Thursday, 31 October 2013

Genetic study reveals that a significant proportion of intelligence is inherited

by Robert Hoskin (University of Sheffield, UK)
Short-listed for Access to Understanding 2013
To what extent do biological and environmental factors influence how an organism develops? This question, often framed as the 'nature-nurture debate', is one of the most fundamental problems that science has to address. Within this debate it is of particular importance to understand how biological and environmental factors contribute to the development of human intelligence, as intelligence plays a substantial role in determining life outcomes. A 2011 study, published in the Molecular Psychiatry journal, has demonstrated that differences in adult intelligence can, to a large extent, be explained by genetic variations between people. The study therefore provides clear evidence that a significant proportion of adult intelligence is hereditary.
Shutterstock Image ID: 154870706 Copyright: Jorgan McLeman
The research was the result of wide-scale collaboration between scientists at 8 different universities, across 3 different countries. They analysed DNA collected from over 3000 unrelated volunteers. Each individual’s DNA was scanned for the presence of a large number of common genetic variations (known as single-nucleotide polymorphisms or ‘SNPs’). These genetic variations effectively encode the biological differences between people. Their study can therefore reveal the genetic basis of individual differences. For example, if a particular gene has a causal effect on a trait (in this case intelligence) then individuals with an SNP within that gene should have noticeably different scores on the trait compared to those who do not. Measures of each individual’s intelligence were ascertained from various psychometric test scores collected from each volunteer during middle to late adulthood. Two separate measures of adult intelligence were computed: ‘crystallised intelligence’, which is a measure of the ability to acquire and recall knowledge, and ‘fluid intelligence’, which is a measure of cognitive skills such as abstract reasoning, logical thinking and problem solving.
The research team were not able to establish a firm relationship between any individual SNP and either measure of intelligence. One SNP (named FNBP1L) was found to predict fluid intelligence, but this relationship could not be replicated using an independent sample of data from Norway, suggesting that the effect may be spurious. The identification of SNPs also however enables a genetic profile of each individual to be created, a process which in effect allows the cumulative genetic variation between individuals to be quantified. These profiles therefore allow an assessment to be made of the extent to which more general variations in genetic makeup contribute to individual differences. Using this method the researchers found that 40% of the variance in crystallised intelligence and 51% of the variance in fluid intelligence between individuals could be explained by genetic differences. Furthermore the predictive information contained within the SNP profile was also able to predict intelligence scores in the independent Norwegian dataset, confirming the validity of the original finding. These results strongly suggest that around half the variation in intelligence between people can be attributed to inherited abilities. Indeed as only common SNPs were analysed, rather than every single genetic variation, the actual proportion of intelligence that is heritable may be much higher than this.

Shutterstock Image ID: 135960185 Copyright: kentoh

The estimates regarding the heritability of intelligence provided by the study are in broad agreement with those obtained from twin and family studies. This study however strengthens our understanding of the heritability of intelligence because it side-steps some methodological issues that exist with twin and family studies, such as the difficultly in parsing genetic from environmental influences when closely related individuals are studied. The study therefore represents the first direct demonstration that genetic differences explain a significant amount of the variance in intelligence between individuals.
As no individual SNPs were found that strongly predicted intelligence, an additional conclusion that can be drawn from the study is that a very large number of different genes are likely to interact to determine our intelligence, rather than there being a small number of ‘intelligence genes’. This is perhaps not surprising as intelligence is a complex trait that is reliant on a number of different cognitive abilities, which are in turn likely to be reliant on a number of different biological processes. The likely influence of a large number of genes does not suggest that associations between individual SNPs and intelligence cannot be uncovered in the future. Instead it suggests that studies with far larger samples, and perhaps looking at more specific cognitive abilities, will be required in order to identify such associations. Nevertheless the study represents an important step in the battle to understand the genetic basis of intelligence. By improving our understanding of the biological mechanisms that support intelligence we may be able in the future to identify ways in which the development and maintenance of human mental functioning can be improved. This may lead to interventions that can help to both promote cognitive abilities in the general population, and preserve these abilities to a greater extent in old age.
This entry describes research published in the following article, selected by the Biotechnology and Biological Sciences Research Council:

