Brain linked machine (Malta Cafe Scientifique)

Less than a hundred years ago electrical activity from a human brain was first recorded. Today, with our improved understanding of brain function and the technological advances that have taken place, we are developing devices, known as brain-computer interfaces, that allow us to control equipment around us just with the use of electrical activity from our brains.

In this presentation we will see how brain-computer interfaces work and how these systems can provide an alternative means of control and communication for individuals with severe mobility impairment. We will also have a look at brain-computer interface applications for healthy individuals and how this technology may become part of our everyday life in the near future.

Come and listen to Dr Owen Falzon on Friday the 15th of May in the Cinema Room at St James Cavalier. Dr Owen Falzon also forms part of the new and approved Malta Neuroscience network. A brain awareness week will be held later on this year in December.

Malta Café Scientifique can be found on Facebook and online. You can now view events and subscribe to our mailing list from the website.

Poster thanks to Toni Gialanze

We would like to thank our sponsors: University of Malta, St. James Cavallier, Sammy’s by Culinary Forward Malta, Inspirations Café, Malta Chamber of Scientists.

Brain Boggling Behaviour (Malta Cafe Sci Talk)

The next science talk in Malta on the boggling brain.

The Malta Neuroscience Network has been founded to help the study of  the human brain, the most complex organ on Earth.  This complexity means it can go wrong easily. A lot of research is trying to understand this mind-boggling behaviour and what factors or triggers can make it go haywire. Professor John Stein (Oxford University) has dedicated his life to neuroscience trying to understand how the brain works and what makes it tick.

Date: Tuesday 21st April
Time: At 7.30pm (doors open at 7.15pm)
Venue: Cinema Room, St James Cavalier, Valletta

He will talk about modern techniques that help us understand the brain, the brain’s plasticity and the genetics which affect day to day activities. Dr Stein will also talk about deep brain stimulation to identify tremors, dyskinesias (involuntary movements) and pain, as well as to discussing how the cerebellum controls our motor functions.

Poster thanks to Toni Gialanze

Share the event on: bit.ly/MCS21April2015

If you haven’t joined our Facebook group, feel free to do so on and be updated on events.

We would like to thank our sponsors: the Department of Counseling, the University of Malta, St. James Cavallier, Sammy’s by Culinary Forward Malta, Inspirations Café, Malta Chamber of Scientists.

For information about the event, email cafesci@mcs.org.mt

For further information and any queries on Malta Neuroscience Network, you may call our offices on 2340 3518/2340 3515 or else email the Coordinator Prof Giuseppe Di Giovanni: giuseppe.digiovanni@um.edu.mt

Sex, Drugs & Rock ‘n’ Roll: a Malta Cafe Scientifique Event

Cocaine, Heroin, Cannabis, Amphetamine, LSD, the contraceptive pill, The Doors and Rolling Stones are children of the 60s. Chemistry fuelled the rise of free love, drug use, and a new ever-resonant culture. But, this culture also has a dark side: sexually transmitted infections, lost potential, and lives.

Interested? Professor Richard Muscat (University of Malta – Pro-Rector for Research) will be talking about ‘Sex, Drugs and Rock ‘n’ Roll’ on the 10th May at 7.15pm, Music Room, St. James Cavalier. The talk will be followed by an open discussion. Free entrance, no special science background is required, and all are welcome.

For over 20 years, Professor Richard Muscat has researched the effects of drugs of abuse on the brain. His research has focused on brain pleasure pathways and their relation to moods. In turn, how drugs affect the way people behave both in the short and long term. The brain chemical dopamine plays a critical role in influencing how people respond to pleasurable situations and unfortunately as a consequence relapse following repeated drug use. Another three important links are the predisposition to drug use, age of first drug use, and anxiety/depression.

The speaker Chairs the Research Platform of the Pompidou Group, Council of Europe, a group that combats drug abuse and illicit drug trafficking. Malta Cafe Scientifique is supported by The Malta Chamber of Scientists and the Malta Council for the Voluntary Sector, and aided by the University of Malta. Email maltacafescientifique@gmail.com or find us on Facebook for further information.

How to stop Multiple Sclerosis in Mice: step 1

Administering neural progenitor cells (NPC) is one of the most promising ways to treat multiple sclerosis. Jingwu Zhang and co-workers1 now report in Cell how these cells release the cytokine leukaemia inhibitory factor (LIF) that reduces disease progression.

