it's been seen that these kinds of things have been clinically linked to risk factors for disease. So we're seeing one potential kind of mechanistic pathway through which this could be acting.

David Fisher: Now you left the students this morning, the young researchers, with a challenge.

Elizabeth Blackburn: Well the challenge was that we focus very much on things that are immediately facing us, and those are big challenges in infectious diseases and challenges to human health in very serious ways. But the better we get at that, as we see with life expectancy, it keeps going up, as we deal with all of these more and more we now leave the field open for all the chronic diseases, and so those ones are now starting to be the big burden in both developing and developed countries; for example, diabetes is now affecting ten percent of all the world's adults, and we're talking in the developing countries as well, so it's not a disease of rich countries. So this is a huge burden. So we have to start thinking about what are we going to do to try and intercept these things as early as possible, and our work with the chronic stress is interesting. It's just very specific example of how you can think about, okay, here's something, here's a causality here, let's think about ways that we can deal with that. This is not the only one, but it's certainly one more arrow in the quiver, if you will, of the armament of things that you can try and use as preventive measures, apart from not smoking, which is the other good one. Well proven!

And yes, as we get better and better at the infectious diseases, these are going to be the big ones. So people with these chronic diseases are going to be around for a very long time, very miserable, very demanding on the system. This is not a good prospect when you think about it, and so the more we can think about not only treating, which is clearly important, I'm not against treating at all, you know I mean tremendous advances, I couldn't be more enthusiastic about the fact that we can treat so many things; but vaccination is the perfect example of that's the best thing you could do is the equivalent of vaccination. That's not going to work for certain chronic diseases of ageing, but something that prevents the disease or at least stalls or intercepts its progression earlier and earlier in disease progression, that's what we should also be thinking about. Pharmacological intervention has been very much money driven; treatments are very much influenced by, you know, there's big money in drugs, right? And there's less incentive to do preventive things. But from a human health and welfare point of view there's every incentive.

David Fisher: Maybe that's where government comes in.

Elizabeth Blackburn: I think absolutely, yes.

Jan Gralton: My name is Jan Gralton, I am from Sydney, Australia. I work in respiratory virus transmission, so when you cough I have a bit of a freak-out, because I know how big the particles are and where they move.

David Fisher: Especially onboard an aircraft or a bus.

Jan Gralton: Oh yes! Aircraft are not a good situation for me. I'm very alert and alarmed at those times. It's been really enjoyable. I'd have to say the talk this morning from Oliver Smithies was a highlight, definitely.

David Fisher: Do you know, he's 86?

Jan Gralton: 86! And still works in the lab on a Saturday morning like me as a PhD student. So that's pretty inspiring to think I'm going to be doing that when I'm 86!

David Fisher: What did you find inspiring about his talk?

Jan Gralton: That he still has that passion for science, and that's what's driving him. He doesn't seem concerned about anything political, he's not driven by funding - he does it for the love of research. And a lot of his major findings have been accidental. He found gel electrophoresis out of laziness.

David Fisher: You're going to have to explain what that is.

Jan Gralton: So when we look for DNA we run it on a gel to see the fingerprint, and originally they used to run it through grains of starch. And he said well there's just going to be too many basins for me to wash, I'm going to melt the starch. And he made the gel. He did it because he remembered his mother used to starch his father's collars and it would be this gluggy material at the end, and that gluggy material is what we use in research now.

David Fisher: So he developed the method that's widely used?

Jan Gralton: And he said it's because he was lazy.

David Fisher: So it's not a bad thing!

Jan Gralton: It's not a bad thing at all! So maybe I'll be lazy and I'll find something along the way too, by accident! Every lab uses PCR and electrophoresis now.

Yedidya Saiman: Yedidya Saiman from Mt. Sinai School of Medicine in New York City. It's really been amazing. Meeting all the young researchers is really most of what it is. The Laureates are just a special prize on top of that. It's been an incredibly collegial environment. I think everyone's guard is almost down, and it's not like a normal conference where everyone's like you just want to see this person, you need to speak to them, maybe I'm going to get a job with them, you know, make sure everyone sees my work. I think everyone doesn't have that. No-one's here to present what they're doing and I think it's just a much more collegial and interactive environment because of that.