PMCID: PMC3182557
Gail Davies,  Albert Tenesa, Antony Payton, Jian Yang, Sarah E. Harris, David Liewald, Xiayi Ke, Stephanie Le Hellard, Andrea Christoforou, Michelle Luciano, Kevin McGhee, Lorna Lopez, Alan J. Gow, Janie Corley, Paul Redmond, Helen C. Fox, Paul Haggarty, Lawrence J. Whalley, Geraldine McNeill, Michael E. Goddard, Thomas Espeseth, Astri J. Lundervold, Ivar Reinvang, Andrew Pickles, Vidar M. Steen, William Ollier, David J. Porteous, Michael Horan, John M. Starr, Neil Pendleton, Peter M. Visscher, and Ian J. Deary
Mol. Psychiatry (2011) 16(10), 996-1005


Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2013 there were 9 articles to choose from, selected by the Europe PMC funders.

The articles are all available from Europe PMC, are free to read and download, and were supported by one or more of the Europe PMC funders.


Look out here and on Twitter @EuropePMC_news for announcements about the competition.

Tuesday, 29 October 2013

“Will you just stand still?” Scientists gain insight into metastatic lung cancer

By Katarzyna Makowska (University of Leeds, UK)
Short-listed for Access to Understanding 2013
Brian J. McHugh and colleagues from University of Edinburgh and King’s College London have discovered a one-protein switch that makes normal lung cells behave like metastatic cancer cells. This exciting finding, published in PLOS One in July 2012, brings us closer to conquering lung cancer.
What are we up against?
Lung cancer is very common and has very high mortality rates. It kills more people than any other cancer in the Western World, including the UK. Small cell lung cancer (SCLC) is an extremely aggressive form of the disease that grows quickly and spreads rapidly to other parts of the body, creating new tumours called metastases. As one can imagine, multiple tumours spreading in the organism are very difficult to deal with, and as a result, only less than 1 in 7 small cell lung cancer patients show long-term survival. This is also why researchers are always seeking new ways to fight the lung cancer.
Shutterstock Image ID: 142544812 Copyright: wonderisland
What makes cancer so dangerous?
Several things make cancer such a serious disease. Unlike normal cells, cancer cells can appear to be immortal, grow uncontrollably and divide almost without limits, but the biggest problem is that they can become more mobile and invasive than healthy cells. Normal cells do not usually move, but cancer cells ‘conquering’ other tissues can cause a lot of damage. The migration of cells depends on many factors, such as the cytoskeleton (scaffolding inside the cell), neighbouring cells or the external environment, generally called the extracellular matrix (ECM). In many cases, although not always, attachment to ECM is necessary to sustain the migrating cells. Several groups of proteins are extremely important for this process, including integrins.
What are integrins?
Integrins are crucial proteins in cell migration, because they are integrated into the cell membrane and are responsible for cells attaching to surfaces, a kind of molecular ‘glue’. Their important role is to integrate, thus the name, the inside of the cell (cytoskeleton) to the outside (ECM and other cells). Integrins get cues about the environment and distribute the information in the cell, so that the cell knows how to behave and can respond accordingly. It is not surprising then that the levels and activities of integrins change in many types of cancer, and help to promote cell migration or metastasis.
How can normal cells mimic metastatic cancer?
Integrins can be influenced by other proteins. In this new study, the researchers focused on Fam38A, which helps to switch on the integrins. They showed that Fam38A is found at high levels in normal lung cells but it is almost absent in small cell lung cancer cells. To discover if this is important in driving lung cancer metastasis, they ‘silenced’ the expression of this protein in normal cells, so that its level was similar to that in cancerous cells. They found that when Fam38A is almost missing, integrins become inactive, and the cells stop adhering to their surroundings as readily as normal cells. Surprisingly, the cells missing Fam38A were also shown to eagerly move around and to be more invasive than normal lung cells.
The next question to ask is how is this possible? How can the cells migrate, when levels of active integrins are low, and cells need integrins to adhere at least in some types of migration? The exciting answer is that their movement no longer depends on integrins. The cells can switch to so-called amoeboid migration, when they move similarly to free-living single celled organisms called amoeba. Amoeboid migration is known to be often used by various cancer types, including small cell lung cancer.
Birds during the migration period
Shutterstock Image ID: 159790823 Copyright: Ki Zel
What does this mean for the patients?
This intriguing discovery shows that the loss of one humble protein causes a fundamental change in cell behaviour. If it has such drastic consequences for cell migration, Fam38A is likely to be very important for lung cancer metastasis. For example, detecting low levels of Fam38A in tumours during screening is likely to mean that the cancer has higher potential to become aggressive and metastatic.
Further studies seem necessary before this finding can be applied clinically. Nevertheless, it certainly helps to unveil the mechanisms behind cancer metastasis and hopefully will contribute to discovering new therapies for lung cancer in the future.

