Wednesday, 28 May 2014

The TBPH gene – Do neurodegenerative diseases have a fly in the ointment?

Image design: Serial/Trash
A number of genes have been implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), also known as motor neurone disease, and Frontotemporal lobar degeneration (FTLD). However, the core biological processes involved in these disorders are extremely difficult to model and this is hampering the effort to develop treatments. If we can resolve this and increase our knowledge about these disease processes it may be possible to develop new and improved treatments.

The gene TDP-43 in ALS and FTLD
The gene TDP-43 has been shown to be involved in the development of the neurodegenerative diseases ALS and FTLD in humans, however the exact way(s) in which it does this still remain unclear. This protein acts as a master regulator of RNA, a precursor to proteins, and can therefore control the expression of genes within cells. A recent study by a group led by Dr. Frank Hirth from King’s College London has shed some light on this by using an interesting choice of organism: drosophila melanogaster, the common fruit fly.

A fly way to model diseases
Researchers in a wide variety of fields are looking to drosophila to model complex diseases. But why choose flies, they couldn’t be any more different biologically to us could they? In fact, fruit flies share many biological processes with us; they have a complex immune system, an intricate brain and can even develop cancer! Genes that are similar in structure and cellular function in flies and human are called homologues. They can be retained from a common ancestor by a process called evolutionary conservation. What makes the fruit fly a great model for studying disease is that it has fewer genes than humans. Where humans often have multiple genes that perform essentially the same function, a feature known as redundancy, flies often only have one gene at each stage of a signalling pathway. This means that if you alter that one gene the effect should be more obvious. Imagine calling in sick for work but no one there is able to cover for you, your work just won’t get done and others will see exactly what your role is!

Altering the function of fruit fly TBPH models neurodegenerative disease
The fruit fly homologue of the TDP-43 gene is called TBPH, and it too has been implicated in neurodegenerative disease. To investigate TBPH the researchers from King’s made fruit flies which either lacked the gene, or had increased gene expression. Interestingly, both types of fly have key symptoms of neurological disorders such as a decreased life span and motor dysfunction – this was measured by videoing the flies walking and then making recordings about the speed and gait of their  movements. TBPH may therefore be considered a “goldilocks gene”, too much or too little can be biologically bad and “just the right amount” is required for normal health.

What mechanism did this study find?
To discover how loss or gain of TBPH leads to altered motility of the flies the researchers began to compare physical features of the normal fly to flies with loss of TBPH. Firstly they noted that there were no visible differences between muscle or synapse structure. This led them to dig deeper into the process of motor function. Using a series of complex experiments measuring the electrical currents generated at the gaps between neurons and muscles (neruo-muscular-junctions) of TBPH expressing, non-expressing or over-expressing flies, the group were able to suggest that the defects exist at the pre-synaptic stage of signal transmission. The flies have trouble transmitting neurological signals from the neurones to the muscles and this causes the physical difficulty in movement; as seen in humans with disorders driven by dysfunctional motor neurones.

Modelling the aging fly
Humans typically develop neurological diseases during old age, a fruit fly model where TBPH loss, or over-expression, was targeted only to a specific area of neurones allowed flies to age normally. It was not until flies had reached an “old age” of 40 days that they started to lose pre-synaptic function. This led ultimately to symptoms of neurodegeneration suggesting TBPH loss or over-expression has a progressive effect on neurological degeneration. Therefore, optimal TBPH levels in neurones are critical for maintaining proper motor neuron function during aging and supports both the TDP-43 gene as a driver of motor neuron disorders. This study elegantly highlights the usefulness of the TBPH fruit fly model as a great way to research the underlying mechanisms behind these disorders. If more is discovered about these mechanisms then new and exciting therapeutic agents could be developed for treating neurodegenerative diseases. It is clear that when it comes to neurodegenerative disease research the flies have it!

This summary by John Foster was shortlisted for Access to Understanding 2014 and was commended by the competition judges. It describes research published in the following article, selected for inclusion in the competition by the Motor Neurone Disease Association:

PMCID: PMC3605831
D.C. Diaper, Y. Adachi, B. Sutcliffe, D.M. Humphrey, C.J.H. Elliot, A. Stepto, Z.N. Ludlow, L. Vanden Broeck, P. Callaerts, B. Dermaut, A. Al-Chalabi, C.E. Shaw, I.M. Robinson & F. Hirth.
Human Molecular Genetics (2013) 22(8), 1539-1557.

Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2014 there were 10 articles to choose from, selected by the Europe PMC fundersThe 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 further competition news and other Europe PMC announcements.   

Wednesday, 21 May 2014

A divorce in development: single regulators can raise arteries alone

Image Source: Serial/Trash
Understanding how blood vessels are born and propagated is vital for the treatment of a whole host of diseases including heart disorders, diabetes and cancer. Scientists from Oxford’s Ludwig Institute for Cancer Research have begun to reveal the mechanism by which the switching on of specific genes leads to the development of arteries. 

A vast network of blood-carrying arteries feeds our body with the oxygen and nutrients it needs to survive. Within a young embryo, this network takes its primitive shape in a series of stages. First, the cell type which will later make up the inner-walls of all blood vessels, the endothelial cells, is generated. Then simple tube-like structures of these endothelial cells must differentiate into either arteries or veins.

But the story doesn’t end there – the process of sprouting new blood vessels continues throughout life and indeed maintaining just the right distribution is critical to our health. Too few, too many or abnormally-developed blood vessels can all lead to disease. Interestingly, although cancer and Alzheimer’s disease are very different conditions, scientists believe that the underlying molecular processes responsible for the defective blood vessel development that comes with them are very similar and therefore exciting targets for research.

All aspects of our development, from the formation of vital organs within the embryo to the healing of wounds in adulthood, utilise similar molecular tools to lay down the pattern which governs how cells and tissues specialise into one of many types – rather like a blueprint. External signalling molecules are deployed to pass instructions to cells depending on where they lie in the overall blueprint. These signals can be sensed by each cell individually via receptor molecules protruding from their surface.

Scientists are confident of the signalling molecules released during artery development. Vascular Endothelial Growth Factor (VEGF) spreads diffusely across tissues and is the primary driver of general blood vessel formation. The Notch pathway, which operates when adjacent cells touch, is implicated in deciding which vessels become arteries. However, signalling messages are short lived – how does an artery know to remain an artery? It is this last link in the chain that until now scientists have been most unsure about – how can several signalling pathways be combined inside the cell so that the correct genes are turned on for operating an artery?

All cells carry a copy of the entire genome, but few genes are required in every cell or all the time. Genes lie adjacent to ‘enhancers’, DNA sequence elements that do not encode protein but rather allow control of when, where and how fast a gene is read. Such control is governed by DNA-binding proteins, which sit on the DNA structure and interact with the gene-reading machinery.

Image Source: Shutterstock Copyright: Crystal Eye Studio

Dr Sarah De Val and her colleagues at Oxford have conducted a series of experiments in mice and zebrafish that reveal which DNA-binding proteins are important in the formation of arteries. They first pinpointed which enhancers are most important for the activation of an artery-specific Notch gene before demonstrating which of the known DNA-binding proteins engage them. These included a DNA-binding component of the Notch pathway and three members of the SOX-gene family, utilised during development throughout the animal kingdom.

By fusing copies of the artery enhancers to a bacterial gene that produces a bright blue protein when activated, it was possible for the researchers to trace the pattern of artery formation at different stages during embryo development. Unsurprisingly, when they cut out the binding sites at which the proteins responsible for formation of endothelial cells associate with enhancer DNA, or chemically disabled the VEGF signalling pathway, the normal pattern of Notch gene activation was completely lost. But intriguingly, deleting the binding sites for the SOX and Notch proteins only had a severe effect when carried out in parallel – loss of regulation by either SOX or Notch individually was of little importance.

This finding was echoed by injecting inhibitory DNA molecules into embryos to simultaneously turn off the genes encoding the DNA-binding SOX and Notch proteins. Although endothelial cells were able to form a network of primitive blood vessels, the principle artery, the aorta, was missing and none of the known genes common to arteries were activated.