David Fisher: Apart from feeling good and being relaxed and having lots of beer, what have you actually got out of it?

Yedidya Saiman: I think it's definitely reinvigorated me in my research, and we saw Edmond Fischer speaking truly in the most simple terms, kind of just describing you know the pathways of phosphorylation, tyrosine kinase phosphorylation. But seeing it from the master who found it is just incredibly invigorating, incredibly inspirational. I mean to see how much, you know, these people really still want to educate us and they're here really for us, and it's just incredibly inspirational.

David Fisher: Do you think it might change your approach to your work?

Yedidya Saiman: I think it'll make you be a little more critical on your data, critical on what you're looking for. You know what so many of them said, oh we found this thing, we had no plan that this was what we wanted to do. Kroto was saying the experiment they were doing to find the buckyball was a mundane experiment that led on to something better, and it's really keep an open mind about it. And I think what most of the Laureates also said that there's no eye on the prize, you know, it's not about winning any prizes, it's really following your passion, doing what you love, and you know the prizes, they're great when they come, but they're really just luck of the draw.

David Fisher: Also a matter of luck, mostly, is whether we make it into our nineties. Christian René de Duve has, and he's sailing quite nicely. He collected the Nobel Prize in 1974 for discovering the lysosome, a structure within animal cells which contains enzymes designed to keep the cell clear of debris and waste products. He spoke to the 500 young researchers about his big concern, and when on stage with a laser pointer that didn't work he solved the problem with his walking stick.

Christian de Duve: Before talking about the future of life, I would like to spend a little time going back. I don't think there's a pointer, but it doesn't matter! (applause) Now I don't know why you applauded, but never mind! Wait till the end of the lecture! We're going to look at population in terms of time. Half a million years ago it's estimated that the human population was about 3,000 individuals. 200,000 years ago, that's the time when we had already separated from the Neanderthals, it's estimated that there were about 10,000 human beings. 10,000 years ago, that's when the first human settlements started, when they started cultivating land and raising cattle, 5 to 10 million individuals. 1600, that's the time of Galileo, of Descartes, half a billion; that's quite a lot already, half a billion. 1830, that's when Darwin was working, one billion individuals. 1930, that's when I was at school, yes, yes! I was almost finished school at that time! I almost entered university - two billion, that's what I learned at school, they said we are two billion. In the meantime it's changed. From 1930 to 1970, that's four years before I got the Nobel Prize, four billion, just in one lifetime, from two to four. 2009, six-and-a-half billion. Tomorrow maybe nine billion, maybe more, we don't know. So this is really a staggering increase in population. It's even more frightening when you see the curve how suddenly you know more than exponential fashion this number has risen.

What this means is that the human species, Homo sapiens sapiens, we are among all the living organisms that have ever existed on this planet, we are the most successful species. We, starting in Central Africa, small bands roaming Central Africa, we have come to invade the whole of our planet, to occupy almost every liveable corner of this planet. We've come to use virtually all the resources that are available for our own benefit. We have really become tremendously successful.

But this success has a price - exhaustion of natural resources, almost complete exhaustion. It's loss of biodiversity, every day living species disappear, deforestation, desertification. We're losing forests in the Amazon at a fantastic rate; the deserts are becoming wider. Climate change - but climate is just a small aspect of this whole tragedy that we have inflicted on our planet. Energy crisis, you know, how we're all trying to find new ways to power our needs because we are using more and more energy. We are polluting the earth to the point of making it unliveable in certain parts of the world. Overcrowded cities, conflicts and wars, I don't have to tell you. I've seen two wars in my lifetime, and today wars and conflicts are raging all over the world. The main problem of our success is that there simply are too many of us.

Is there something that we can do? First do nothing. That's what we're doing today almost - do nothing. Well, if we do nothing I think what will happen is easy to predict. Things will only get worse, and they will very soon get so bad that life will become very difficult on this planet, that the conditions for life will be menaced and dangered more and more and that we, the human species, will progressively move towards extinction. You've seen that all those that preceded us ended by becoming extinct, the Neanderthals only 35,000 years ago. Why not us? Well that's a good question, but you have to remember that if 10 billion individuals have to go extinct, that's not the same thing as 10,000 in Central Africa. 10 billion all over the world, that means that before we become extinct the most unimaginable apocalyptic events can take place, fights and epidemics and whatnot. If we let things go there won't be enough food for everyone. So we are doomed if we don't do something about it.