This entry describes research published in the following article, selected by the




Chief Scientist Office of the Scottish Government:
PMCID: PMC3390408
Brian J. McHugh, Amanda Murdoch, Christopher Haslett, and Tariq Sethi
PLoS One (2012) 7(7), e40346


Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2013 there were 9 articles to choose from, selected by the Europe PMC funders.

The articles are all available from Europe PMC, are free to read and download, and were supported by one or more of the Europe PMC funders.


Look out here and on Twitter @EuropePMC_news for announcements about the competition.

Sunday, 27 October 2013

How heels help people walk

By David Daversa (Institute of Zoology, University of Cambridge, UK)
Short-listed for Access to Understanding 2013
Most people may not think very much about reasons explaining the shape of our feet. For evolutionary biologists and designers of prosthetic legs however, this topic is of major interest. A recent study, led by Dr James Usherwood from the Royal Veterinary College in England, provides new evidence that our feet are specifically designed for walking.
To understand why however, requires a brief overview of human walking 101. Just as people dance with certain styles, we also walk with a certain style. This movement is no hokey-pokey, however. Rather, scientists call our walk the inverted pendulum. Inverted pendulums are characterized by objects that move in an arching, rainbow-like fashion overtop of a fixed pivot. A catapult exemplifies an inverted pendulum. Likewise, while walking our bodies act as a weighted object that propels forward over our feet, which serves as a fixed pivot. Imagine the way a wiper blade moves across a car windshield.  Such is the motion made by both walking people and inverted pendulums.
Shutterstock Image ID:10341253 Copyright: V&V
Yet, this confusing concept may be best grasped while actually walking. So, let’s do the inverted pendulum (imagine beat of “the hokey pokey”): 

We put one foot out, and place the heel down.
We push our bodies forward with the foot on flat on the ground.
Arriving overtop we stand with bodies and legs erect. 
We pivot further forward, lifting our heel and using the toes to push off into the next step.