Multiple sclerosis is an autoimmune disease that attacks the central nervous system causing inflammation, loss of myelin sheets, and the eventual degeneration of neurons. These symptoms are linked to specialised cells of the immune system called helper T cells. A subset of helper T cells, T helper 17 (Th17), release interleukin-17 (IL-17), a key inflammatory factor in the development of multiple sclerosis.

Neural Progenitor Cells (NPC) help to reduce disease progression of MS. The researchers found that NPCs secrete a factor which inhibits specific cells in the immune system. The picture shows spinal cord sections, on the left untreated diseased tissue, on the right treatment with NPCs. © Cell.

The role of IL-17 in disease progression was cleared observed in several studies performed using mice with chemically induced multiple sclerosis (experimental autoimmune encephalomyelitis; EAE). Removal of IL-17 delayed disease onset and reduced its severity. On the other hand, the disease was worsened by the increased expression of IL-17 or a greater number of Th17 cells.

So, how do NPCs reduce multiple sclerosis? Currently, they are thought to migrate to damaged neurons and differentiate into myelin sheets that protect the neurons. However, only 5–10% of NPCs form myelin sheets. To discover any additional mechanisms, the researchers injected NPC cells into diseased mice. The cells migrated to the spleen and reduced symptoms by inhibiting Th17 cell formation, which suggested that the NPC cells must release a secreted factor. This was confirmed by treating the mice with irradiated NPC cells and an NPC cell supernatant, which also inhibited the disease.

To identify the factor responsible, the researchers tested several NPC secreted proteins on Th17 cell differentiation, identifying LIF. Recombinant LIF was then injected into diseased mice that suppressed disease progression. These mice had lower levels of Th17 cells, but normal levels of other immune cells. Conversely, inhibiting LIF with a neutralising antibody reserved this recovery.

Further studies showed that LIF works by binding to CD4+ T cells and preventing their differentiation into Th17 cells. Upon binding to the LIF receptor, LIF triggers the extracellular signal-regulated MAP kinase (ERK) signalling pathway that increases the level of suppressor of cytokine signaling 3 (SOCS3). SOCS3 prevents the phosphorylation of Janus kinase-2 (JAK-2) and signal transducer and activator of transcription 3 (STAT3) inhibiting differentiation of the Th17 cells.

Finally, the researchers tested whether LIF has the same role in humans. They first purified healthy CD4+ T cells and then added either recombinant human LIF or NPC supernatant. Similarly to the mouse, these treatments prevented Th17 cell differentiation, which was negated by adding a LIF-neutralising antibody. These results were repeated in cells from 18 subjects with multiple sclerosis, confirming their relevance to human disease.

This important work shows how LIF inhibits Th17 differentiation in both mice and human models. The advantage of LIF is its selectivity — it specifically inhibits Th17 cells and does not affect other immune cells. Other studies specify how LIF can stimulate a neural repair mechanism, which also improves neuronal survival. The researchers suggest that this dual action makes LIF a strong candidate to develop a better therapy to treat multiple sclerosis.

References
Cao, W. et al. Leukemia inhibitory factor inhibits T helper 17 cell differentiation and confers treatment effects of neural progenitor cell therapy in autoimmune disease. Immunity 35, 273–284 (2011).

doi: 10.1016/j.immuni.2011.06.011

When Kangaroos and humans said: hello, goodbye

These are placental mammals (Wisconsin Historical Images; http://tinyurl.com/6ekftw7)

Biologists obsessed with mammalian evolution have been having a debate that sometimes gets nasty. They’re fighting over when placental mammals, that includes you and I, diverged from the marsupials, those cute and cuddly kangaroos, koalas and Tasmanian devils. But a new fossil unearthed in China [http://tinyurl.com/6dh5poy] by Zhe-Xi Luo in the USA and researchers in Beijing might force them to put their gloves down.

This debate has been raging on for quite a while, in March 2002 a small, 125 million year old, tree-climbing mammalian fossil was found. This pushed back mammalian evolution by around 50 years. Placental mammals were much older than anyone expected.

By 2007, even this date was being challenged. DNA sequences from several different placental mammals, marsupials, monotremes (platypus and short-beaked echidna) were compared to each other, which pushed back the marsupial-placental split another 20 million years.

This challenged the dogma that marsupials and placentals diverged recently and that the death of the dinosaurs allowed them to flourish. It’s a logical conclusion, but this is another case of truth being stranger than fiction.