Fortunately we have received from natural selection a gift no other living species possesses. We of all the living organisms on this planet that have ever existed, we are the only ones to receive the ability to do something natural selection cannot do, we can look into the future, we can make predictions about what will happen if we do something or if we do something else. We can make decisions about the future and we can act according to those decisions, so we can act against natural selection. We are the only living organism on this planet that has the ability to intentionally, willingly, consciously act against natural selection. And therefore that is what we have to do before it becomes too late.

The religions have been very much involved in educating the young and even the adult. Some religions, like the Catholic religion, can influence one billion people in this whole world, so they have a huge ability or power to do what is needed, the education. And here I think the religions are not doing their job properly. I think they are more busy defending their own beliefs, their own ideologies, their own doctrines, their own hierarchies. They're much more involved with their own survival than with the survival of the world. They're more involved with your being happy in the next world, but not in this world. I hope there will be a change. I think there should come from people like you an influence that goes up to the hierarchy and tell those old men there's need for a change!

All the ills that I have mentioned are due to one single cause - there simply are too many human beings in the world. It's staggering, it's frightening to see how quickly our numbers have increased just in my lifetime - four-fold increase just from the time I was born till today. It's terrifying, so we have to do something about it.

The writing is on the wall. If we don't act soon to overcome our genetic tendency to intragroup selfishness and intergroup hostility, the future of humanity and of much of life on Earth will be gravely endangered, possibly leading to total extinction under conditions that can only be visualised as apocalyptic.

Here I turn to the young. This is the most wonderful thing about these Lindau Nobel Meetings, and as long as I am physically able to come I will come back, because here is where we meet the young people of the world. And I would like to turn to all you young people in this audience and say I want to tell you, my generation has made a mess of things. It's up to you to do better. The future is in your hands. Good luck.

Annette Baudisch: My favourite one was Smithies.

David Fisher: Oliver Smithies?

Annette Baudisch: Yes, that was really great, because I found that he hit the balance between being really personal, but not too much, I like that; and the one yesterday by-

David Fisher: Christian René de Duve?

Annette Baudisch: Yes. It's a difficult name!

David Fisher: So what was it about his talk?

Annette Baudisch: Well the way that he really said well there are really important problems and if we don't solve them we're going to go extinct. I mean it's a fact!

David Fisher: Is it a fact?

Annette Baudisch: For me it's a fact. I study population dynamics and structures. I'm a demographer, and for me it's pretty obvious that there's exponential increase in people and linear increase in resources, so at some point the lines cross; that you don't want to have to happen.

David Fisher: So you don't think he was overstating the situation?

Annette Baudisch: No, I don't think so. I think he was pretty much right.

David Fisher: So what should be done?

Annette Baudisch: Oh my God! That's a lot over breakfast! I think that we need to slow down. We had a long phase of growth and now there needs to be a reasonable phase of restructuring and maybe sort of some de-growth. I don't know whether-

David Fisher: But the whole economy is based on a model of growth and people's wealth and prosperity increasing.

Annette Baudisch: People to need in maybe like half the size or just make people much more happy.

David Fisher: What's your name?

Sukhdeep Singh: I'm Sukhdeep Singh, originally from India, but now in Germany I'm doing my post-doc over there.

David Fisher: How has the week been for you?

Sukhdeep Singh: Wonderful really. It is one of the best meetings I have ever attended.

David Fisher: Why is that?

Sukhdeep Singh: Because it's so diverse. Normally when we go to a conference or to a meeting, then we are really so focused. And for example I'm a chemist, so the public is from chemistry area always. So here I met many other diverse fields. It was really a very great thing, because science at the moment, it has to merge altogether to bring some useful things for the society. So I feel that it's good to have ideas about other fields and what we can all contribute in that.

Ting Zhang: I'm Ting Zhang from China. We are doing biology and medicine. But actually the fields are quite different, so I can learn more from them and I can share the Chinese culture with them, and let them know that China is very good and we can make more friends and more improvements in the future. Our lab is working on projects of synthetic biology. We want to make normal bacteria by transplanting artificial genome into the bacteria, and if they can live then we have some new discovery, and then we make new bacteria. That's a very big success.