As a general rule, developmental characteristics tend to emerge in cells located in regions where two or more necessary signals overlap. This research, proclaiming that proteins of either the SOX or Notch pathways alone are sufficient for much of artery function without the other, intriguingly contradicts this.

Highlighting the fact that the vascular system is extremely sensitive to genetic fine-tuning, Dr De Val’s study reveals some of the first molecular targets for potential vascular disease therapies. At the same time, it exposes some unusual molecular intricacies that will continue to excite scientists for some time.

This summary by Christopher Waite was shortlisted for Access to Understanding 2014 and was commended by the judges. It describes research published in the following article, selected for inclusion in the competition by the British Heart Foundation:

PMCID: PMC3718163
N. Sacilotto, R. Monteiro, M. Fritzsche, P.W. Becker, L. Sanchez-del-Campo, K. Liu, P. Pinheiro, I. Ratnayaka, B. Davies, C.R. Goding, R. Patient, G. Bou-Charios & S. De Val.
Proceedings of the National Academy of Science USA (2013) 110(29), 11893-11898.

Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2014 there were 10 articles to choose from, selected by the Europe PMC fundersThe 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 further competition news and other Europe PMC announcements.    

Friday, 16 May 2014

Now available: use DOIs with our External Links Service

Our External Links Service enables links to be created from articles on Europe PMC to free third-party resources that enrich our articles. Since launching the service last July we've been joined by providers who have set up links to an ever widening range of useful resources, including data underlying articles, press releases and plain English summaries, and article full text not otherwise held by Europe PMC - to name but a few. We now have 14 providers enriching 33, 000 articles with links out to additional information.

A recent development makes setting up these links even easier. Whereas previously you needed to have a PMID or PMCID associated with the information for which you wanted to create a link, we've enabled links to be created using DOIs, a commonly used, stable document identifier. The first provider to create links using DOIs is PANGAEAa data publisher for earth and environmental science.


Image source: Shutterstock Copyright: Thomas Reichhart
As always we welcome your feedback, and we would be delighted to hear from you if you want to get involved in this free service - at labslink@europepmc.org.

To stay up-to-date with Europe PMC news you can also follow us on Twitter @EuropePMC_news.

Wednesday, 14 May 2014

Reforming rheumatoid arthritis treatment: a step in the right direction

Image Source: Serial/Trash
There is good news for rheumatoid arthritis sufferers: scientists are a step closer to predicting which patients will benefit the most from a particular type of drug using just a urine sample.

Imagine being in pain whilst carrying out routine, daily tasks such as opening a door, reaching for something in the cupboard, or writing. On top of this, imagine that this pain often comes on quickly and intensively, but not being able to predict when this will happen. This is what thousands of people with rheumatoid arthritis have to cope with every day.

Usually, the cells of your immune system protect your body from invasion by harmful viruses and bacteria, acting as your body’s army. Rheumatoid arthritis occurs when some of these immune cells start to attack your own cells, specifically in the healthy tissue around your joints. This results in the affected joint and surrounding area becoming swollen, painful and stiff. These symptoms often intensify very quickly and without warning, resulting in severe discomfort for the person concerned. What causes these sudden ‘flares’ and the onset of the disease in general is still largely a mystery.

There are currently several different types of drugs available to treat the symptoms of rheumatoid arthritis. Unfortunately, it can take a period of trial and error to find out which drug works the best to reduce symptoms in each patient. Doctors and scientists are currently trying to find out why some drugs work very well in some people, but not in others. This research is important as it will ensure that in the future, patients are more likely to be given a drug that works the best for them; wasting less time than trying treatments by trial and error.

TNF-alpha inhibitors are a group of drugs currently used to treat moderate to severe rheumatoid arthritis. TNF-alpha is one of the proteins responsible for creating the swelling and pain in joints affected by rheumatoid arthritis. These drugs block the TNF-alpha protein, and so in turn reduce the symptoms associated with rheumatoid arthritis. They work very well in reducing symptoms in some patients, but do not work for many others. This latest research reveals a potential way to identify which people with rheumatoid arthritis are most likely to respond well to the TNF-alpha inhibitor drugs, by looking at their urine.
Image Source: Shutterstock Copyright: MILA Zed 
The researchers decided to see if they could find any differences in the amounts of certain molecules in the urine of rheumatoid arthritis patients who responded well to the TNF-alpha inhibitors, compared to the urine of those who did not respond well. They chose to look at the patients’ urine as a similar approach has already been successful with other diseases. Obtaining a urine sample is also very quick, easy and not intrusive to the patient.