This is a marsupial mammal (OZinOH; http://tinyurl.com/5scay8r)

The recent find by Zhe-Xi Luo and co-workers puts the nail in the coffin on this idea. They unearthed a fossil called Juramaia sinensis (Pictured), a tiny tree-climbing mammal that weighs in at around 12 to 15 g. It’s really tiny. Its teeth, jaw and heel bones are similar enough to ours to be grouped with us. On the other hand, it is different enough from other placental fossils to be stamped an ancestor. With enough fossils evolution can become very clear. Remarkably its also 160 million years old.

Juramaia Sinensis a 160 million year old placental mammal (from: http://tinyurl.com/6dh5poy)

Such an old time frame matches the molecular data perfectly, and it also pushes back our own ancestors by another 35 million years. Placental mammals diverged from marsupials in the Middle to Late Jurassic before flowering plants existed; when Allosaurus roamed, the big meat-eating daddy preceding T. rex; when the 40 ton long-necked giant sauropod Supersaurus roamed America; and, when Archaeopteryx was testing its wings (As a side note: Archeropteryx is no longer the ancestor of all birds, just closely related — instead other vegetarian dinosaurs are their ancestors). J. sinensis must had had a tough time competing with these dinosaurs and was even smaller than some of the insects they might have been trying to eat. But, was a mammals life really that tough?

The evidence suggests differently. It seems that in the early and middle Jurassic, a few million years leading up to J. sinensis, mammalian evolution was exploding. Several different mammalian forms developed, though in true Darwinian fashion, only a few survived. By around 100 million years ago, they were petered down into three classes: the monotremes, placentals and marsupials. After 100 million years ago, the dominance of mammals might just have been inevitable. The asteroid that wiped out the dinosaurs was simply a lucky break.

Sources

A Jurassic eutherian mammal and divergence of marsupials and placentals

The delayed rise of present-day mammals

Robust Time Estimation Reconciles Views of the Antiquity of Placental Mammals

Evolution of birds: Digging up the roots

Tips about Science Writing, Podcasting and Film (WCSJ2011 Day 1)

“So what do you do? Are you a journalist”. “Ehm, I’m not sure, not really, I’m freelance” I said. Not the best of answers, come on you can do better than that — a bit more confidence. “I’m a science writer, editor and I’ve setup a science cafe in my home country”. “So where is that?” said Samuel. “Malta, Malta” … blank stare … “it’s an island just below Italy, north of Libya a fusion of European and Arabic, but we’re in the EU, and you where are you from Samuel”. “Ghana, I’m a science journalist, I work for and I write freelance article for SciDev.net” Fuck, I thought “that’s amazing”

This was the first person I met, strangely I made a friend in one day. And, it was just the beginning. I’m at the World Conference of Science Journalists (WCSJ) in Doha, Qatar, which is amazing [add gorgeous picture of Doha here]. It has the highest GDP per capita, is advanced, clean, ordered, safe and has the most amazing architecture I have ever seen — and I’ve been to Beijing’s Olympic Village.  Though Doha is a strange place, only 20% of it’s citizens are from Qatar the rest are migrants.  But, this doesn’t feel like a function city, it feels like a perfect city.

Back to the bus leading to Education City — a series of huge complex whose architecture are simply astounding [show picture of education city] that the Qatar foundation is building to put this country on the science map. By 2030 Qatar will become a knowledge based economy – much better vision for oil wealth than Iran (have to admit).

I walked in late, scurried to the back of the room, no places, tip toed to the front. Nancy Shute was talking about online resources for science journalists, most are free:

• 10000words.net
• Mashable.com
• ReadWriteWeb.com
• Amy Wbb Webbmedia.com free and paid sections
• WGBH lab sandbox for independent filmmakers
• TECH.TV.MIT.EDU

Find more on: NANCY SHUTE (multimedia) – find on slideshare.com/nancyshute nancy@nancyshute.com @nancyshute

Then Beryl Benderly talked about how to get good reliable sources for science journalism:

• NIh.gov — The best!
• Pubmed Central — classic academic tool, if you can understand the paper it is the best source
• Free medical journals.com
• Science.gov — stuff like all earthquakes in last 7 days)
• Data.gov — information dump
• newswise
• eureka alert (publish science mag, releases on studies, embargoed release service. This resource sounds great!
• National library of medicine

Then we had a great exercise in podcasting by John Bohannon a science correspondent for science magazine. Great guy, so gave us a few good tips: Podcasting is cheap and easy, all your need is great content, decent equipment. Also remember not to speak to fast and give a decent intro. He got us to talk about a made up science story, ours: A pepertual motion machine as been built and energy has seeped into inanimate objects making them come alive. Rock monsters in Ghana and baby-eating carpets in Saudi Arabia. Idea adapted from Terry Pratchett.