David Fisher: What's the point of making new bacteria?

Ting Zhang: Actually bacteria can be used in some very good way. For example it can be be used to make oil, produce oil, it can help us treat disease. We change some genes in the bacteria and then the bacteria can produce oil. It has not been worked out totally and so it's just a try.

David Fisher: But as we've heard this week, so much happens that is unexpected. And half of these people didn't realise they were going to discover anything, and they discovered something great and changed the world. Maybe you'll do the same.

Ting Zhang: Me? You mean my project? I think my project is not as important as the Nobel Laureates', but I think at least it's a small move. But in the future, after many of these small moves, I will someday make a big discovery to astonish the world!

David Fisher: Ting Zhang, one of the 26 young researchers at Lindau from China. Back to population, and not everyone is convinced it's our number one problem.

Hans Rosling: I'm Hans Rosling, Professor in International Health at the Karolinska Institute, but now mainly working with the Gapminder Foundation, providing teaching material on the web. The problem with world population is that people don't understand it! World population is flattening off at around 9 billion. We may be 8, 9 or 10 billion in a hundred years from now. But there are already an average of 2.5 children per woman in the world today, and the number of children born per year hasn't increased for the last 20 years! The few countries that still have large families are compensated by billions of people in Asia and Europe that have less than two children. So we have two billion children, and that won't increase. What we are doing now is just adding adults, and we are adding adults to cities in Africa and Asia. Then it's we have come to an end and after that it will decline. But these things change slowly. You cannot use population to solve the challenge of climate change, because that's too big a challenge and it's too soon we have to do something.

David Fisher: You're saying climate change is a more urgent problem and population is a longer term problem?

Hans Rosling: Yes, population is half to one century. Energy we have to do something now, not to be in deep shit within 30 to 60 years. So the focus on population is drawing the attention in the wrong direction.

David Fisher: We've got 500 of the world's best young researchers here. What's your challenge to them?

Hans Rosling: It is that they should think in new ways. We said now they had an idea about the new drug and the big pharma wouldn't finance it - well go to the Indian venture capital, they think in new ways. Find financing from China. I told them that China and India now come and invest in research at the Karolinska Institute, because it's innovative and it's curiosity driven. Big pharma has not been so effective, and small pharma can grow out of Brazil, out of India and China.

David Fisher: So are you saying big pharma is actually an old world model?

Hans Rosling: And they know it themselves. It's a very interesting change taking place now. You find Pfizer for instance that have two new business areas, Emerging Markets and Established Products. During the patent period they learnt to produce the drugs so cheap that they continue to earn money on it afterwards - that's clever. They also put another price on the patented drug when they sell it in middle income countries, so it's affordable, they don't lose money on that. So they start to rethink also, and I asked them why? Because we have to, we are not earning enough money. This is interesting. Big pharma is not the success any longer. They have a decrease in their return on investment, and a lot of the money in big pharma is pension capital. I ask my students, should we hit big pharma because they don't deliver drugs for malaria? Yes, they say, hit them! Yes, but who should you hit? You have to be precise. Shall I hit the staff? No, no, no, hit the CEO they said. But he's elected by the board. Well, hit the board then! Well the board is elected by the stockowners. Well, hit them then! But who are the stockowners? They don't know. Well it's pension funds. Go home and hit grandma. It means that pension funds in the richest countries are those who have placed the money in big pharma to a big extent, and those are responsible.

I was concerned that so many at this meeting thought that population could solve the climate issue and the environmental issues. It will not. It's a constant, population. We have to get rid of poverty. Family size has to come down in Afghanistan and in Africa. Yes, that's right, but that's a minor thing. It's only 16 percent of world population that live in countries with three or more children per woman. 85 percent of world population live in countries with less than three children per woman, and the number of children is not growing any longer in the world. So what we need to do is to go directly and look at human behaviour in the richer part of the world. The services we use to support that behaviour and the technology that makes those services possible, that has to be much more green - much, more more green. And there's no way we can solve it by population. Population is a change of +/- 20 to 30 percent. The change in energy system we have to do is a question of 200 to 300 percent. We have to go for the big thing. And the agricultural subsidy is a shame. That's US$300 billion a year in the oeCD countries and it's much, much less than goes to green research. To me it's appalling to see that the most concerned national leaders when it comes to climate change is the Politburo in China! Now there are many other things that they are not concerned with, so don't think that I'm a Communist because I say this, you know! I'm really concerned about human rights in China. But they think that climate change is dangerous because it's dangerous for China, it's a national issue for them. And they invest in solar panels from basic research all the way up.