Sixteen rheumatoid arthritis patients were chosen to participate in the study. They each gave a urine sample before commencing treatment with one of two TNF-alpha inhibitor drugs, which continued for one year. After this time, a doctor assessed the patients and decided, based on their symptoms, who had responded well and who had not. At the same time, scientists analysed the urine samples the patients had given at the beginning of the study. They did this using a technique called nuclear magnetic resonance spectroscopy. This takes advantage of the notion that different molecules behave differently when they come into contact with a magnetic field. When a magnetic field was applied to the urine samples, all the different molecules in the urine separated and a machine identified exactly which molecules were present, and in what amounts.

Three different computer programs analysed the results to make sure the final conclusions were accurate. In the patients who responded well to the TNF-alpha inhibitor drugs, all three computer programs agreed that these patients had more histamine, glutamine and xanthurenic acid molecules in their urine, but less ethanolamine molecules, compared to those who did not respond well. These findings mean that, if this test was used in the future, a doctor could take a urine sample from a rheumatoid arthritis patient to help him or her decide if the TNF-alpha inhibitor drugs are likely to ease the symptoms of the patient.

This study was small, so the next step is to test these findings on a larger group of rheumatoid arthritis patients. These initial findings are exciting though, and not just for those patients who are most likely to benefit from the TNF-alpha inhibitors. For patients where the drugs are not likely to work, this will be known quickly, and an alternative can be suggested instead. This means that each patient is more likely to receive a treatment that helps his or her symptoms as quickly as possible; something which is invaluable.

This summary by Elizabeth McAdam was shortlisted for Access to Understanding 2014 and was awarded second prize. It describes research published in the following article, selected for inclusion in the competition by the Arthritis Research UK:

PMCID: PMC3715109
S.R. Kapoor, A. Filer, M.A. Fitzpatrick, B.A. Fisher, P.C. Taylor, C.D. Buckley, I.B. McInnes, K. Raza & S.P. Young.
Arthritis & Rheumatism (2013) 65(6), 1448-1456.

Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2014 there were 10 articles to choose from, selected by the Europe PMC fundersThe 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 further competition news and other Europe PMC announcements.   

Tuesday, 13 May 2014

Simplicity is sometimes best

By Elizabeth McAdam, a postdoctoral researcher at the Cancer Research UK London Research Institute, UK

Note: Elizabeth was awarded second place in this year's Access to Understanding competition. Check back tomorrow to read her winning entry. Congratulations Elizabeth!

Writing always terrified me. Growing up, I didn’t enjoy English at school; I positively hated it. It all seemed to be about big words and complex detail. But I didn’t really care; I was going to be a scientist! And who needs to worry about being good at writing when you’re a scientist?


Elizabeth receiving her award from Sir Mark Walport ©The British Library Board
Fast forward ten years to my doctoral studies. I found myself becoming increasingly frustrated reading poorly written research articles. Scientists were desperately trying to look impressive by using long complex paragraphs of words to explain work that could easily be summarised in a sentence. I would spend hours reading and re-reading a single article trying to get my head around the unnecessary (and often wrong) use of words, all the while wondering how an interested member of the public might fare. Someone newly diagnosed with a particular disease may be curious as to what the latest research means for them, or maybe a scientific documentary inspired another to read on further. Whatever the reason, these people would find the jargon filled, over complicated, research articles impossible to understand. 

Often, the media is the messenger between scientist and non-scientist, and is usually fairly accurate in its reporting. Unfortunately however, many newspaper articles describing current scientific findings are headed by misleading, sensationalised titles and content, particularly when it comes to medical research. ‘Food X causes cancer!’ or ‘Food Y prevents cancer!’ can be weekly occurrences in some heavily read tabloids, at best misleading the public; at worst outright scaring them. 

