The earliest film, Onwards to Victory, 1953, most closely resembles government war propaganda from the Ministry of Information and the newsreels shown during the Second World War. The film exploits the viewers’ patriotism and builds on the metaphor of science and technology’s contribution to Britain’s victory. The public are asked to give generously in support of the campaign to defeat the peacetime ‘menace’ of cancer.

The second film, The Modern Crusaders, 1958, celebrates the heroic struggle of the white-coated ‘mid-twentieth century crusaders’ against cancer. The voice-over, by an unseen male narrator, explains how much money is needed to cover the cost of the high-tech equipment shown. Despite the reassurance of scientific progress, the film communicates an urgent and ‘anxious’ appeal for funds. It was shot at the British Empire Cancer Campaign’s Chester Beatty Research Institute at the Royal Cancer Hospital (aka Royal Marsden Hospital), Surrey.

The Fight against Cancer: An appeal by Margaret Leighton, 1959, is an appeal by the British celebrity Margaret Leighton, who would have been familiar to cinema audiences during the 1940s and was critically acclaimed for her theatrical performances in the 1950s. Complete with her clipped accent, pearls and fur stole, she gives a very personal appeal to the public to contribute to the funding effort. The endorsement of charitable causes by famous but more accessible actors became more prevalent around this time: Harry Secombe appears in Penny Parade, 1964, an appeal on behalf of the Spastics Society, which became later became Scope, a charity for those with cerebral palsy, which also campaigns for equality for disabled people.

A trend in health communication is to have a more patient-centred approach and use the testimony of the patients themselves. Television and the Internet are much more intimate spaces – the emotional impact of these real stories can be more powerful. A compilation of Cancer Research UK’s television commercials can be viewed on their YouTube channel. A selection of videos made for patients about cancer, including testimonies, can be viewed on the NHS Choices website.

Angela Saward, Wellcome Film

You can learn about the Wellcome Film project here. If you would like to make use of this archive footage in your own projects, please visit the Wellcome Library catalogue to download the original files, which are distributed under a Creative Commons Attribution-Non-Commercial 2.0 UK: England & Wales licence.

In the latest of our shortlisted entries to the 2011 

Its surface is white as snow and covered in ice. Large expanses are smooth and unblemished, belying a history of constant meteorite bombardment. In one site near this moon’s south pole there are cracks tens of miles long. Ice and water, from vast underground oceans, are constantly spewed out of these cracks into the blackness of space.

Sounds like something from Doctor Who, right? Well, this moon actually exists, and it’s closer than you might think.

Enceladus is the second smallest of Saturn’s major moons. Until the Voyager 2 satellite passed in 1981, we knew little about it. Now, with the Cassini-Huygens satellite performing having performed several close fly-bys, the story of Enceladus is beginning to become clear.

Enceladus has one of the most reflective surfaces of any object in the solar system. It is also one of the most geologically active solar system bodies. This may seem counterintuitive at first, but it is no surprise to the scientists that study Enceladus — geological activity is what makes the moon so pristine and reflective in the first place. Ice volcanoes are able to constantly replenish the surface, covering up the scars of meteorite bombardment.

As it orbits Saturn, the pull of the planet contorts Enceladus. Saturn inflicts so much force on the tiny moon that ‘hotspots’ are created near its south pole, creating four giant cracks. Each is around 80 miles long, a mile wide and 500 metres deep. These cracks, affectionately known as ‘tiger stripes’, are 100°C hotter than the rest of the moon.

Cassini took the first clear pictures of the tiger stripes in July 2005. Their signature however, had been seen a few months earlier. In February 2005, small changes in the magnetic-field data revealed Enceladus had an atmosphere containing water vapour. There was something a little out of the ordinary about it, as the atmosphere was concentrated around the moon’s south pole, right above the tiger stripes. Ultraviolet images later confirmed what scientists had suspected: the stripes were the source of the giant plumes of water vapour and ice being ejected into space.

In the 1980s, scientists had some idea that these plumes might exist. During its time around Saturn, Voyager 2 searched for them but found no conclusive evidence of their existence. Scientists working on the Cassini mission decided that they could not take any chances — a fly-by had its path altered, bring it closer to the surface of Enceladus. It flew through one of the gas clouds created by the plumes and confirmed the presence of water, dust and molecules containing carbon and hydrogen.

One of the few things that we knew about Enceladus before Voyager 2 and Cassini was that it was icy. Since the discovery of the tiger stripes and plumes, scientists have speculated that there is also liquid water beneath the surface.

Although the forces exerted by Saturn on Enceladus are insufficient to explain the heating occurring around the tiger stripes, combing their effect with that of a vast ocean beneath the surface, able to transport heat more efficiently, might explain the phenomenon.

Evidence of a hidden ocean was suggested in December 2008 when scientists noticed that the tiger stripes had moved. They think that something similar to the movement of Earth’s tectonic plates is occurring on Enceladus, with the surface of the moon splitting and material coming up from underneath to fill the gap. On Earth, the material that fills the gap is molten rock. On Enceladus, it could be water.

Yet more evidence came a few months later. Unusually high levels of salt were discovered in water from the plumes. Salt tends to come from large bodies of water; oceans are big enough to have significant amounts dissolved within them, while ponds are not.

Liquid water, combined with heat and the organic molecules seen in the plumes, increases the chance that life might develop on Enceladus. If water does exist on Enceladus, it will join Mars and Europa, a moon of Jupiter, at the top of the list of places to look for life in the solar system.

We are discovering more about this moon all the time. Earlier this year, for example, it was revealed that the ice volcanoes on Enceladus create an electrical circuit between the moon and its planet. This produces aurora, better known as the northern lights here on Earth, on Saturn.

If these recent discoveries are anything to go by, Enceladus is only going to get more interesting. The Cassini mission was originally meant to run for four years, until 2008. It has now been extended twice, and will keep exploring Saturn and its moons until at least 2017. Watch this space.

Kelly Oakes

This is an edited version of Kelly’s original essay. Views expressed are the author’s own.

Find out more about the Wellcome Trust Science Writing Prize in association with the Guardian and the Observer and read our ‘How I write about science‘ series of tips for aspiring science writers.

Over the coming months, we’re publishing the shortlisted essays in this year’s inaugural competition.

Image Credit: kokogiak on Flickr

Understanding these health impacts is a challenge for science. Communicating and acting upon that information is a challenge for all of us. Artists have been helping with this important process, for example the 2005 visit to the Arctic by a joint group of artists and scientists, which produced the novel Solar.

Video games have, in their own way, responded too. There are games that look specifically at the health issues (such as Climate Health Impact by the Wellcome Trust and Playgen) and games that put the player in the position of trying to persuade the world’s countries to act together (Fate of the World). But there are also games that use the changed world as a narrative setting.

Brink is a first-person shooter. Most such action games use aliens, World War II or terrorism as their setting. Brink uses climate change. I asked the game’s writer, Edward Stern, why. 