David Fisher: They're the world leader in solar now.

Hans Rosling: Yes! Because in the richest parts of the world we work with lobbyists to keep the old system, to keep the oil flowing and the cars running. We are not planning for the future. We are just planning to win the next election.

Isaac Kinde: My name is Isaac Kinde and I am from Baltimore, Maryland. I attend Johns Hopkins University.

Claire Robertson: I'm Claire Robertson, I am from the University of California at Irvine in California.

Catherine Howard: I'm Bree Howard, I'm from New Orleans, Louisiana, and I attend Tulane University.

Claire Robertson: Oh it's been awesome. It's been wonderful meeting our colleagues from around the world and hearing how science differs in different countries.

David Fisher: What about some particular lectures that really stood out?

Isaac Kinde: More so than the lectures, I think what really stood out was just eating, just having meals with the Nobel Laureates, just sitting at their table and discussing science and life, and just having these wonderful conversations that I don't think you would have access to otherwise.

David Fisher: Which Laureates did you have dinner with, or lunch or breakfast?

Isaac Kinde: So I had a meal with Harry Kroto and Peter Agre and also Werner Arber.

David Fisher: What about you guys? Did you have a meal with a Laureate?

Catherine Howard: I also had dinner with Dr. Kroto and his wife. I thoroughly enjoyed the discussions outside of the realm of science. I feel like the conference is really meant to connect the delegates, these are the other people around the world that we're going to be doing collaborations with, and the Laureates are able to guide not just the science that we do but how we're going to conduct our lives as researchers.

David Fisher: Did any of you go to the final presentation by Christian René du Duve?

Isaac Kinde: Yes.

Catherine Howard: No, that was unbelievably inspiration, and what he had to offer to us was more an advice on how to be responsible scientists and how to focus our efforts, and remind us that what we're doing is for the benefit of the world in general.

David Fisher: There was a standing ovation, it was amazing to see.

Catherine Howard: It was well deserved. It was well earned. He is a tremendous individual. I went to his discussion section afterwards, and his advice on living life as a scientist and how we can communicate to the general population, that's also our duty is to lead, be leaders in science, but also be leaders in society.

David Fisher: Do you think that's happening? Is the communication happening well enough?

Isaac Kinde: Certainly not. We don't receive a lot of training in communication and it's something that you have to practice I think in order to effectively communicate to people that don't understand science. Sometimes scientists have problems communicating science to other scientists, so it's even more difficult when you're talking to someone that has less experience. I think a lot of the Laureates have touched on this, that it's important to get others involved, whether they be in your field, in another scientific field, or have nothing to do with science.

Clare Smith: We didn't know what to expect from the Laureates. Like what are they actually like as people? And so we got to have some lunches with them one-on-one, and some of them were fantastic. They were asking, you know, so Clare, what are you doing? You know, what do you want in life? They wanted to know what the next gen, what we're going to be doing. It wasn't just about them.

David Fisher: Who were some of the Laureates who joined you one-on-one like that?

Clare Smith: So I got to speak to Elizabeth Blackburn one-on-one, and that-

David Fisher: From your home town!

Clare Smith: Yes, another Hobart girl. That was really cool to hear that, you know, it doesn't matter where you come from, she's a Nobel Laureate, she's doing great work, she's got family, she's loving life. She's an inspiration!

Jan Gralton: I got to speak one-on-one with Harald zur Hausen who discovered the link between cancer and viruses. He was fantastic. He has no problem with advocating his findings and disseminating that out to the public, and he's just an everyday person. That's the common message I think we can all say, they're all just like you and I, and they're just somebody who's found a discovery. That's the inspiring part of it.

David Fisher: How's the week been for you, Phillip?