That is what the inverted pendulum is all about.
What has specifically confused scientists is why humans are flat-footed, with heels that touch the ground while walking and standing. As ostriches illustrate, such a foot is not essential for doing the inverted pendulum. These large, flightless birds known for running at impressively high speeds use the inverted pendulum style to walk as well, but their heels are always elevated off the ground. Furthermore, women in high heels still do the inverted pendulum as well. Thus, the ground-touching heel is inessential. Moreover, ostrich feet may actually be preferred, as the need to spend energy lifting the heel off the ground is eliminated.
What these past studies fail to consider however, is the burden that walking places on the leg muscles. Therefore, James Usherwood, from the Royal Veterinary College in the United Kingdom, and colleagues examined muscle use throughout the inverted pendulum walk, to see whether any insights into the function of the heel could be afforded. They did this by first breaking down the inverted pendulum into 3 steps.  In Step 1 we place our heel down on the ground. In Step 2 we stand overtop of our feet with bodies and legs erect. Finally, in Step 3 people push off the ground, lifting our heel and using the toes, into the next step. Then they determined when and how lower leg muscles were put to work during each step. What they found was that the shin muscles were used in Step 1 to absorb the initial impact of hitting the ground with our heel.  In Step 3 the calf muscles were triggered for the push off. Interestingly, during Step 2 these muscles were relaxed.  Furthermore, the heel, then positioned on the ground, absorbed the pressure placed on the foot by standing on top of it. Therefore, Usherwood and colleagues concluded that the grounded heel functions to provide a brief respite for our shin and calf muscles during the inverted pendulum walk.  Coincidentally, this finding explains why people can stand for long periods of time without getting sore shin and calf muscles.
Shutterstock Image ID: 94554937 Copyright: Kasza
These results provide new insight for human evolution. Recently, some scientists have argued that humans are specifically adapted for running. These findings however, offer new evidence that human bodies are more likely to be designed for walking.
Such findings also have important implications for the design of prosthetic legs for amputees. In light of the results, prosthetic legs would best be designed with so that the heel touches the ground behind the leg, correct? Actually, the opposite is the case. Prosthetic legs do not incorporate muscle-like components as our bodies do. Thus, the value of the ground-touching heel (to reduce the amount of work placed on the leg muscles) is eliminated. Rather, its planted position represents a cost, since lifting the heel off the ground requires unneeded effort.
For this reason, Usherwood and colleagues propose that designs for prosthetic legs mimic ostrich feet, keeping the heel permanently lifted off the ground. Such designs have already been put to the test and are proving effective. The prosthetic leg used by accomplished Paralympic athlete Oscar Pistorius, known as the blade runner, mimics a raised heel form. This South African sprinter holds the world record time for several track and field events. Now that is no hokey-pokey.
This entry describes research published in the following article, selected by the Wellcome Trust:
PMCID: PMC3427509
J. R. Usherwood, A. J. Channon, J. P. Myatt, J. W. Rankin, and T. Y. Hubel
J. R. Soc. Interface (2012) 9(75), 2396–2402

Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2013 there were 9 articles to choose from, selected by the Europe PMC funders.

The articles are all available from Europe PMC, are free to read and download, and were supported by one or more of the Europe PMC funders.


Look out here and on Twitter @EuropePMC_news for announcements about the competition.

 

Friday, 25 October 2013

Breast cancer: Two-face ER

By Luisa Robbez-Masson (Barts Cancer Institute, Queen Mary University, London, UK)
Short-listed for Access to Understanding 2013

Oestrogen is a female hormone, produced in the ovaries, that stimulates the formation of the female sexual characteristics at puberty. It also triggers the growth of the breast tissues during the reproductive cycle and during pregnancy. However, oestrogen exposure in a woman’s lifetime has been linked to breast cancer risk for many years. During the development of breast cancer, oestrogen feeds the breast tissues and the tumour indiscriminately and consequently helps its progression. Treatments that block oestrogen receptors have been successfully used in the clinic, however the response is difficult to predict and some patients eventually develop resistance to those drugs. Understanding how oestrogen and its receptor work is key to developing new effective therapies against breast cancer.
Microscope view of ductal Breast Cancer cells in tissue culture
Shutterstock Image ID 71178904, Copyright: Paul Hakimata Photography



Scientists at Cancer Research UK in Cambridge have discovered that the oestrogen receptor (ER) activates a different set of genes in breast cancer patients who died compared to patients who survived. This important study could help scientists understand why a disease that appears superficially identical, has such differing outcomes in terms of response to treatment and, ultimately, survival.