That’s the beauty of Access to Understanding. It promotes simple, yet accurate scientific writing intended for interested members of the public often bewildered by the science which directly impacts upon their daily lives. The competition requires entrants to summarise a research article in plain English, which is then checked for its scientific accuracy and judged. I chose an article from Dr Stephen Young’s research group at Birmingham University, which detailed some exciting possibilities for alleviating rheumatoid arthritis, something I knew almost nothing about beforehand. This was actually beneficial, as I needed to simplify the information to understand it myself. 

The competition has raised an important issue, and hopefully in the not too distant future, scientists will be asked to provide a lay summary when they publish their work, to help make research accessible to anyone who is interested in it. Encouraging the next generation of scientists to write in plain English will help immensely, which, I was pleased to hear, is already happening at Dr Young’s University.  

Writing no longer terrifies me quite as much as it used to. Access to Understanding has helped me to realise that a good piece of writing doesn’t always involve fancy words and in-depth descriptions. Sometimes, keeping it simple is best. After all, what’s the point of writing something if most people can’t understand it?

Look out here and on Twitter @EuropePMC_news for further competition news and other Europe PMC announcements.

Wednesday, 7 May 2014

How healthy eating could starve out cancer

Image Source: Serial/Trash
Skin is not the only thing to wrinkle with age. Our genes also show signs of ageing – a process that can lead to cancer. A new study indicates that healthy eating can prevent cancer development and explains how this works.
When genes get old
Thanks to modern medical advancements, our average life expectancy has increased dramatically in recent decades. However, there is a paradox in our longevity: we now live long enough to develop cancer. Cancer is a genetic disease and, as we age, our genes – like our body – become more vulnerable. Some genes accumulate genetic mutations: if you think of genes as cookbooks for proteins, then these mutations are like typing errors in the recipe. Others acquire epigenetic modifications, which affect the way a gene works rather than its content – which, to use our analogy again, is like not being able to open and close the cookbook anymore. Both genetic and epigenetic changes can lead to cancer; however, the latter are especially interesting because they are affected by environmental factors that we can actually control, such as our diet.
How can we keep our genes young and prevent cancer? This is what Dr Nigel Belshaw, at the Institute of Food Research in Norwich UK, wanted to discover. His team looked for environmental factors that affect epigenetic markers associated with early colon cancer – a common and lethal cancer, responsible for over 610,000 deaths worldwide each year. Preventing colon cancer with small lifestyle changes would be a cheap, highly effective, and low-risk approach that turns the tide against this disease.
 Image Source: Shutterstock Copyright: Sebastian Kaulitzki
Lifestyle and cancer risk: the mystery unfolds
The researchers analysed a specific type of epigenetic modification called DNA methylation. Like other epigenetic markers, DNA methylation is a genetic switch: it can turn genes on and off, it can make the cookbook readable or make it impossible to open.
Our genes are hidden in tightly-wound DNA which is about two metres long in every single cell of our body. In this state, genes cannot be read and used by the cell to make proteins. Epigenetic switches can turn genes on by unwinding them, or turn them off by folding them back up, as in the case of DNA methylation. While this process is essential to our health, faulty folds in the DNA, much like wrinkles, can disturb gene function and lead to cancer.
What lifestyle factors might influence the formation of these epigenetic wrinkles in colon cancer? To answer this question, Belshaw’s group examined the cells lining the gut wall in healthy, cancer-free volunteers who consumed their usual diet without any supplements. The researchers looked at eleven risk genes, that, when their methylation is turned on, increase the risk of developing colon cancer.  They then quantified the relationship between methylated genes and cancer risk factors such as age, diet and obesity. Age was associated with the highest gene methylation, which fits with the observation that colon cancer risk increases exponentially after 50 years of age. However, other factors had small but significant effects. High body fat increased cancer-related methylation whereas high levels of the mineral selenium and vitamin D reduced it. This is consistent with what we know about the link between obesity and a high risk of colon cancer, as well as with the protective effects of vitamin D and selenium observed in previous studies.
Surprisingly, high blood folic acid, a vitamin found in leafy vegetables like spinach, increased gene methylation associated with colon cancer. We have been told that these foods are good for us, so how could they promote cancer? It is actually still unclear whether folic acid is a friend or a foe as previous studies indicate it may even have a protective function. This is an important issue as some countries add nutrients such as folic acid to food and this may expose people to increased risk of developing cancer. In a follow-up study, Dr Belshaw’s team will try to shed light on the potential dark side of excess folic acid intake.
Healthy ageing starts in the kitchen
Overall, these findings support the idea that healthy ageing is affected by what we eat. As we age, the epigenetic status of some genes can change leading to disease like cancer. Our diet seems to affect this process and bring important ingredients into our genes’ recipe. As Dr Belshaw says, “This raises the exciting possibility that lifestyle interventions may reverse age-related DNA methylation and consequently reduce the risk of disease”. An apple a day might be more effective in slowing down the ageing process than an anti-wrinkle cream.