Phillip Fitzgerald: So my name is Phillip Fitzgerald. I'm based at Johns Hopkins University where I'm doing a MD/PhD.

David Fisher: Where Peter Agre is!

Phillip Fitzgerald: Yes. He nominated me.

David Fisher: He nominated you!

Phillip Fitzgerald: Yes.

David Fisher: And how's the week been for you?

Phillip Fitzgerald: It's been amazing. It's just been a wonderful opportunity to put a face to the top of science.

David Fisher: Although you knew what Peter looked like!

Phillip Fitzgerald: Yes, I knew what Peter looked like. And to put a face and personality and the more personal and social aspect of doing science and doing it at a high level, that's what I'll take away most from this.

David Fisher: Tell me about some highlights, some lectures that stood out.

Phillip Fitzgerald: Smithies.

David Fisher: Oliver Smithies?

Phillip Fitzgerald: Oliver Smithies. I thought he had a personality, he was funny. I liked how he used pictures of his notebook to show how his work progressed.

David Fisher: We saw his notes written with a fountain pen before the ballpoint pen had even been invented!

Phillip Fitzgerald: Yes, and also just how he just showed his true love of doing science, and how he was always there on the weekends on Saturdays and how it just came across that this wasn't work for him, this was a labour of love.

Clare Smith: He called himself still a child of science and he was nearly 90, you know, and still running around the lab with his wife, who's also a scientist. They would be pretty amazing to work in the lab with.

David Fisher: Clare Smith and Jan Gralton from Australia, and Phillip Fitzgerald from the United States. Oliver Smithies, I've spoken to many of the young researchers, almost all of them mention your talk. What did you say to them?

Oliver Smithies: Well I don't know that I said anything very special in a way. I tried to take them through a lifetime of being a scientist, and that meant I started at the same age as they are. And so they could hear the things that happened to me when I was their age, and I think that maybe was the thing that in a sense caught their mind and their enjoyment, because I was talking to them as if I was at the same age as they were.

David Fisher: And it was a completely different world.

Oliver Smithies: Well, yes, it was a very different world scientifically. I mean things were not understood nearly as well as they are now in terms of biological science. For example, my thesis problem stemmed from some experiments which suggested one protein could be converted into a different protein just by putting it in the ultracentrifuge, and I mean we would call that completely crazy now. But it was the basis of the work that I did for my PhD.

David Fisher: How much time did you spend on that problem?

Oliver Smithies: I spent all my time on the part of the problem that I eventually was assigned. And I don't think assigned is the right word, because it was very much a choice as well, and I developed a new tool and I was very proud of it. So I was talking about making tools, and I think maybe they enjoyed the fact that I told them the tool I invented for my thesis work was published, but the paper has a record. And nobody every referred to it, and nobody ever used the method again and I never used the method again. And they enjoyed that thought, and I told them it doesn't matter what you do for a PhD, you're learning to do good science. It's not what you actually do that matters.

I talked about my first paper, which nobody quoted, and then I talked about my second paper which four people quoted. But it had one interesting sentence in it about an automatic pipette. The sentence was that the work described in this paper was made easier by an automatic pipette, however all the results presented were made with the manual pipette, so the automatic one was never published. But I made one and it was like the one that we all call the Eppendorf Pipettes now. It had a disposable tip and it would repetitively deliver one millilitre and it was accurate to a quarter of a percent. But as I told them, I never published it and I never patented it, and somebody else invented it later and became a millionaire!

David Fisher: Damn!

Oliver Smithies: The major thing that I had a hand in that was an important tool was gel electrophoresis, and that I invented in a sense by accident when I was in my first job in Toronto and I was having a problem with proteins sticking to filter paper, which was the medium for electrophoresis in those days for separating proteins. And I remembered helping my mother to starch the clothes as a child, and I thought well it sets into a gel, and maybe if I make a gel here the proteins won't stick to the starch gel. And that's indeed what happened and that was the beginning of gel electrophoresis, which is a tool that's still used all over the world. And that was the first of the major tools that I had a part in. I did have a part in others.

David Fisher: What were some others?