This was followed by Diane Finch on data visualisation. Data visualisation is a process to display information in a manner understandable to a general audience. For a science journalist this means you got to do some research. Find the data, run some stats, find some interesting story within the data. Then Visualise it. A good picture is an easy sell.

Find data from Worldbank or WHO.

There is lots of software she recommended:

• Excel
• filemaker pro
• Google refine for BIG messy data

Another tip: geomap the data. This links your XML file (a spreadsheet from excel) to a location, turning it into a .KML file. Will help you connect data with neighbourhoods. Best tools for this seem to be google maps, google eat and google fusion tables. (also geocommons, openheatmap and GAPminder.org). More software for geo mapping and data visualisation:

• ARCview
• ArcGis
• Quantum GIS – MapWindow
• Phython/Django and R —more advanced and FREE (SPSS has become redundant)

• For Timelines: Simile and Timeline software

Then we had Randy Olson talking about science films and documentaries. This guy was yet another great speaker, very succinct, best to list tips:

STORYTELLING:

1. Why? (non literalism)
2. What? (is a story, what is not)
3. How? (Study structure)
4. Why (Film/Video)
5. The Nerd Loop – (refers to 4 organs)

What is a story? A story is a fact wrapped in an emotion ( Fact — literal, emotion — nonliteral)

A story has 3 structures A Beginning a Middle and an End.

Act not think = emotion, plus there are 4 organs for acting. The head which is cerebral and its ideas must go to the muscle (action), the gut (instinctual) and the genitalia (visceral) i.e. must have sex appeal. Sex sells.

A very important point to film making, writing, podcasting — is that story telling comes from the Greeks (and other ancient cultures). To remember a story orally it had to be riveting to the speaker, so the Greeks had tragedy and comedy, plus Simple Ideas and a good take home message. This is really the Hollywood formula — Hollywood unfortunately has no brains.

It is more important to arouse people with film and video, than bombard with messages. This is why Al Gore’s An Inconvenient Truth has failed to change the minds of so many. Sadly enough. Randy Olson’s answer was Sizzle. We had a free screening, and it was a fusion of Borat interwoven with a climate change message i.e. MENTAL!

I loved this movie, and I’m a scientist. Apparently most climatologists hated his film, because Randy’s approach is so unique and clever. First he lets you listen to the skeptics. Then shows them up for what they really are: charlatans, petroleum drunk, cocky, aggressive and liars. Watch this film, it’s a must.

By the end of the day I met people from Malaysia to Mexico to Nambia to Denmark. If science journalists from so many nations can be in one room and enjoy each others company, why can’t our politicians and the countries they represent?

So that’s it for today. I hope these tips help in the quest to find the next story that simply must be told. Please note that this is a very very rough draft and I hope to expand/flower/shorten this. Comments are welcome 🙂

Follow me on Twitter: username DwardD for real time updates on the conference, just search #WCSJ2011

For some Photos Samuel has already uploaded mine to: http://www.facebook.com/media/set/?set=a.2200291491520.130734.1374292926

Edward Duca,

Doha, Qatar

26th July 2011

WCSJ2011

GM fish coming to your plate? So?

If I read another article about Frankenfish or Frankensalmon I might just design a Trojan to bring down any website/ computer / mobile / tablet that hosts them.  These articles bring to mind images of double-headed Salmon and seven-finned abominations.  Why all the fuss?  The FDA (Food and Drug Administration, USA) are close to agreeing to the production of genetically modified (GM) salmon made by AquaBounty on a land-based Fort Knox in Panama, and sold – unlabelled – to the US market.

The villain of this story is an Atlantic salmon (Salmo salar) that has a single-copy of a growth hormone gene from the Chinook Salmon (Oncorhynchus tshawytscha) inserted into its genome.  This growth hormone is under the control of an antifreeze gene promoter from the eel-like ocean pout (Zoarces americanus).  The promoter keeps growth hormone production switched-on all year round instead of only in the warmer months.  So this salmon can go from an egg to your plate in just 18 months instead of the normal 3-year process.  Simply more fish in less time; economically it’s pretty brilliant.