“We knew the narrative backdrop for Brink had to be visually distinctive and explain why people are fighting, what they’re fighting for, and why they don’t just leave. All of this seemed to require resource scarcity and isolation. Perhaps an island of some sort, but why would people be on an island?

“I’d read about the Sea Standing Institute and seen some other terraforming/engineering solutions to rising sea levels on Jeff Manaugh’s BLDG BLOG. So that lead to the Ark, Brink’s techno-visionary artificial island – built to combat climate change but cut off from the outside world and running out of spare parts… it wasn’t anything I’d seen in a game before… But it also plugged into current concerns.”

Given how much the science drives what you know (and don’t know) about climate change Stern looked for credible sources to inform his writing, but sorting what’s reliable in a controversial topic like climate change was a challenge for a non-expert.

“My training, such as it is, is as a Historian,” says Stern. “So my test for researching a topic is; have I read the primary sources, or am I relying on secondary sources, or have I just read one book, or have I read several web posts but they’re all misquoting each other?

“I used to follow the science and the culture/media brouhaha surrounding [climate change] as best I could, mainly starting with Science Blogs and Real Climate and following links from there. I couldn’t understand absolutely every detail of the Mann ‘Hockeystick’ and the stolen CRU emails, but I went through them as thoroughly as I could, keeping as open a mind as I could. If I couldn’t be an active combatant in the information wars, I could at least be a well-informed civilian.”

And how does the wealth of scientific information contribute to the creative aspects of the game?

“There’s the old statistics joke that the plural of anecdote is not data. But from a writer’s point of view, the singular of data is not anecdote – you can’t just invoke a scientific buzzword and hope that will make things seem credible or dramatic to a player/reader. It has to be something you can show or tell within the game.”

“I love it when a game connects to the non-gaming bits of the brain. I always cite Deus Ex as the first game I played where I genuinely didn’t know what to do. Not just what the game would reward me most for, or what would move the action along, but because I genuinely didn’t know how I felt about the real world choices and issues the designers had put in their game for my character to deal with.”

I’ve completed Brink and the setting of the game, and the characters’ responses to the world they’re in is credible and engaging. Given that climate change is a hot political issue, and will be for some time, its a bold decision to place the issue front-and-centre in a key part of popular culture – gaming. This is key as a growing number of people play games and see games as a primary source of understanding about the world around them. As Stern told me, “I was trying to make it as easy as possible for players to let the game stick in their minds, to plug into their existing concerns and prejudices about real world issues. And few people know or care absolutely nothing about climate change, whatever their outlook.”

Tomas Rawlings

Tomasis a Video Games Consultant for the Wellcome Trust. You can read the full version of Tomas’s interview with Edward Stern on his blog. See also his previous posts on games and science.

Find out more about the Wellcome Trust’s support for games.

Sue Horner

What is the role of inquiry-based learning in an inspiring science education? And what are its boundaries and limitations? In the last of our Perspectives essays, former Director of Curriculum Sue Horner outlines the difficulties in developing clear policy that can be easily interpreted and implemented.

A central challenge in writing a National Curriculum is one of definitions: what do we want the core content to be and how can this be best explained to a range of users? This is in addition to the challenge – common to all education policy – of offering a legislative framework that raises standards. For it to be respected, the framework needs to be intellectually cogent, realistic and practical to implement, and to attract sufficient support from the scientific and teaching communities.

One of the conventions of the National Curriculum is that it specifies the matter to be taught but not how it should be taught. The supposition that any subject can be ‘pedagogically blind’ is simplistic for two reasons. First, learning is constructed through pedagogy and the nature of a subject is conveyed by how it is taught. Second, the way the curriculum is written has implications for the classroom: the importance of scientific inquiry is inferred from how it is represented in the National Curriculum. The 2007 curriculum (1) emphasises ‘scientific thinking’, ‘practical and enquiry skills’ and ‘critical understanding’, and these rightly have clear implications for pedagogy. 

Scientific inquiry in the science curriculum

The National Curriculum seeks to capture the essence and scope of the study of science in school. Integral to that is the nature of inquiry and its relationship to scientific knowledge, derived through experimentation and observation. Students therefore need to understand not only scientific ideas but also how they are constructed.

Inquiry is essential to the development of scientific ideas and essential for understanding the world. This means that inquiry is more fundamental to real science than other pedagogies or classroom activities. It has always been hard to represent the integration of content and process in the curriculum.

The challenge for teachers is to select teaching methods that promote students’ understanding of how scientific knowledge is constructed. This gives greater significance to the pedagogies used in science, as they affect learning in more fundamental ways than those in other subjects may.

The curriculum is a framework that, before being implemented, needs interpretation by intermediaries – such as continuing professional development providers, awarding bodies, textbook writers and teachers. Of course, different intermediaries, with their own views of the subject, may emphasise the aspects they favour  There is a tendency for different groups to argue for content but not process.

What is defined in law is intended to provide a shared understanding of science. It also has to serve many purposes, for teaching and assessment, and a recent criticism of the science curriculum (2) is that lack of detail has led to inadequate guidance for these different purposes. Judgements, however, do have to be made about what is the irreducible core of science. This has been a constant struggle, especially because ‘new’ areas of knowledge will continue to appear, leading to a temptation to specify too much content. Alternatively, rigorous inquiry could be at the core – enabling students to tackle a subset of knowledge in depth and to develop skills that will enable them to understand science more broadly.

What is progression in science and how can it be assessed?

Progression in inquiry means, for example, students making more rigorous observations, taking account of more experimental variables, analysing more complex evidence and ensuring that conclusions are more scientifically valid. Poor articulation of this progression can lead to repetition rather then progress.

Assumptions about progress are most exposed in assessment. To support learning, assessments should recognize the complexity of a subject, but current qualifications mostly assess knowledge through written examinations and skills through set practical experiments. These methods of assessment do not therefore reflect the integration of knowledge and inquiry upon which science relies.

Recent critical events in assessment have exposed some of the problems:

• GCSEs have recently had to be rewritten as, according to Ofqual, there was too great a reliance on multiple-choice questions. (3) They seemed to focus on recall of information; by age 16 this was not considered sufficiently challenging since it reveals nothing about the thinking required to explain processes, ideas and the significance of evidence.

• Key Stage 2 science tests came under fire because it was thought that a reasonably knowledgeable pupil who had studied no science at all could answer some of the questions based on ‘common sense’. There were also concerns that tests were too susceptible to cramming information. Again, as with GCSE examinations, remembering the facts or making simple deductions was considered inadequate.