Oliver Smithies: Well, the one for which I was jointly awarded the Nobel Prize with Martin Evans and Mario Capecchi was the tool of showing how it was possible to alter genes in a living cell. And eventually that tool enabled us to alter genes in mice, so we could see what happens when a gene is changed in a mouse to make it behave differently, maybe make it not work or make it work stronger than normal or less strong than normal. And that tool, which is called gene targeting, was the tool that was important for the Nobel Prize in 2007. There are probably more than 20,000 different types of experiments have been done with this method, but basically the easiest way to think of it is that if you want to find out what something does, perhaps the simplest experiment you can do is to take it away and see what happens. If you want to find out what gene x does and you take it away and you find that the only thing that happens is the mouse tail gets a little shorter, perhaps you think it's not very important. But on the other hand, if the mouse starts to have behavioural problems and runs around in circles, then you begin to think well maybe this gene is important, and so you learn what different genes do by knocking them out.

David Fisher: Now people were amazed that you're still working at the age of 86. It sounds like retirement isn't even on the radar?

Oliver Smithies: No, it isn't on the radar for me, because I'm doing what I enjoy most.

David Fisher: And you run your own lab at the University of North Carolina with staff and your own young researchers. What are you working on these days?

Oliver Smithies: Well I'm working on something in relation to the kidney. I'm making little gold particles, which is rather fun chemistry, I have a Bachelor's degree in chemistry, and then I can make particles of different sizes, and I want to see what sizes can be discriminated by the kidney. Because the kidney is rather clever and it can excrete small molecules while keeping back big molecules. So when you pee, you don't pee away your antibodies for example. So there's some part of the kidney that does this and there's disagreement about where that is, so then I make my little particles and my post-doc injects them into a mouse and we see whether they go past the kidney or whether they don't go past the kidney, and we learn more about it. And that's the type of work I'm doing at the moment.

David Fisher: Oliver Smithies, from the University of North Carolina, in his 87th year, and working six days a week to understand more about how our kidneys work, preparing perhaps for his second Nobel Prize!

Martin Weissenborn: Martin Weissenborn. I live in Manchester, but I'm from Germany. It was one of the best weeks ever. I mean it all started with this amazing ceremony with Bill Gates and then the Federal Minister here and everything and the Countess was giving a speech. Then all the day we heard various Nobel Laureates, amazing talks really which really widen the horizon. There are so many amazing people who are just so interested in science, any discussion here improved my knowledge. I mean and then this boat trip today, we were on an island here on Lake Constance. I couldn't think of anything which could top it.

David Fisher: What will you take away from this week?

Martin Weissenborn: First of all, the fascination of science. I mean I was always fascinated about science, but seeing those Nobel Laureates which are like 90 and still go every day in the lab and love it just, yeah? And when we ask them where do you get your passion from, and they say which passion do you mean? I mean I just love what I'm doing. It's not that I work hard, and I'm not working more than 12 hours because I have all this free time, because I do what I like.

Everyone here I think will agree that the best speech was from de Duve, and it was not science related really. I mean it was more like of global health and how we can solve the problems of the world basically. But I mean this man is over 90 and he was so amazing. He was not using a pointer, he was using his stick, which he usually limps on, yeah? It was like listening to your grandfather which you really adore, and that was the best speech. But I mean science-wise I loved Jean-Marie Lehn. We had a discussion afterwards and he was playing the piano for us. He was like you're treating us as a collaborator, I have the feeling. I mean he was saying something on mass spectrometry and I said there's a new technique, and he came and like asked me, like can you explain it to me? And then we had a discussion about it. I mean he is a Nobel Laureate and he asked like a stupid student now over the technique. So it's amazing.

We had a couple of panel discussions. There was a question raised whether like everyone should do something like malaria, because we have to all cure malaria, it's very important to cure it, or cancer, shall we all work against cancer now? And then they said a very important thing. They said for example that if Bill Gates would be blind and he would spend like $250 billion, it wouldn't be for sure that he spends the money to an optician, then it wouldn't be sure that he gets it, because in the end what helps people to get sight again was the guy who invented the laser. So that means basically in any direction you go you could possibly cure malaria, you could possibly cure cancer. So it doesn't mean that you have to go in this direction. Maybe it's even better to go left or right.

David Fisher: So basically don't set out with an aim like that?