The consumer should get more fish at a lower cost, however consumer groups are roaring “[they] jammed up the White House telephone lines last week protesting any approval” said Eve Mitchell, European food policy adviser at Food and Water Watch Europe.  The two main concerns about GM fish are its effects on human health and the environment.

I’ve read over 20 articles about these fish and most journalists seem to assume that GM fish are bad for you, and implied that these fish might be highly allergic since the human body has never been exposed to this salmon before.  My opinion: wishy-washy bull****, no data backs these claims, most proponents link allergenicity with seafood being highly allergic.  The only decent article that discussed health was Henry Miller’s ‘Turning gene science into a fishy business’ in The Observer.  His conclusion? Till now GM food has not resulted in huge health epidemics, although some cases of earlier imprecise genetic techniques, such as traditional crossbreeding, have resulted in new vegetable varieties with elevated toxin levels or disease weaknesses.

The FDA have given this GM salmon a clean bill of health, and the FDA has made the data publically available to appease critics.  On the other hand, AquaBounty claims a lot without backing it up with publically available data (that I could easily find): Ron Stotish, the chief executive of AquaBounty “This is perhaps the most studied fish in history … Environmentally this is a very sustainable technology.”  So my concerns started rising here.

The greatest fear is that these salmon could escape and cause the collapse of wild Atlantic salmon stock.  This fear is based on the ‘Trojan Gene’ hypothesis initially coined by Howard and Muir in their seminal PNAS study in 1999.  They inserted a salmon growth hormone gene into the Japanese medaga (Oryzias latipes) that makes the fish grow bigger and stronger.   Predictably this resulted in dominance over wild type males and more less fit young being produced from GM males.  The data was plugged into a computer model and extended over multiple generations.  The result was extinction in nearly 50 generations if the GM males have a 4-fold mating advantage over wild type fish.

If applied to AquaBounty’s GM salmon an escape could lead to quick extinction of wild type Atlantic salmon.  AquaBounty have already predicted this scenario and their facility is land-based.  Unless these fish start evolving very quickly there is little chance they will escape.  AquaBounty also subject their eggs to high pressures that results in eggs with 3 sets of chromosomes and 98% of adult salmon are rendered sterile.

The problem is that for AquaBounty to become profitable they need to sell their eggs to be raised on other farms in a number of countries. The U.K. has already banned GM fish from being grown in sea- or river-based pens, but will other countries have the appropriate legislation?  Escapes are not uncommon.  In the U.K. 100,000 farmed Atlantic salmon escaped in March.  If these were Aquabounty’s GM salmon potentially over 2,000 fertile adults could of escaped into the wild, a catastrophe.

AquaBounty says that even if they do escape their GM salmon are more susceptible to the environment.  They also say that male salmon do not gain mating advantages due to size.  A study by Thomas et al. (1997, Proc. R. Soc. Lond. B) proves them wrong.  Such blatant misinformation coupled with the companies desire not to release all of its data simply breeds mistrust.

AquaBounty are also trying to sell the idea that these fish are environmentally sustainable since they remove pressure on wild fish stocks.  Theoretically this makes sense, replace our need and love of that pink flesh from wild salmon to GM salmon.  The GM salmon will be cheaper, people will buy more, and so less wild salmon will be caught.  Wrong.  Since the 1990’s fish have become harder and more expensive to catch.  Fish stocks have been dwindling worldwide.  On the other hand, governments have been subsiding fisherman to keep them afloat and consumers are willing to pay more for their wild fish.

GM salmon are also unlikely to relieve wild fishing pressures any time soon, since farmed salmon are fed on fishmeal and fish oils that are made from wild stocks of makerel, sardines and smaller fish.  Until this changes the proposed environmental benefits are very opaque.

These companies are only shooting themselves in the foot.  People just won’t believe the data from AquaBounty, but no other third party research has been allowed on these salmon.  Greater openness and collaboration with academics is sorely needed for the environmental (perhaps even health) issues to be addressed.  Otherwise we will all be doomed to read about yet more Frankenfoods and the PR catastrophe that was GM crops will be repeated.  If GM foods are truly harmless then they should be labelled and the public informed.