A completely different model of assessment underpinned the criteria in Assessing Pupils’ Progress (APP). (4) Instead of specifying knowledge separately and recognising process, the assessment criteria focus on effectiveness in aspects of inquiry, including ‘thinking scientifically’, ‘communicating and collaborating in science’, ‘using investigative approaches’ and ‘working critically with evidence’. This is the best attempt so far to describe progression in these skills. The apparent lack of content in APP initially caused anxiety, but it soon became evident that students could only progress if they used and developed their scientific knowledge. In fact, APP provided a framework within which knowledge was activated and teachers collected more varied and richer evidence of what their students actually knew. This, then, was a way of integrating knowledge and inquiry in assessment.

Techniques for assessment need to be sufficiently sophisticated to support a complex view of learning in science. If scientific inquiry is inextricably linked to knowledge and understanding, then assessment needs to find ways to test this. If not, inadequate assessments will continue to inhibit teaching and learning.

Inquiry and the whole curriculum

The processes of inquiry are not solely the purview of science, with common ground clearly evident in 11 of the 12 subjects in the 2007 National Curriculum (the exception being modern foreign languages). No skills or processes can be learned in a vacuum and, although the kinds of question and the methods of investigation may vary between subjects, students are being asked to undertake similar thinking. Students benefit when connections enable them to develop and apply skills across subjects, since they are not relearning but applying and adjusting their learning to a different context.

The importance of these skills is underlined in the QCA’s Personal, Learning and Thinking Skills (PLTS), (5) which see ‘independent enquirer’ skills as essential to success in life, learning and work. Even though these are non-statutory, many schools see them as important for their students, and employers are keen for applicants to demonstrate these skills. Pupils, too, have voiced their preference for active, participatory and collaborative learning, as evidence from NFER6 and CUREE7 shows. So, scientific inquiry not only animates learning in science but also contributes to the development of the wider skills needed by all learners.

The National Curriculum seeks to set out what we, the nation, want our young people to know, understand and be able to do. The 2007 version sought to include the necessary knowledge and skills for those who will become scientists or take up science-related work, as well as providing a basis for all students to make sense of the world. Integrating scientific ideas and knowledge with rigorous inquiry methods can promote this, and policy can support this approach. What policy can’t do is ensure that everyone agrees and that all the intermediaries interpret the curriculum in the same way.

With the National Curriculum now potentially moving into a new phase, it is the responsibility of all those with a stake in science teaching to use their judgement and autonomy to make sure inquiry is fully integrated into science learning.

Sue Horner

Dr Sue Horner is Former Director of Curriculum of the Qualifications and Curriculum Authority. She has worked in national policy roles on curriculum and assessment for 18 years, during which her priority was to find ways to take forward thinking and practice in teaching and learning. She also works in the arts and is on the Board of several national charities.

The original version of this essay appears in the newest issue of our Perspectives on Education series, in which four authors explore these questions from their perspectives as a teacher, an international education expert, a policy maker and a researcher. We’ll be publishing each essay here on the blog, but you can download the full publication for free on the Wellcome Trust website. 

References

1. The National Curriculum statutory requirements for key stages 3 and 4. QCA, DCSF; 2007.
2. Oates T. Could Do Better: Using international comparisons to refine the national curriculum in England. Cambridge Assessment; 2010.
3. The new GCSE science examinations: Findings from the monitoring of the new GCSE science specifications: 2007 to 2008. Ofqual; 2009.
4. Department for Children, Schools and Families. Assessing Pupils’ Progress. 2009 [accessed October 2011].
5. Qualifications and Curriculum Authority. Personal, Learning and Thinking Skills. 2008.
6. Lord P, Jones M. Pupils’ Experiences and Perspectives of the National Curriculum and Assessment. Final report for the research review. National Foundation for Educational Research; 2006.
7. Centre for the Use of Research and Evidence in Education. Building the Evidence Base. Qualifications and Curriculum Development Agency; 2010.

Professor Fiona Powrie

Professor Fiona Powrie, a Wellcome Trust Senior Investigator at the University of Oxford, is one of two scientists who will be awarded the 2012 Louis-Jeantet Prize for Medicine at a ceremony in Switzerland in April. She will receive CHF 625,000 (£430,000) for her research and CHF 75,000 (£50,000) as a personal award.

Fiona wins the prize for her work on “the interactions between the bacterial intestinal flora and the immune system”. Her research looks at why the immune system does not usually attack the numerous beneficial bacteria that live in the gut, and how we can improve treatment for conditions caused when the immune system gets it wrong. Inflammatory bowel diseases such as ulcerative colitis and Crohn’s disease are caused by an inappropriate immune response in the gut.

I interviewed Fiona last year and will be posting a feature on her work in the next week or so. It is fascinating research, not least because the immune system in the intestines in not quite the same as it is in the blood, which is where it is more usually studied. Immune cells and signals do different things according to where they are. As Fiona said, it’s all about location, location, location!

Fiona was one of the first people to receive a Wellcome Trust Investigator Award and she has made important contributions to immunology throughout her career. As a DPhil student in Oxford, she discovered the role of regulatory T cells in suppressing inflammation, and later she developed some of the first mouse models for inflammatory bowel disease. Today, she is Head of the Experimental Medicine Division and the Translational Gastroenterology Unit at the John Radcliffe Hospital in Oxford, as well as being the inaugural Sidney Truelove Professor of Gastroenterology.

Many congratulations to Fiona, and to Professor Matthias Mann, a German researcher who also wins the Prize this year for his work on developing the use of mass spectrometry in proteomics.

Image credit: Wellcome Images

Alex Bateman

In a world in which anti-science appears to be on the increase, it is imperative that scientists improve how they engage with the general public about their research. A traditional way to do this is to give talks at science fairs and engage directly with schools. A problem with this ‘standard’ public engagement approach, however, is that the reach can be quite limited and is often a case of preaching to the converted.

Of course, if your research is ‘hot’ enough you can push stories through the mass media, such as TV and newspapers, hoping that the results don’t get too garbled in the telling. I believe that these limitations, combined with the fact that many of these activities are time-consuming, inhibit many scientists from communicating effectively with the public.

If you really want to let the public know about your science then the only way is Wikipedia. For better or worse, Wikipedia has become the central repository of knowledge on the internet. If you don’t believe me then try the following experiment. Pick a word and type it into Google. For most terms – e.g. ‘malaria’, ‘research’ or ‘opinion’ – Wikipedia is the top hit.

If you want to get a quick overview of a topic, it’s likely you’ll go straight to Wikipedia. Now think about the hundreds of millions of internet users out there who will, at some point, want to find out something about science, technology or medicine. I’m afraid that they will almost certainly not be heading to your latest research article to do so.

Editing Wikipedia can seem daunting at first. Some researchers might be put off because their first impulse is to tackle editing an article there the same way as they would write a research paper – perfect it and then let others review it before final publication. Wikipedia doesn’t work that way. You don’t need to rewrite the history of a science article, just add a sentence here, a reference there. You can make a useful contribution to Wikipedia without making a large investment of your time.