Martin Weissenborn: Exactly, exactly. Do what you want, what you're passionate for, and not what sounds good or what people like to hear.

David Fisher: Did you find it interesting that serendipity has come up in the stories of so many Laureates?

Martin Weissenborn: Actually I found it more interesting that there were some Laureates which didn't have the serendipity.

David Fisher: Why is that?

Martin Weissenborn: Because I mean, for example, Elizabeth Blackburn, she was doing her work over 40 years and you saw her paper, her publication, like every two years an amazing publication about telomerase, and then consequently she got the Nobel Prize. With the serendipity you know, obviously I mean they told us keep your eyes open, and we will do this, but I mean it is hard to count on serendipity, isn't it? I would rather go the approach which Elizabeth Blackburn did for example, or also like which Oliver Smithies did, he had so many inventions in his whole life. So what more, go this way and if something pops out, obviously then I go for it. So it's probably easier to go there, as the Elizabeth Blackburn way, and if you find something then go for it.

Phillip Fitzgerald: I really appreciated the Laureates that were willing to use their clout and their name to advance the field of science overall, such as Sir Harold Kroto, Christian de Duve who had written the book on overpopulation. There are multiple ways of helping to ensure that we are training the next generation of scientists and that this field and process will continue on after they are gone and after even my generation is gone and retired. With that Nobel Prize they have a power to affect public opinion about scientists and about the scientific discipline. Some of the scientific organisations have been very active, but at the same time I just don't think that that is as effective as having a charismatic person that people can connect to and see their face, you know? We have all these organisations with their acronyms such as American Association for the Advancement of Science and the International Union of Concerned Scientists and Engineers, but I don't think any acronym can stand up to some charismatic politician that's on the television screen every day saying evolution is a myth, or we should not do stem cell research because it's killing babies, even though an embryo is only like two days old and it's only like eight cells. So I really appreciated the scientists that were really willing to put their face to their position and go out into the public and try to change public opinion. I also want to say that the Laureate Dr. Blackburn, Elizabeth Blackburn from the University of California, San Francisco, did that during the mid-2000s when she spoke out in advocating stem cell research. So there were a good handful of Laureates that were doing that, and I see how public opinion doubting climate science has held the world back from really tackling that issue at a substantial level, and the embryonic stem cell research issues of the 2000s before the Obama administration came in, and how that prevented good scientists from having the resources to do robust research.

David Fisher: So is the Nobel Prize the career pinnacle for a scientist? Hans Rosling from Sweden's Karolinska Institute spoke in a panel discussion on global health, which we'll hear later in the year on The Science Show. Here's his take on the ultimate reward for scientists and medical researchers.

Hans Rosling: The personal highlight was to sit on the podium next to Professor zur Hausen. He's my hero. He found the cause of a major disease and he found a way to prevent it - cervical cancer in women. And when I worked in Africa I saw so many women dying painfully of cervical cancer. The only thing I could do was to give them aspirin. It was so embarrassing and so tragic. Cervical cancer is so common. Actually if we could cure that, it is as important in many African countries as HIV. But you could see that the man is not fully satisfied, you know. And I asked him, wouldn't it be a greater prize for you if your vaccine could be made available cheap enough so everyone could get it? Oh yes, that would be the best prize, he said. You know, he said, my grandmother died from cervical cancer, so I always knew how painful it was. And it's interesting, a Nobel Prize is not the most important for a researcher - it is that his research really reaches to the people in need, and it's sort of sad to come half way, you know? The tragedy for him is that he got the Nobel Prize, but most people who need his result can't get it. That's tragedy. And what is interesting with this, to make it available is not about aid, it's about doing one more step of research and see how you can produce that wonderful vaccine at the lower cost and against the viral types that exist in each country, and then find the economical model to do that. And perhaps aid would be best used to develop that cheap way of doing it, or to give a free licence for the Indians to do it, because they're very capable.

Robyn Williams: Hans Rosling from Sweden. He'll be on The Science Show again ,as David said, in November. You should bottle that enthusiasm. And never malign a 90-year-old again, that previous Nobelist, Christian de Duve. Our thanks to the Australian Academy of Science and the Lindau Nobel Laureates Foundation for their assistance with that event.