This summary by Lucia Aronica was shortlisted for Access to Understanding 2014 and received the People's Choice award. It describes research published in the following article, selected for inclusion in the competition by the Biotechnology and Biological Sciences Research Council:


PMCID: PMC3572581
H.S. Tapp, D.M. Commane, D.M. Bradburn, R. Arasaradnam, J.C. Mathers, I.T. Johnson & N.J. Belshaw.
Aging Cell (2013) 12, 148-155.

Access to Understanding entrants are asked to write a plain English summary of a research article. For Access to Understanding 2014 there were 10 articles to choose from, selected by the Europe PMC fundersThe 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 further competition news and other Europe PMC announcements.   

Tuesday, 6 May 2014

Challenging language barriers

By Lucia Aronica, Max F Perutz Laboratories, Austria

Note: Lucia won the first ever Access to Understanding People's Choice award. Tomorrow the blog will feature her popular piece!

My research field is epigenetics, which means that I am interested in understanding how environmental factors can influence our genes and thereby impact both our health and predisposition to diseases. This scientific passion inspired me to write about Dr. Nigel Belshaw’s study ‘Nutritional factors and gender influenceage-related DNA methylation in the human rectal mucosa’. This research makes an important step towards preventing cancer with a cheap, highly effective, and low-risk approach: diet intervention. Hippocrates said "let medicine be the food and let food be the medicine" and I believe that modern research is finally uncovering the scientific foundation of this ancient wisdom.

Lucia and guests after winning her award.

Winning the People's Choice award was a big achievement for me. Lay people were the intended target of my writing efforts so to have their votes was incredibly rewarding. What inspired me to enter the competition was giving taxpayers insight into the science their money is funding. This is an imperative, often forgotten, issue and I am glad that initiatives like Access to Understanding remind us of its importance.

As English is not my mother tongue, I am especially proud of being shortlisted and winning the People’s Choice award. After the German Famelab 2009, this is the second time I have won a science communication competition in a non-native language. I hope this encourages other scientists to challenge their communication skills across language barriers.

Thursday, 1 May 2014

World Health Organization joins Europe PMC

Additional new funders joining Europe PMC further expand the perspective and scope of the resource.

Two new funders have today formally announced that they have joined the Europe PMC funders group, and in doing so the outputs of the research they fund will be freely available via Europe PMC. This brings the total Europe PMC funders to 26, and marks a steady growth in the open access commitment of research funders.

Image source: Shutterstock Copyright: Konstantin Chagin
The World Health Organization (WHO) is the United Nations health agency. It  provides leadership on global health matters, shapes the health research agenda, articulates evidence-based policy options, and monitors and assesses health trends. In the 21st century, health is a shared responsibility - and by making their research outputs available from Europe PMC, WHO is enabling more people to access and act upon relevant health information, and providing the opportunity for timely interventions and developments that build on this available information.

The National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC3Rs) is an independent scientific organisation. They support innovation and technological developments that replace or reduce the need for animals in research and testing, and lead to improvements in welfare where animals continue to be used - and by joining Europe PMC, these advances can be shared and incorporated more widely, thus contributing to ethically sound research practise.

We're delighted that WHO and NC3Rs have joined Europe PMC!

Europe PMC is a free, worldwide biomedical and life science information resource. A single search covers all the PubMed abstracts, PMC full text articles, and additional content including biological patents records.

A press release is also available here.