So if you are interested in helping the public understand what your research is all about then I urge you to learn how to edit and improve Wikipedia. Find the relevant article and make whatever changes you think are needed to ensure that the content is scientifically accurate and up to date. It doesn’t take a lot to make a big difference, and you get to fulfil some of your public engagement responsibilities in the process too.

Alex Bateman

Dr Alex Bateman is a research scientist at the Wellcome Trust Sanger Institute.

Neglected tropical diseases (NTDs) affect the world’s poorest people, causing death, disability and prolonged disadvantage. Many of these diseases lack effective treatments but the rising profile of NTDs means more resources are becoming available for research and development. However, the challenges of finding new drugs for NTDs go beyond funding, as Michael Regnier reports in the fourth post in our NTDs series.

A handful of NTDs – schistosomiasis, trachoma and hookworm, for example – have effective drugs available for treating them. For these diseases, the challenge lies in acquiring and distributing sufficient doses to treat the millions of people suffering with them. However for many, if not most, NTDs either there are no drugs or the drugs we do have are old, cause significant side-effects, are very expensive, or are losing their potency because the parasites, viruses and bacteria that cause the diseases are developing drug resistance.

Professor Alan Fairlamb

Professor Alan Fairlamb, Co-Director of the Wellcome Trust-funded Drug Discovery Unit (DDU) at the University of Dundee, says that only a handful of NTD drugs are truly fit for purpose: “Many compounds were originally developed with a different indication in mind, maybe from cancer research or anti-fungal drug discovery programs. The target product profile for these original indications does not take into account the association with poverty and the rural setting where most NTD drugs are needed.”

The cost of new drugs is another significant issue. “Expensive drugs are good for the odd safari but too costly for the local population,” he adds. “People often can’t afford the treatment, so they don’t complete the course and this drives resistance. The challenge is to develop cheaper and safer drugs.”

The Dundee Unit works with scientists who have discovered a promising target but perhaps don’t have the know-how or the infrastructure to do drug discovery. “Our vision is to take excellent basic science and turn it into useful medical products,” explains Fairlamb. They work directly with industry and through product development partnerships such as the Drugs for Neglected Diseases Initiative (DNDi).

“The product development partnership is a good model,” says Fairlamb. “It is starting to transform the situation with respect to new drugs [for NTDs]. But there is a five-year cycle of funding, they need to demonstrate success and, understandably, are therefore slightly risk-averse to early stage drug discovery. The DDU fills this gap.”

The Unit’s most successful project to date is based on an enzyme called N-myristoyltransferase (NMT), which was developed as a target for new drugs to treat leishmaniasis and other diseases at Imperial College London by Professor Deborah Smith, now at the University of York.

Journey of drug discovery

“We sequenced genes from Leishmania parasites transmitted by sand flies and screened for molecules produced exclusively in the infective stage of their life cycle,” Smith explains. “We found one molecule that had to undergo a specific modification in order to be presented on the surface of the parasite cells. That modification was catalysed by NMT, which we knew had been previously developed by Pfizer as a drug target for fungal pathogens.”

Although Pfizer had developed inhibitors of NMT, they were each specific to particular species of fungus. Doctors would have had to identify the type of fungus infecting their patient before treating them with the right NMT inhibitor. Because fungal infections can be difficult to distinguish, Pfizer had instead turned its attention to developing general antifungal drugs that would work against multiple species.

Knowing that Pfizer had already worked on NMT meant Smith and her colleagues could be confident that it was a strong candidate for development. The specificity of NMT inhibitors would be less of a problem because, while there are different species of parasite that cause leishmaniasis, they cause distinctly different symptoms in different parts of the world.

Smith persuaded Pfizer to share some of their compounds for her research to confirm that NMT is vital to Leishmania parasites. Then she discovered that the enzyme is also found in the parasites that cause human African trypanosomiasis (sleeping sickness) and may even be a target in Plasmodium, the parasite that causes malaria.

Professor Deborah Smith

“Will one key enzyme be a target for multiple parasites? There’s still a long way to go,” says Smith. Even if the work on NMT does not lead to a viable drug for all these diseases, however, it will be valuable research. “We’re doing the groundwork for future potential opportunities,” she concludes.

A large consortium is now working on drugs to target NMT in the various diseases. Work on human African trypanosomiasis is being led by the Dundee Drug Discovery Unit, while Smith is leading work on leishmaniasis and Plasmodium in York in collaboration with colleagues at Imperial College London, the Medical Research Council National Institute for Medical Research in London, and the University of Nottingham.

Safeguarding treatments

Professor Paul Kaye, Director of the Centre for Immunology and Infection at the University of York, has been doing research into leishmaniasis for many years and knows that new targets like NMT are rare and clinical trials even more so. “Poverty is a major driver both in the disease and in limiting investment,” he says. “We don’t have the money to do iterative testing as in other diseases. Malaria has seen 20 to 30 trials in recent years, whereas we’re seeing the first clinical trial in leishmaniasis to be funded in ten years.” As with all NTDs, it is crucial to keep pursuing other avenues of research.

Professor Paul Kaye

For example, Kaye and Smith are working together on developing a therapeutic vaccine for leishmaniasis, targeting a different arm of the immune system to that focused on by most previous research (CD8 rather than CD4 T cells) and using new vectors to deliver the vaccine. It is one of just two second-generation vaccines in development for leishmaniasis and they hope to start phase I trials this year.

“We need to protect the drugs we have,” says Kaye. “We only have three leishmaniasis drugs and there is already resistance to the commonest drug in parts of India where visceral leishmaniasis is endemic. Second-line drugs are being used but while these are very effective, they do have some side-effects and are costly. A therapeutic vaccine given in combination could help protect the drugs’ lifetimes. Also, we could use lower doses or a lower number of doses or expect greater compliance, which would all help to minimise resistance.”

Underpinning this work are years of basic research. Kaye himself has spent 25 years looking at the fundamental immunology of why chronic disease develops from some leishmaniasis infections and not others. “Most people are well-protected and don’t show any symptoms,” he says. “What makes others susceptible?”

Smith’s postdoctoral research was in molecular biology, looking at the control of gene expression in Drosophila (fruit flies). “I became interested in the potential for applying the tools I was using in fruit flies to sand flies and the parasites they carry,” she explains. “We are basic, fundamental biologists working on pathogenic organisms. Our long-term goal is to have an impact on human disease, work that is desperately needed. We’ve been to these countries and are aware of the constant and continuing challenge these diseases present.”

This is one of a series of blog posts accompanying a Wellcome News feature on neglected tropical diseases. Next week: Approaching the problem from all angles – why a number of approaches are needed to tackle any one NTD.