ER belongs to the family of transcription factors, which means that it can travel to the cell nucleus, when partnered with oestrogen, and reach the DNA molecules that harbour all our genes. Like all transcription factors, ER has the capacity to attach to some specific “target” genes, and lead to their activation or inhibition, which will in turn tell the cells how to behave. ER is aided in reaching its nuclear targets by the pathfinder transcription factor FOXA1, which opens up the DNA molecule for easy access. It is known that this collaboration between ER and FOXA1 involves many genes and is very dynamic, but the importance of its role in cancer development is still unclear.

Using molecular biology tools, scientists can “capture” a transcription factor together with the DNA to which it is bound. It is then possible to read the DNA sequence obtained from these binding events in order to identify target genes of specific transcription factors. This technique, previously used in cancer cell line models, was applied for the first time by the team in Cambridge to biopsies from breast cancer patients that all possessed ER and FOXA1. These patients were carefully chosen according to how aggressive their cancer was: eight patients with good prognosis, seven patients with bad prognosis and three who had a relapse and developed metastases were selected.

The team identified the target genes of ER and compared them between the different groups. The results showed that 484 binding sites (i.e. spots on the DNA where ER is bound) were common to most of the patients, but that the strength of the binding was more important in poor outcome and relapse patients compared to good outcome ones. The experiment also indicated that the different outcome patients can be well characterised by a specific set of ER bound genes: 1,192 binding sites were predominantly found in the poor prognosis group and another, distinct 599 binding sites were representative of the good outcomes. The authors also observed that the pathfinder FOXA1 was more often binding near the poor outcome ER binding sites than the good ones.

The experiments revealed that ER was responsible for a double whammy; activating the poor outcome genes but also inhibiting the genes in the good outcome group, meaning that the binding of ER at those specific binding sites was biologically relevant in term of regulating cell behaviour.
Estrogen (estradiol) female sex hormone, molecular model
Shutterstock Image ID 159232019, Copyright: Iculig


In order to validate these finding they turned to well established cancer cell line models that were either drug sensitive or drug resistant, reproducing what is seen in patients. However, contrary to what they had hypothesised, the drug sensitive cell model was more similar to the poor outcome patients group, in term of ER binding sites, possibly suggesting that these models constitute an intermediate category of tumours, with an ER binding profile resembling more advanced tumours, on their way to acquired drug resistance. The events that led to this intermediate category might have been caused by the presence of other stimuli, such as other hormones or growth factors for instance, in the patients from whom the cell line models were established. By treating drug sensitive cells with some of these chemical stimuli, they were able to shift the ER binding profile, and observed an increase in new FOXA1 binding sites.

We have known for many years that ER can play a critical role in orchestrating the behaviour of breast cancer cells, but the emergence of FOXA1 as the principal conductor sets the stage for novel approaches in targeted therapy.

This entry describes research published in the following article, selected by Cancer Research UK:

Caryn S. Ross-Innes, Rory Stark, Andrew E. Teschendorff, Kelly A. Holmes, H. Raza Ali, Mark J. Dunning, Gordon D. Brown, Ondrej Gojis, Ian O. Ellis, Andrew R. Green, Simak Ali, Suet-Feung Chin, Carlo Palmieri, Carlos Caldas, and Jason S. Carroll
Nature (2012) 481(7381), 389-393


Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2013 there were 9 articles to choose from, selected by the Europe PMC funders.

The articles are all available from Europe PMC, are free to read and download, and were supported by one or more of the Europe PMC funders.


Look out here and on Twitter @EuropePMC_news for announcements about the competition.

Thursday, 24 October 2013

Medical research charities and Open Access

This post is by our guest, Dr Stephen Pinfield, a Senior Lecturer in the Information School at the University of Sheffield. In this post he introduces us to his recent paper 'Medical research charities and open access' where he reports on a survey he carried out to assess the Open Access (OA) policies and activities of medical research charities in the UK, including several of the Europe PubMed Central (Europe PMC) funders.