There are currently a dozen GM fish in the pipeline, 2 produced in China and Cuba.  There is also a cow that has been modified for resistance to mad-cow disease and a so-called Enviropig.  As its name suggests this pig is beneficial to the environment since it produces less phosphorous in its faeces.  But unless we have more information and good scientific research performed on these animals I doubt anybody is going to be convinced about wanting to eat Enviropig bacon, no matter how good, cheap or beneficial they are.  The anti-GM scare journalists are too great.

 

 

The Science Thesis Blog: Procrastination got worse not better

I’ve been lazy. I was nearly sticking to my deadlines till I decided to come to Malta.  That’s the closest place I’ve got to home – I’m a nomad and I’ve never truly felt home anywhere in this world (closest places are scenes of natural beauty with people I love, China, Germany, Edinburgh, Malta, Dubai, Libya, all have touched me).  Malta has got my parents and old friends.  I’ve learnt many things, which friends I was closest to and were most special to me. How I’ve changed since I left Malta four years ago. How my parents have changed. How I love the new house – I can actually go for walks and take pictures of beautiful things: http://www.flickr.com/photos/38042871@N08/4244958081/in/photostream/.

I’m enjoying the return and it’s teaching a lot about myself.

This is all me, me, me, me what about thesis, thesis, thesis? Ha! 3 weeks after I was meant to start and this is the only week I’ve managed to actually get some work done.

Materials and methods: 90% done, 1st draft (Francesca – the post doc who rescued my PhD – suggested a lot of changes so I had to notch it down from 100% to 90% – I hadn’t been slacking off that much!)

Mitochondria Chapter: 70% ready.

Figures for all Chapters 60% ready.

Meeting deadlines: 1 month late…

A month a whole bloody extra month. I’m pretty pissed off with myself. Will that provide motivation, will I finally sit down, switch of twitter, facebook, msn, skype, emails and get cracking on it. Hardcore cracking, that’s What i’m referring to. Will power! That’s what I need, but how do you force yourself to do something you do not want to do. Now that’s something to ponder. Or is it another desperate attempt at procrastination?

ED

The Science Thesis blog: start.

I’ve decided to start a blog about writing up my thesis.  It’s likely another endless distraction to force myself to take double the time to write it up.  Or perhaps it will loosen my writing brain cells and beautiful academic language will plop out of my brain.  Check these posts to find out.

Materials and methods: 90% ready, 1st draft

Rest: 0% ready

Meeting deadlines: 1 week late.

 

ED

Viking Genes, Gout and Heart Disease: How are they linked?

Last week, Dr. Jim Wilson (University of Edinburgh) an Orcadian, gave a talk at the Western General Hospital in Edinburgh, about a 10-year genetic study that he has led called ORCADES, that sampled the population of Orkney.  The data his team has gathered matches genetic data with clinical data.  He spoke about some recent findings on gout and heart disease.  When we think of gout, great arthritic pain and the gluttony of 17th and 18th century Aristocracy, typically comes to mind.  However in 2008, this study combined with data from studies in Croatia and Germany complicated this picture.  They managed to narrow down 7 gene variants which resulted in a grossly elevated level of uric acid in blood.  High levels of uric acid are linked with gout, which affects millions of people around the world.  This study helped uncover an added role for a known sugar transporter, called SLC2A9, finding its dual role as a uric acid transporter in our cells.  This was a significant step for the treatment of gout.

Yet this study has not stopped there.  Data gathered by ORCADES has also been used to identify 22 genes, 16 known and 6 new genes, linked to heart disease.  These 22 genes were turned into a diagnostic tool which was as good as the current gold standard of measuring cholesterol levels.  In a few years genetic diagnostics are predicted to become cheaper than measuring cholesterol level; another major benefit is that genetics can be detected at birth, not when the patient decides they can no longer bear the pain.

The links between the underlying factors in our genome and disease will continue to be unravelled by this study, especially as technology and science continue to advance.  The study of these underlying factors could lead to new therapies.  Excitingly, the data collection by ORCADES is still ongoing and has been expanded to bone disease, obesity, age-related diseases, myopia and others.  The scope of this study is breathtaking; how does Dr. Jim Wilson manage it all?

Links to nature genetics papers:

http://www.nature.com/ng/journal/v40/n4/full/ng.106.html

http://www.nature.com/ng/journal/v41/n1/full/ng.269.html

More about ORCADES (bit old):

http://www.phgfoundation.org/news/1423/

http://www.orkney-mcn.org/CHD/ORCADES.html