Related resources:

Frearson, J., Brand, S., McElroy, S., Cleghorn, L., Smid, O., Stojanovski, L., Price, H., Guther, M., Torrie, L., Robinson, D., Hallyburton, I., Mpamhanga, C., Brannigan, J., Wilkinson, A., Hodgkinson, M., Hui, R., Qiu, W., Raimi, O., van Aalten, D., Brenk, R., Gilbert, I., Read, K., Fairlamb, A., Ferguson, M., Smith, D., & Wyatt, P. (2010). N-myristoyltransferase inhibitors as new leads to treat sleeping sickness Nature, 464 (7289), 728-732 DOI: 10.1038/nature08893

The Wellcome Trust website has a number of scientific animations showing the life cycles of many parasites, bacteria and viruses that cause diseases including some NTDs. Eg:
Leishmaniasis – fly / human
Human African trypanosomiasis – fly / human
Malaria – mosquito / human

Prof. Elaine Fox

What causes mental illnesses such as anxiety disorder or depression? Are some people more likely to develop these conditions than others? What is the best way to treat them? These are just some of the challenging questions that Professor Elaine Fox, a psychologist at the University of Essex, is trying to answer. She and her colleagues have recently found that a variation in the gene that encodes a particular protein could make some people more sensitive to their emotional environment – and more susceptible to anxiety disorders – than others. I spoke to Professor Fox to find out more.

Which protein have you been studying?

We’ve been looking at the serotonin transporter, a protein that ‘recycles’ serotonin [a neurotransmitter] during nerve signalling. When a nerve signal is passed from one neuron [nerve cell] to the next, serotonin released by the first neuron carries the signal across the gap to the second neuron. Afterwards, serotonin transporters remove serotonin from the gap and return it to the initial neuron, ready to be released again when another nerve signal is transmitted.

Why were you interested in it?

We’ve known for a while that the gene that contains the instructions for making the serotonin transporter seems to play a role in increasing the risk of a person being emotionally vulnerable, particularly in relation to depression and anxiety.

This gene varies across the population. Some people have short versions that result in them having fewer copies of the serotonin transporter, and therefore higher concentrations of serotonin in the gaps between neurons. Others have long versions of the gene that lead to more copies of the serotonin transporter and lower serotonin levels.

About a year ago Arne Öhman, and his group from the Karolinska Institute in Sweden, published a paper that showed that people with short versions of the serotonin transporter gene learnt to fear [by exposure to a “highly annoying but not painful” electric shock] much more quickly than people with long versions.¹ Their findings suggested that these people have brains that are much more reactive to threat.

I thought it would be really interesting to look at this link between the serotonin transporter gene and how the brain learns in the context of the attention bias modification (ABM) procedures that I was already using.

What are attention bias modification (ABM) procedures?

They are techniques that can be used to change the amount of attention a person pays to something, known as an attention bias. ABM training typically involves using a computerised training programme to alter a participant’s attention bias.

It’s normal for healthy people to have low levels of ‘trace’ attention bias, which may focus their attention slightly more towards either positive information [if they have a positive trace attention bias] or negative information [if they have a negative trace attention bias].

People with anxiety disorders have a very strong bias in their attention towards threats [a negative attention bias that is much larger than the trace levels found in healthy people]. The interesting question is: do people with anxiety disorders have a strong negative attention bias because of their anxiety, which tunes them into things that are threatening, or are these biases part of the reason why people have developed anxiety in the first place? The evidence now indicates that the biases can indeed cause anxiety problems to develop.

We want to find out whether ABM techniques can be used as a treatment to reduce negative attention biases in patients with anxiety disorder, and therefore reduce their emotional vulnerability. It may be that they won’t be used as a stand-alone intervention, but might actually be very powerful if combined with other techniques, like cognitive behavioural therapy [a talking therapy] or drug therapy.

What did you do?

We combined ABM training with genetic testing for the first time, to investigate the relationship between the serotonin transporter gene and how quickly people can “learn” to develop a bias in attention².

Our experiment involved testing two groups, each of 57 healthy people. We used computer-based tasks to test whether the volunteers had an initial trace attention bias towards either positive or negative images, and then gave them ABM training to induce a positive bias in one group and a negative bias in the other. We then re-tested participants to see if their initial attention biases had changed, and whether their performance varied according to which version of the serotonin transporter gene they had. Both groups contained some people with short versions of the serotonin transporter gene and others with long versions.

Attention bias testing involved briefly presenting two images at the same time, side-by-side on a computer screen. One image was highly positive [e.g. a smiling baby] and the other was highly negative [e.g. a snarling dog]. Both images disappeared after half a second and one of them was replaced with a symbol. We measured how quickly a participant was able to identify the symbol, and used this to calculate their attention bias. For example, if someone was more tuned into the positive, they were slightly faster at finding the symbol when it appeared in the location where the positive item had been, compared to when it appeared where the negative item had been.

Each participant’s response time was measured 128 times, in which there was equal probability of the symbol replacing either the positive or negative image.

ABM training was conducted in almost the same way as attention bias testing. Over hundreds of trials, people saw pairs of images flash up on the screen, followed by a symbol. The difference between this and the testing was that the symbol always replaced the positive image during positive attention bias training, and always replaced the negative image during negative training.

We were orientating people’s attention system towards either positive or negative information [depending on which training group they were in], even though they weren’t really aware that the symbol was always appearing behind the same type of image.

What did you find out?

People with a short serotonin transporter gene developed stronger biases over an hour’s training session than those with long versions of the gene. The unexpected finding was that this was true for both negative and positive information. In other words, people with short forms of this gene were more sensitive to the emotional significance of their surroundings, irrespective of whether that environment was positive or negative. This means that they are likely to be far more reactive to very negative situations, such as a car crash, putting them at higher risk of developing emotional vulnerability.

On the other hand, when they experience something very positive such as a supportive relationship, they may be able to benefit from it far more than someone with a long serotonin transporter gene would. This supports the idea of short serotonin transporter genes as ‘adaptability’, rather than ‘vulnerability’ genes, or what you might call a “make you or break you gene”.

In healthy people, a trace attention bias is not likely to have a dramatic effect on a day-to-day basis. The idea is that these biases are not particularly damaging in themselves, but over time they really do start changing brain states. If you imagine someone with a small negative attention bias who experiences negative events 8 or 9 times every day, over a month, a year, or many years, that could really build up to produce a different brain state and a different world view.

We’re arguing that the kind of biases that people have in their attention plays a causal role in the development of emotional vulnerability. In other words, if people are tuning into the more negative aspects of their surroundings, it can make then more reactive to stress.

What are you planning to do next?

I’m hoping to follow up this work. The idea is to look in more detail at how patients with different versions of this gene respond to various therapies for anxiety disorder and depression, such as ABM procedures, cognitive behavioural therapy and drug therapy. It would be really nice to see whether the type of serotonin transporter gene that a patient has makes a difference to how beneficial those treatments are.

That would be the first step towards a much more ‘personalised medicine’ approach, in which genetic information about a person with anxiety or depression could help with decisions about how to treat them. I also think that there is a lot of work to be done to understand the basic science behind cognitive biases and how they impact on emotional disorders.