Open access has come a long way in the last decade and the funders of medical research have often been at the forefront of developments. However in the last two years there has been a heightening of the OA debate internationally, as many funders have strengthened their positions on OA and as OA has begun to enter the mainstream of research communication for many disciplines. In the UK, the Finch Review and the Research Councils UK OA policy, and in the USA, the Federal Fair Access to Science and Technology Research bill and the Office of Science and Technology Policy OA policy memorandum, are examples of developments that have increased the momentum towards the ‘mainstreaming’ of OA.

In this context, and following discussions with Europe PMC and the Association of Medical Research Charities, I decided to carry out some research to assess the OA policies and activities of medical research charities in the UK. How are they responding to recent developments? What do they see as the main opportunities and challenges? Where are they taking their organisational policies?

I asked these and related questions in a survey of UK AMRC and Europe PMC members, and received some very interesting responses. There is clearly a lot going on and some of this is described in an article recently published (and available in open-access form) in the journal Learned Publishing.
shutterstock_128925893

The results presented in the paper show that OA is an important issue for many medical research charities and a large number already have or are developing policies which encourage OA. Some clearly see OA as a really important way of getting the research they fund out there and used. Trends on a wide range of issues from compliance monitoring to licensing are also discussed in the paper, providing a snapshot of the current state of play in the sector.

However, there are concerns. In particular, there are concerns about costs and resource requirements to support OA. Some of the data presented in the paper provides provisional evidence of the size of the cost challenge for different organisations. "Provisional" because what the article illustrates amongst other things is the need for more and better data in this area to help create a reliable evidence base to inform policy development. There is still some way to go.

Of course, the debate currently happening amongst medical research charities in many respects reflects wider debates about OA: Gold versus Green, IPR, roles and responsibilities and so on. However, medical research charities have an important perspective on the discussion and can make a valuable contribution to it. I hope this research helps to get their voices heard.
Pinfield, S (2013). Medical Research charities and open access. Learned Publishing, 26(4), 285-302. doi: 10.1087/20130409 http://dx.doi.org/10.1087/20130409

Stephen teaches on several postgraduate programmes and pursues research in a number of issues including scholarly communications (particularly OA), research data management, and information strategy. Before becoming an academic, Stephen was for 23 years an information professional, latterly Chief Information Officer at the University of Nottingham where he managed a converged library and IT services Department. At Nottingham, he was founding Director of the Centre for Research Communications, which runs a number of OA-related services, such as SHERPA RoMEO, and carried out research and development projects in various areas of scholarly practice and communication futures. Stephen has been active for a number of years in OA developments at institutional, national and international levels.



Monday, 21 October 2013

5 annoying things about Open Access

To start, I should say that all at Europe PMC support Open Access. This is just a short list of some issues that can be frustrating…

1.    The often incorrect definition of green and gold routes to Open Access
I am a relative newcomer to Open Access having only been working in this area for a couple of years. Before that I was a research scientist, and the movement had largely passed me by, with the exception of noticing that I didn’t have to click through the university journal subscription pages to download some articles.
Having said that, I have now lost count of the number of meetings I’ve been to about Open Access where the introduction has included an incorrect definition of the distinction between green and gold open access. ‘Green’ often gets described as free, whereas ‘gold’ you have to pay for. I’ve already said that I’m a newbie in this area, so I will refer you to Peter Suber’s Open Access for a definitive explanation.
In brief, green is self-archiving in a repository and gold is open access delivered by journals. There may be associated costs, but that is not the defining difference.

2.    The constant argument between Open Access advocates about which route, green or gold, is best.

It is an important discussion, but sometimes it can diminish the central message about the benefits of Open Access – some of which are being highlighted this week by the Accelerating Science Award Program (ASAP) which recognises individuals who have applied scientific research – published through Open Access – to innovate in any field and benefit society.