This study was funded by a University of Essex Research Promotion Fund Grant and a Wellcome Trust Project Grant.

References

• Lonsdorf TB, Weike AI, Nikamo P, Schalling M, Hamm AO, & Ohman A (2009). Genetic gating of human fear learning and extinction: possible implications for gene-environment interaction in anxiety disorder. Psychological science, 20 (2), 198-206 PMID: 19175757
• Fox, E., Zougkou, K., Ridgewell, A., & Garner, K. (2011). The Serotonin Transporter Gene Alters Sensitivity to Attention Bias Modification: Evidence for a Plasticity Gene Biological Psychiatry, 70 (11), 1049-1054 DOI: 10.1016/j.biopsych.2011.07.004

In the latest of our shortlisted entries to the 2011 

It all starts with an apple pie. That fresh-from-the-oven baked crust, curling around the rich, succulent fruit. Steaming corkscrews of warmth bring the aroma to our nose, ringing bells of desire. Get to work salivary glands! Ready the battleground for a scrumptious engagement.

Success. We’ve managed to load the perfect ratio of pie crust to apple filling onto our dessert fork. A quick pitstop into the vanilla ice cream and we’re good to go. Oh, sensory jubilation!

A plethora of food molecules dissolve, each compound melting onto our taste buds, home of the taste receptors. Our gustatory system – the sensory system for taste –  has evolved to help us decide whether our food is inedible or is worthy enough to be swallowed. Like keys on a piano, each receptor plays a specific note, with each note representing a different taste. A harmonious combination of ingredients will release Beethoven’s fifth symphony within your mouth.

But let’s return to our apple pie. As we chew the tasty morsel, sugars flow over our taste buds and find their match, the sweet receptors. Carbonyl groups from the sugars bind to the sweet receptors resulting in an electrochemical signal that travels to the brain, carrying a tantalizing delivery. This glorious chain of events is responsible for our perception of sweetness and for many a failed diet.

Again, let us not abandon our pie. In addition to the sugar, ascorbic acid from those juicy apples tickles our sour receptors. Hydrogen (H⁺) ions are found in all acidic food. They flow through the ion channels on the receptors and activate specialised sensors, which ultimately lead to the release of a neurotransmitter that signals the brain. The result is a sensation of quenching tartness that counteracts the sugary pastry. Well played, chef. What’s next on the menu?

How about a fifth taste? For years, the conventionally accepted tastes were sweet, sour, bitter and salty. However, at the turn of the century a mysterious new taste was identified by Kikune Ikeda of Tokyo Imperial University. It wasn’t until the year 2000 that researchers from the University of Miami discovered that the receptor for the fifth taste was activated by L-glutamate. This is an amino acid found naturally in fermented products like soy sauce, Worcestershire sauce and many meats and cheeses, it triggers a sublime savoury sensation. This fifth taste is known as umami, the Japanese word for ‘delicious’.

Most receptors in our taste buds made of molecules known as G protein-coupled receptors. These receptors need a specific protein to activate them, beginning a chemical cascade that eventually reaches our brain. More specifically, it is a protein known as gustducin that’s responsible for our perception of bitter, sweet and umami.

Intriguingly, gustducin is similar to transducin, a G protein naturally expressed in the retina. This suggests that taste may have evolved in a similar way to sight. Perhaps not so astonishing, given how our senses frequently interact. It’s no secret that the appearance of our food influences our perception of its taste, but texture and temperature also contribute to the overall flavour of a meal. This type of cognitive impact is the bread and butter of creative chefs like Heston Blumenthal, if you’ll excuse the pun. Anyone who is familiar with his lavish banquets is aware of how his meals tease all of our senses, including our sense of humour.

Chefs delight in confusing our taste buds, blending tangy acidic tidbits with mellow, sugary compounds. Sometimes it works, sometimes it doesn’t. Flavour fusions like cheddar and chutney or Italian basil and tomato, are fine examples of matches made in heaven. Cooking, like painting, is an art of many nuances. Physical chemist Hervé This has turned it into an exact science. A man who is equally dedicated to science as he is to casseroles, he coined the term ‘molecular gastronomy’, the science of cooking. In his laboratory at the Institut National de la Recherche Agronomique, he discovered the perfect temperature at which to cook an egg, 65°C, so that the yolk remains liquid as the white solidifies. Besides teaching us how to make scientifically delicious mayonnaise or poach an egg in whisky, he is passionately devoted to understanding the molecular mechanisms at work during cooking. So while his research may not cure cancer or baldness, it might help your next soufflé rise.

This is an edited version of Jasmine’s original essay. Views expressed are the author’s own.

Find out more about the Wellcome Trust Science Writing Prize in association with the Guardian and the Observer and read our ‘How I write about science‘ series of tips for aspiring science writers.

Over the coming months, we’re publishing the shortlisted essays in this year’s inaugural competition.

Image credit: Matt McGee of Flickr

In this post, broadcaster and journalist Quentin Cooper talks about the search for a good story .

After starting my career as a news trainee with the BBC I went on to present the arts programme ‘Kaleidoscope’. Interestingly for me, when I interviewed a photographer, visual artist or film maker nobody ever asked what my qualifications were, they just accepted I was there.

For the first three years that I presented ‘Material World’, at least half of the interviewees wanted to know if I had a scientific background. As it happens I do, but it’s interesting that we have this strange attitude that unless you’re a scientist you’re not allowed to talk to other scientists.

During that time I never looked at an arts story as more interesting than a science story, or vice versa, I just asked, is it a story first of all? Why do we have to apply labels rather than asking if it’s an interesting story? In my opinion, there’s no such thing as a non-science story. I don’t like the way the boundary around science applies to festivals either.

I’ve done events at science festivals that have gone really well, but I’m convinced that, within a five-mile radius of the venue, there are thousands of people who would love the event but who would never walk through the door because it’s in a science festival. This is one of the things I like about Cheltenham: that the festivals of jazz, music, science and literature are linked.

I’m involved in LabOratory, a project to get biomedical science across the four festivals. A think-tank including writers, musicians and scientists creates highly innovative events – both in content and style – that cross boundaries and I think there’s a great deal of potential for it to go further.

Sometimes it’s said that science is unappealing to certain audiences, but I believe that people care passionately about it. They may not know they’re caring about science, or may resent the label, but there are always amazing stories.

Are any topics too difficult? I don’t think so. You can be lazy and concentrate on stories about dinosaurs or space, but even something about a new laminate or property of a material can be interesting – if you think hard about the best way to pitch it.

I find it ridiculous that we say we don’t like science. We don’t like the difficult bits, the complicated equations, but there are difficult bits in everything – even the plots of soap operas. Science isn’t always easy, but these kinds of objections aren’t anti-science, just anti-difficult.

As told to Chrissie Giles. This feature also appears in issue 69 of ‘Wellcome News’.

Image Credit: Charlie Chan

Three mitochondria surrounded by cytoplasm

When new scientific understanding makes novel medical treatments a possibility, it is right that society should have the opportunity to debate whether the new treatments should be adopted. This is especially important if the technology involved could present ethical concerns.

Such democratic debate, as much as the final decisions made by policy-makers, should be based on a proper understanding of the science behind the treatment. That is not always helped by the way potential medical advances are reported in the media.

Two announcements were made yesterday concerning a potential new technique using in vitro fertilisation (IVF) to prevent children inheriting mitochondrial diseases. We announced a £4.4 million award to establish the new Wellcome Trust Centre for Mitochondrial Research at Newcastle University. A large part of the centre’s remit is to undertake research necessary for the new treatment to be introduced, building on years of previous work by the centre’s scientists funded by the Trust, the Muscular Dystrophy Campaign and others.

At the same time, the Government has asked the Human Fertilisation and Embryology Authority (HFEA) to run a public dialogue exercise to gauge views as to whether this kind of treatment would be acceptable.

The technique has been reported before – notably last year when it was the subject of a report by an HFEA expert scientific panel. Their study concluded that while there was no evidence to suggest the technique was in any way unsafe, more research was needed before it could be licensed because it was a new technique for use on human embryos and, while any new medical technique has associated risks, these risks should be managed to be as small as possible in this case.

Many media reports of the panel’s 2011 conclusions described the proposed procedure as ‘three-parent IVF’ (here are some examples: BBC, New Scientist, Independent). Several reports of yesterday’s announcements repeated this phrase (see the Financial Times, Daily Telegraph, Channel 4 and the BBC, who have since changed their wording to “Three-person IVF”), which is in danger of becoming a common, but flawed, concept of the technique.  

1 + 1 + 0.00001 ≠ 3

While it is correct that genetic material from three people contributes to the resulting child’s DNA, the mitochondrial DNA that comes from a donated egg is such a tiny component of their total DNA that, if you really want to count parents according to their genetic contribution, you might say a child born using this technique would have 1 father and about 1.00001 mothers. Added to that is the fact that the mitochondrial DNA produces only proteins used in the mitochondria – it has no influence over physical or psychological attributes of the child such as hair colour or taste for brussels sprouts.

Mitochondria are often described as being cells’ batteries – they provide the energy our cells need to work properly. It is a good analogy and in this new technique, we have a way of changing faulty batteries before they do irreversible damage to the body they are in. And just as changing the batteries in a torch doesn’t change the colour of light it shines, switching mitochondrial DNA won’t change a person’s appearance or personality.

This is not to say that there is no ethical dimension to the technique and the researchers leading this work welcome public discussion of it. The Nuffield Council on Bioethics has also launched a call for evidence on the ethical issues raised by the technique for consideration by its Working Group of experts. Clearly, human DNA is transferred from one egg to another in order to eliminate the mutated DNA that would otherwise cause a mitochondrial disease in the resulting child. If the child is a girl, she will pass on the donated mitochondrial DNA to any children she, in turn, may have.

To some, the benefits of eliminating the risk of these debilitating and often deadly mitochondrial diseases will far outweigh any possible ethical concern; for others, manipulation of human genetic material is just beyond the pale, no matter what potential good it might do. The important thing is that these positions (and any others in between) be reached with a proper understanding of the science involved and not in response to casually constructed headlines about ‘three-parent’ babies.

The Wellcome Trust’s position was clearly set out this morning by our Director, Sir Mark Walport, in an article in The Times: “Medical procedures that introduce a donor’s biological material into the body are … long accepted. If a child with donated mitochondria can be said to have three parents, then the recipient of a heart transplant could be said to have four.”

So here’s the science…

The aim of doing both research and consultation in parallel is that there should be no delay in introducing the new therapy, assuming it is proved to be safe and effective as well as acceptable to the UK public. It is vital that both processes be done with as accurate an understanding of the science and the ethics underpinning this groundbreaking therapy.

For a more detailed account of the science of mitochondrial DNA and disease, have a look at this open-access review in the Journal of Pathology by authors including Professor Doug Turnbull, Director of the new Wellcome Trust Centre for Mitochondrial Research at Newcastle University:

Greaves, L., Reeve, A., Taylor, R., & Turnbull, D. (2012). Mitochondrial DNA and disease The Journal of Pathology, 226 (2), 274-286 DOI: 10.1002/path.3028

Image credits: Top image – Dr David Furness / Wellcome Images; Diagrams – Prof Mary Herbert, Newcastle University

Food has evolved to be experienced as something that is, on the whole, delicious. But in addition to enlivening taste buds, food and the calories within are the source of power needed to make us move, think and live. Every cell in the human body (barring red blood cells) contains the means to convert carbohydrate into the energy needed by cells to perform their basic and vital functions: mitochondria.

These numerous, self-contained ‘organelles’ inhabit our cells, churning out molecular energy to be used in the daunting number of tasks a normal cell must achieve every second in order to ensure its smooth running. But more than mere ‘batteries’, mitochondria have their own genetic identity, their own DNA separate from that in other cells in the body, affording them a touch of independence from the vast genetic repository of the cell’s nucleus.

Where there’s DNA there’s also the possibility for mutation and mitochondria are not exempt. In around one in every 6500 women (because mitochondria are passed directly from the mother’s egg to the foetus) such mutations in the mitochondrial DNA pass unrepaired from mother to child. Unfortunately, many of these mutations result in the child inheriting any one of a number of associated, debilitating mitochondrial diseases – the result of mitochondria not being able to live up to their cell’s energetic expectations. This can set in motion an evolutionary domino effect, with successive women carrying such mutations, passing the disease onto subsequent generations.

In this film, recent research from Professor Doug Turnbull and his team (now part of the newly-announced Wellcome Trust Centre for Mitochondrial Research at Newcastle University explain the  safe, permanent, way they’ve developed to stop the passage of faulty mitochondria once and for all.

What struck me when I spoke with Doug and Professor Alison Murdoch, Professor of Reproductive Medicine at Newcastle University and Head of Newcastle Fertility Centre at Life, was the apparent controversy surrounding such work; it seems the mere mention of ‘human embryos’ is enough to spark controversy without regard for the precise nature and potential of the work being carried out.

The human material they use for this research is provided entirely voluntarily and, were it not used, would simply be discarded. Doug, Alison and others are pioneering a way to eliminate human misery and suffering, removing a biological albatross from families throughout the UK. Isn’t one of science’s greatest achievements this ability to improve lives through such advances?

In the latest of our shortlisted entries to the 2011 

It’s hard enough having to spread yourself thinly during your normal daily activities – work, sustenance, childcare, rest, the list goes on. Luckily for us monogamous types, our efforts in the bedroom are most often directed towards one individual. Imagine, though, the dilemma of having to divide your reproductive resources between many partners. If you were a male seed beetle (Callosobruchus maculatus), you might face this very problem. You would have a limited supply of ejaculate, numerous females of differing ages and reproductive states, lots of rival males, and about a week to live. To fulfil your evolutionary potential and achieve reproductive success you need to prioritise your sexual encounters – do you allocate a little of your seed to several different females, which may offer fairly decent returns, or do you use up all your sperm on one ripe, virgin female in the hope of fertilising each one of her hundreds of eggs?

Sperm is not a limitless resource. Males often have to use it economically to maximise their lifetime reproductive success. In many insects the situation is complex because females store sperm internally from several different mates, much of which is surplus to requirement, so not all males that achieve copulation can be guaranteed paternity. However, males can sometimes bolster their chances, by adopting certain strategies to overcome this sperm competition.

As a promiscuous insect it is essential to assess your surroundings. For example, if you were a male cricket (Gryllus veletis) you might want to allocate lots of sperm when copulating if there is another male waiting his turn with the female, in attempt to father a greater share of the resultant clutch than he does. If there are ten rival males around, you’d probably be better holding onto your ejaculate for now and saving your sperm for other, less competitive situations.

Now imagine you’re a bush cricket (Kawanaphila nartee). That large female you can see might look appealing and you might think she has a lot to offer in terms of egg number and offspring quality. However, all the males think that. If you all mate with her many of you will lose out because she can’t use all the sperm. It might be wiser to reduce your sperm allocation and instead offer more of it to a smaller, less desirable female. With her, your sperm will be unlikely to face competition and you’ll probably father all her offspring.

Age also matters when it comes to females. If you were a meal moth (Plodia interpunctella), you’d assess female age upon mating and allocate your resources accordingly. Give more sperm to young females – they have more eggs in storage and more time to lay them. Your resources might be wasted on old females who could die before getting the chance to use your sperm on their few remaining eggs.

You also need to think about the non-sperm constituents of your ejaculate – water, nutrients and other chemicals. As a locust (Locusta migratoria), you could flush out sperm inseminated by males that have gone before you by allocating a large volume of water to your semen. It you were a swallowtail butterfly (Papilio machaon), you could delay a female copulating subsequently with a rival by inseminating a large ejaculate – she’ll be too full to accept another mating for a while.

Don’t forget about seasonality – the reproductive worth of females can change with the weather. As a small white butterfly (Pieris rapae), you can judge how many sperm and what quantity of nutrients to invest in a female depending on the period of the mating season. If you’re quick off the mark, the females you encounter are likely to be virgins so you can inseminate just enough sperm to fertilise all their eggs but include lots of nutrients to provide nourishment for your resultant offspring. Conversely, later in the season when females will have already mated with rivals, you should allocate more sperm but fewer nutritional resources – greater numbers of sperm will out-compete those of your rivals but there’s no point spending nutrients on offspring that might not be yours.

With all these things to consider you might be glad not to be an insect. If you are indeed a monogamous type things might appear more black and white. You might feel more empathetic towards the faithful Adélie penguin (Pygoscelis adeliae). Little does your partner know, however, that while allocating small numbers of sperm to her you are saving most of them for sneaky matings with others, in attempt to spread your genes far and wide.

As a male Homo sapiens you might think you have no control over the attributes of your ejaculate. However, with some suggestion that sperm numbers are increased when men return to a female partner having been away for a lengthy period, you might have more in common with an insect than you thought.

Fiona Lethbridge

This is an edited version of Fiona’s original essay. Views expressed are the author’s own.

Find out more about the Wellcome Trust Science Writing Prize in association with the Guardian and the Observer and read our ‘How I write about science‘ series of tips for aspiring science writers.

Over the coming months, we’re publishing the shortlisted essays in this year’s inaugural competition.

Image Credit: Richardus_H

Mark Hahnel introduces a new free service aiming to push forward open access.

The Wellcome Trust has a strong view on open access and scientific data, expecting authors of research to “maximise the opportunities to make their results available for free”. Other funders have statements along similar lines and the UK’s science minister, David Willetts recently declared a “commitment by the coalition [government] to transparency and open access to publicly funded data”. Yet scientists are notoriously secretive, due in no small part to the current model of scientific publishing.

Scientists carry out research to push the boundaries of knowledge. In the current model of dissemination, a small fraction of this knowledge is handed over to journals in the form of scientific articles, or ‘papers’, for them to sell at a profit (with profit margins increasing).

Journal subscriptions and profits 1986-2008. Source: Association of Research Libraries. 2008.

Is this how science should be disseminated? The current process is based on a 17th century model, which was undoubtedly the best way to share this knowledge at the time. But today, the internet offers new ways to publish scientific data that many argue to be better.

Over the last decade, open access publishing has flourished, perhaps even begun to dominate, scientific publishing – it was recently claimed that PLoS ONE may be the largest journal in the world in terms of article numbers.

Yet one problem that remains is the amount of data that remains unpublished, unshared and essentially wasted. But why is this? As Professor Colin Blakemore suggested in a Radio 4 interview recently, “Memory is getting cheaper, access to information is getting much, much easier. So why shouldn’t we just simply put the raw data for everything that scientists do up on the web, accessible to every other scientists, so that they can scrutinise it, use it, data-mine it, combine it with other information and gain more useful evidence?”

This is where our venture comes in. Figshare is a free service allowing researchers to publish all of their research outputs to the web in seconds in an easily citable, sharable and discoverable manner. We aim to show researchers that they can get the credit for all of their research, whilst at the same time moving research forward in a more efficient manner.

Researchers can publish figures, datasets, tables, videos, anything. All file formats can be published, including videos and datasets that are often demoted to the supplemental materials section in current journals. Up to 1GB of data can be stored privately for free, and users have unlimited space for publicly available research.

Using this, researchers could easily publish null results, avoiding the file drawer effect and helping to make scientific research more efficient by opening up the peer review process.

We also use Creative Commons licensing to allow frictionless sharing of research data, while allowing researchers to choose when and if they make data publicly available. Scientists are notoriously secretive – as Professor Peter Murray-Rust of Cambridge points out, “the primary purpose of publication for most academics is self-advancement”. Yet the idea that secrecy in research will ultimately lead to individual success means that scientific research as a whole is suffering.

We focus on giving users credit for all of their research. There’s increasing evidence for open access increasing impact. By using both traditional measures of impact (i.e. the number of citations) alongside new ones such as altmetrics, Figshare gives researchers a greater level of information, and realtime measurements, of the true reach of their research, without having to wait for other researchers to cite it in another research paper.

New and established methods of tracking impact are recorded on figshare.

For the first time in over 300 years of academic publishing, we could access the sum of all scientific knowledge. By providing a way to store all research data in the cloud, and share it in a quick and simple manner, we hope to help make this possible.

Mark Hahnel

Dr Mark Hahnel is Product Manager of Figshare.

Figshare is supported by Digital Science, a sister company of Nature.

Figshare is not affiliated with the Wellcome Trust. Views expressed in this article are the author’s own.