Crucially, Europe PMC enables both green and gold routes to Open Access. So, researchers (or their funders) can choose which route to use - most funders offer the flexibilty of both routes.

Of course, it’s more complicated than that, as the ‘choice’ is often affected by publishing options, for example. But, just for today, the simple take-home message is that you can go ‘green’ using the Manuscript Submission Service via Europe PMC plus, or ‘gold’ by publishing Open Access with a publisher who deposits their contents or individual Open Access articles with us (you can find out more on the journal list).


3.    That Open Access can be so much effort!
In theory it’s a matter of a few mouse clicks to make an article Open Access, but in reality a researcher needs to understand the impact that funder, institutional and publisher Open Access policies can have on each other.  And they already have enough to do carrying out their research.
We know that the current system is not perfect, and that the researcher is usually the one at the receiving end of sometimes conflicting advice in this area. We don’t have a solution just yet, but hopefully it’s worth sharing that the 24 Europe PMC funders are talking to each other, and to publishers and institutions to try and reach agreements that will make things easier on researchers in the future. These conversations can take time, but they are happening.
 
shutterstock_127171886

4.    This next one is not an irritation with Open Access, but with the mis-guided conflation of Open Access with poor or no peer review.

This reared its head again only a few weeks ago in a (non-peer-reviewed) article published by Science where the author had submitted a spoof paper to a sub-set of Open Access journals. His conclusion was that there is 'little or no [peer review] scrutiny' at many open access journals'. Others have already made a far better job than I could of addressing the flaws in the design and conclusions described in that article, for example, here and here. My impression from comments on Twitter and blogs is that there is generally agreement that the research calls into question the integrity of the peer review system, and is nothing to do with Open Access (beyond the fact that the only journals included in the study were Open Access). In fact, some Open Access publishers are taking the lead in trying to address some of the problems long-associated with the peer review process, such as eLife and the Nature Frontiers series of journals.

Last, and by no means least:

5.    Articles about Open Access that are not themselves Open Access. 

I know I’m not the only person to find this odd/frustrating/completely counter-intuitive. But, really? Is it some kind of elaborate joke on the part of the authors?
 
To read about some more frustrations with Open Access, this time from the perspective of a science librarian dealing with Open Access content, I recommend reading this post ('How open is it?') by Elizabeth Newbold at the British Library - we sit near to each other, so it's been interesting comparing notes this week!

There are a lot of exciting things happening during Open Access week (21-27 October 2013). I hope everyone has a good week, whatever they’re doing and wherever they are in the world.
I will be busy getting ready to launch our science-writing competition, Access to Understanding 2014, in partnership with the British Library. Look out here and on Twitter @EuropePMC_news in November for further announcements.


Tuesday, 1 October 2013

New funders join Europe PMC

We're delighted that 4 new funders have joined Europe PMC, bringing the total to 24! The new funders are:



Worldwide Cancer Research (formerly AICR), who fund research into the causes of cancer. The AICR is UK-based, but funds projects all around the world, supporting the best scientists wherever they are.


Breast Cancer Campaign, who fund research into breast cancer and will support research at any centre of excellence in the UK and the Republic of Ireland. The charity has a particular interest in supporting innovative research and will fund the best breast cancer research in the UK and Ireland, providing that it is of the highest quality.




Diabetes UK, who focus on research with the potential to make a difference to the lives of people with diabetes. They provide funding to scientists and clinicians working in universities and hospitals throughout the UK.


Prostate Cancer UK, who fund vital research into tests, treatments and the causes of prostate cancer. They support researchers in the UK with an emphasis on innovative research aimed at extending and improving the lives of men who are diagnosed with prostate cancer.


Scientists and clinicians funded by these four funders will join thousands of others who make their published research articles freely available from Europe PMC as soon as possible, and in any event within six months of publication.
For more information about joining Europe PMC, visit our website: