The confirmation of a 100 year-old theory of Albert Einstein renders any blog or website posting pretty inconsequential. While the global news machine rolls on, champing out articles about Zika, Trump, refugee crisis, there is now a fervent subsection dedicated to reporting on the discovery of gravitational waves.

The import of the discovery is condensed into stylised, eye-catching and somewhat bewildering numbers. "The announcement is the climax of a century of speculation, 50 years of trial and error, and 25 years perfecting a set of instruments so sensitive they could identify a distortion in spacetime a thousandth the diameter of one atomic nucleus across a 4km strip of laserbeam and mirror," cries The Guardian.

Why should we care? "While the political displays we have been treated to over the past weeks may reflect some of the worst about what it means to be human, this jiggle, discovered in an exotic physics experiment, reflects the best," says the New York Times Sunday Review, through the patient and poetic words of Lawrence Krauss.

The New Yorker delivers an exciting narrative of the human stories behind the science. "David Reitze, the executive director of the LIGO Laboratory, saw his daughter off to school and went to his office, at Caltech, where he was greeted by a barrage of messages. “I don’t remember exactly what I said,” he told me. “It was along these lines: ‘Holy shit, what is this?’ ” 

XKCD delivers a swift dose of black line science snark, while NASA release a succinct dose of no-nonsense reporting.

One UK tabloid takes a typical run at the story. "Einstein was RIGHT!" screams the Daily Mail.

A thousand ways to tell this story. The science, now captured by observation and theory, enters the human narrative. You can read LIGO's richly detailed press release here, if you too would like to try your hand at capturing the "waves that propagate at the speed of thought."

Day 2 introduced some of us to a full night's sleep, and thus restoration of our full powers of intelligence, wit, humour and beauty. However this day also brought our remaining wayward fellow students to Erice, in much the same state of delayed-flight sleeplessness and jetlag as we earlier arrivals had been.

The first talk was of 'a very special candle' – synchrotrons, as explained by Francesco Sette of ESRF. Synchrotrons are facilities that fire incredibly intense beams of light through objects. Synchrotron radiation is capable of illuminating research down to the atomic level, to explore the shape of molecules and to clarify the structure of viral ribosomes. This ability can also be used to piece together larger pictures, such as by revealing hidden van Gogh paintings, and reading the writing inside ancient scrolls from archaeological digs. Francesco led us through a potted history of synchrotron facilities, from the first tabletop-sized synchrotron of 1947, to the massive facilities that exist today throughout the world. Modern synchrotrons can generate radiation which is 100 million times brighter than the first described x-rays of 1885. Most facilities are distributed throughout Japan, the USA, and Europe. Later on, we would be introduced to a notable synchrotron being built in the Middle East.

But next, Nicola Nosengo bade us to consider why light technology prevails, or fails. The invention of the blue LED in the early 1990s is considered so significant that it scooped a Nobel Prize in 2014. The invention of red LEDs, those red spots punctuating the everyday machines of our households and the glittering eye of HAL, did not win anything. For the combination of red LEDs, green LEDs and blue LEDs means that now white LEDs can be created. White LEDs are heralded as an efficient, energy and money-saving means to illuminate our environments and lifestyles. This steady improvement continues to uphold Haitz's Law, which predicts a steady increase in the light LED technology can produce against falling costs. This is the simple economic ideal, that better science leads to better technology at cheaper prices for all, and that more efficient, cheaper lighting will be a massive mainstay against global warming. But when our environment presents us with new benefits, we tend to change our behaviour to take advantage. This is Jevon's Paradox, quite simply, the message being that increasing fuel efficiency can increase consumption. So should we believe the hype about how beneficial LED lights will be? “Innovation in a single technology is one thing. Innovation in a technological system is another,” Nicolo warned.

Similarly, just look at the impact that cars had on society, and our behaviour in this strikingly brilliant film...

Luca Serafini delivered the second and final lecture on Extreme Light Infrastructure, focusing on the development of the ELI-NP laser in Romania. His first talk on ELI had been a crash-course in incredibly brilliant lasers operating at numbers and timescales of bewilderingly high and short scales. My brain was still trying to get to grips with these notions when it began learning about the ELI-NP laser. This laser will fulfil the nuclear photonics 'research pillar' of ELI, which means its research focus will be to explore and manipulate atomic nuclei. That's the easy part. The difficult part to comprehend is that this will be a uniquely powerful laser at the very forefront of research, producing the shortest and most powerful laser flashes, such that the acceleration of photons achieved over 10km of accelerator can instead be generated from 1cm pulses of plasma. The mechanism by which this is achieved emulates the gamma-ray bursts of distant galaxies, the brightest radiation events in the universe. Luca introduced a present and near future where relativistic optics become ultra-relativistic optics and eventually QED optics. The words he used dipped in and out of my uneven grasp of self-taught physics like the hazy plot of a badly dubbed film. My consciousness was rooting through slightly abandoned reserves of my brain, hurriedly seeking more mental yardsticks for scale and wonder. I stared at a helpful analogy for electrons surfing waves to understand this high-level physics. It was reassuring in its simplicity, a pictoral pacifier. Again, how helpful analogies can be used to translate physics for non-mathematicians, I thought, reassured. Sketching out futuristic ideas for high-energy lasers, such as to scan sealed containers and detect nuclear fuel, Luca reflected that the ELI-NP laser is also a prototype, at the front-line of technological progress. How its technology will come to be adopted and refined by industry remains to be seen.

There is some light we definitely do not need. Light pollution, melting away the view of the stars.  Drivers who leave their foglights on while approaching you at high speeds.   Flickering fluorescent lights when you're stuck working late in the office you don't particularly like anyway.  I would also like to nominate the unexpected light at Rome Fiumicino airport on 7th May 2015.  This was caused when a fire chewed through a baggage hall in Terminal 3.  There were no serious injuries, but the travel plans of thousands of international travellers were duly consumed in the process.  Surely, most terrible of all, was the damage done to the travel plans of a particularly special group of international science communicators.

Some slipped through unscathed.   Others arrived in the early hours of Monday morning, bleary-eyed and lurching through the darkness of the Sicilian night.  Others lost entire days in a nadir of intercontinental time zones, batted back and forth between delayed flights, cancelled flights, and interminable airport stays.  But one by one, our heroes eventually made it to Erice International School of Science Journalism 2015.

Following this shaky start, we were all extremely appreciative to arrive to the lecture hall and receive Fabio Turone's welcome speech.  We were also grateful for the inclusion of coffee breaks on our schedules, liberally provided so that we could consume plentiful cups of the magical juice of wakefulness.  The first day began with a talk by Luca Serafini, Research Director of INFN – Milan. (He is also the star of Extreme Skiing on Orobie – mind you I didn't have to delve far to find this fact, it's on his INFN profile...).  With his talk about the Extreme Light Infrastructure, he launched us into the 2015 course. His talk detailed the different research areas of ELI and the science of lasers. He led us gently into this world of high energy photons by weaving in beginning references to Blade Runner's poetic androids and mysterious C-beams to illustrate the great challenge facing him.   How could a physicist explain physics without using the language of mathematics?  And for that matter, how could C-beams be visible in space, if light cannot interact with itself, which also topples the hopeful hearts of millions if it destroys the fantasy of light sabers?  But I can assure Luca that he succeeded in his endeavour.   I know now, for example, the definitions of power, intensity, and brilliance, the reason why the sky is blue, and that there is a 300 TW laser FLAME at INFN.  It has a greater brilliance than the Sun.  Just... just as a laser pointer does...


After this slice of heavy science came Fred Balvert of Erasmus MC Rotterdam. Through his talk he invited us to discuss the intentions and order of questions to consider when promoting science. 

I think one of the easiest forms of science communication is explaining research science in clear or interesting ways. Indeed, mediums such as television often focus heavily on translating and transmitting that interest of research into full-blown wonder. I'll just leave this here as an appreciative nod to the wonder, and this here as a cautionary tale that science, as entertainment, is a two-edged sword. But how can we best communicate the relationship between research, society, and industry to the public?  Scientists do not toil alone in their labs, but are funded by and responsible to society.  But who can see how research might benefit society?  CERN and Tim Berners-Lee created the World Wide Web, but they did not have to describe this intention in several rounds of detailed grant applications to get there. (Of course, it is really the fault of scientists for not inventing that useful time-travelling machine yet). 

Science is both fuelled by, and the food of modern industry and economics.  However faceless pharma and large corporations do not inspire trust easily. The EU has specified that all funded research projects must contain a plan of communications.  Perhaps difficulties can arise when scientists must apply opinions and commentary to issues of science, since this contrasts with the objective, results-focused approach of the scientific method.  A journalist's role is to describe, monitor, comment, and challenge issues.  As science journalists, we bridge this gap.

Our first coffee break promised refreshments to combat the lack of sleep.  However nothing could be more effective for a tired mind than this stunning view from the terrace. 

A book I'm re-reading lately is My Beautiful Genome by Lone Frank.  Essentially, I recommend it, and here's why.

My Beautiful Genome is an account of Lone Frank's journey into finding out what our genomes can say about what, who, and why we are.  Or I suppose it would be more accurate to say, what scientists know about what our genomes can say about what, who, and why.  It's just over 10 years on since the Human Genome Project and Celexa laid out the human genome in its confusing glory- 23 chromosomes, 30,000 genes, 30 billion base pairs- and thanks to techniques, technology and t'internet, times have changed a lot since.  The original human genome took 3 billion dollars and 13 years to complete.  Nowadays a human genome can be sequenced for almost 1000 dollars in a few hours.  So all right, supposing I have a spare 1000 dollars and connections to a world-class lab.  Should I get a proof of my own molecular recipe?

Lone, a Danish science writer, sets out to see what can be seen.  The easy narrative of the book follows her physical journey to various labs and doctors, countries and universities.  It's low on jargon and enjoyable to read, a science travelogue imbued with Lone's own descriptions and inner thoughts, which add a hint of narrative drama to the interview scenes.  James Watson gazes at her from thickly bespectacled "golf ball eyes" that are nonetheless "clear without a hint of the common confusions of old age".  Lone admits her own faults, an honest personality deemed "cruel" by a close friend.  She describes her fear as she waits to find out if she has BRCA mutations that would show a susceptibility to breast cancer.  She reflects openly on mental illnesses in her family and her own experiences in it.  She is a likeable, cynical investigator.

The short answer is that genetics still can't reveal much about the average person, but that there are plenty of hints.  I daresay that still holds true.  This book was published in 2010 so in scientific terms it's a little out of date, especially with a field as fast-moving as molecular biology.  Still, I found plenty about the business and politics of genetics that I hadn't been aware of.  And Lone's journey contains many interesting tidbits from various research areas.  For instance, is intelligence inheritable?  Sure, studies indicate that 80% of a person's intelligence is down to genes.  Which genes?  Don't know!  20 years of study failed to find any 'IQ genes'.  Best case scenario?  In another few years, the researchers might whittle it down to a few hundred genes that explain 3-5% of a person's intelligence.  

Another surprising fact is that where some genes are concerned, such as a gene that affects how likely you are to get diabetes, it matters who you inherited them from, your father or your mother.  You could be more likely to get diabetes if you inherit this gene variant from your father.  But you are less likely to get diabetes if you inherit this gene from your mother. 

Lone explores the services of a few different companies and research schemes.  The Genographic Project can tell you about your ancestry as well as answering bigger, older questions about where early humans lived and moved to.  Then there is the big, attractive question of genes and health.  Can your genes predict what diseases you might be prone to?  Lone receives a few interpretations of her genes.  She has variants that increase her risk of lung and skin cancer, worry and depression, a small hippocampus and obesity.  She also has variants giving her higher resistance to malaria and TB.

Lone admits to a few depressive episodes.  On the other hand, Lone has always been slim, has a normal-sized hippocampus, and has never had skin cancer.  Genomic medicine is still in its infancy, a mix of ambiguity and intrigue.  This book cannot be used by a reader as a manual of certified gene variants, but it is scattered with interesting insights from the modern scientists who are wading through the legacy of the human genome project.  

Should people get their genomes assessed for probability of diseases?  The research continues.  Governments such as the UK are funding genomic medicine centres.  There's also a scramble of entrepreneurship and commercial ventures.  Companies like 23andMe are hoping to be the new Microsoft of personal genetics, offering direct-to-consumer genomic testing.  Another genomics motion, deCODE is cataloguing the genomes of most of Iceland.  But to me, it seems most of these companies do not provide value for money or time of thought.  Studies such as by Erasmus University have shown vastly different results in the answers of your genome analysis, depending on which company you use.  Processing errors have happened, resulting in some alarming results and alarming scenes at the consumer's homes.   A ruling by the FDA has put a halt on health screening by 23andMe in the USA, but the company is branching out in the UK and Canada.  

How long should it be before genomes screening for health is carried out, to prevent misinterpretation and misunderstandings?  "It is inevitable that we will come to use it.  It would be criminal to decide that people must not use this knowledge before we know how it will affect them biologically, psychologically, and socially," Kari Stefansson, founder of deCODE, argues to Lone.  He believes the best way to treat disease is to prevent it, and all would agree.  How far back can we prevent disease?  Armand Leroi, a geneticist at Imperial College London, has judged the risk of finding disease by screening embryos for known mutations to be around 1 in 256.  Lone points out that this level of risk is sufficient to justify cervical and breast cancer screening.  Is the stage being set for large-scale embryonic screening?

Then there's the popular topic of how genes influence our behaviour.  It's the classic nature vs nurture debate, a popular topic among biologists, psychologists, anthropologists, sociologists, parents, teachers, politicians, everyone... This debate is continually updated with increasingly detailed genetic data, and occasionally thrown to the public forefront by popular books like Richard Dawkins's seminal book, The Selfish Gene.  His book launched a thousand debates about whether we were all fleshy vehicles steered by a control-box of self-replicating genes.

"As soon as people hear the word 'heredity' or 'genetic', it immediately gets transformed into 'unchangeable' somewhere in their mind, and that is not the message at all," warns Gitte Moos Knudsen, research director at Center for Integrated Molecular Brain Imaging at Copenhagen University.  Lone has gone to see her to see how a personality questionnaire, brain scans, and her genes may be linked up.  You'll have to read the book to find out what she discovers.  But there's an intriguing mention of a study indicating a genetic basis for differences in behaviour between two major cultures.  Gitte also points out that even ostensibly negative genes- like a variant linked to 'oversensitive' behaviour- must give the owner some advantage.  Else why would so many people still have this gene?

The media gleefully reports behaviour-gene associations that make the best stories.  A discovery of an 'infidelity gene', for example.  But there is still no consensus on how to divvy up their own behaviour between nature and nurture, and I suspect there never can be.  I think we do have free will.  We also have brains housing that free will.  Brains are made from both genes and general living.  There will just be new and interesting ways to look at our brains from a genetic standpoint.

"People cannot stand the complexity of a nuanced problem.  There is a huge desire to lean back and say, 'It's my genes, it's not my fault,'" sighs Kenneth Kendler, a psychiatric epidemiologist at Virginia Commonwealth University, during a discussion on genes, growing up, and psychology.  He and Lone discuss the difficulty of linking a person's psychology to their genes.  There is no single gene variant responsible for causing Alzheimer's, for instance.  Most diseases will involve multiple genes acting in ways scientists still don't understand.  The same issue will apply for behavioural traits, or psychiatric conditions like depression.  

But studying behaviour from a genetic standpoint will help build up the overall understanding.  Kenneth mentions the serotonin hypothesis as an example.  The major theory is that depression is caused by low levels serotonin, a molecular messenger, in the patient's brain.  Drugs that alleviate the symptoms of depression affect serotonin levels.  But scientifically speaking, it's not known why this works.  There is no 'normal' level for serotonin throughout the brain.  Lone reveals a rather striking quote from David Healy, a psychiatrist specialising in antidepressive remedies.  "The theory that serotonin levels are the cause of depression is as well founded as the theory of masturbation causing insanity."  This doesn't mean we should toss out our antidepressants or stop the self-love, though.  It means that the picture is complex and genes are part of the complexity.

Studying genes in detail could also provide a new way to monitor psychiatric therapy.  "Psychiatrists used to ask people endless questions about their mothers, as if we could make good predictions on that basis.  At least, genes are objective," said Daniel Weinberger, neuroscientist at NIH.   And it does not have to stop at what genes each person has from birth.  Epigenetics adds another layer of complexity.  Studies have shown that life experiences can alter how your genes behave.  In a nutshell, this is caused by life adding molecular labels onto your genes.  Moshe Szyf, epigenetics expert at McGill University points out benefits of tracking the labels.  "If we know the epigenetic signatures and markers - for abused children, for example - we can design behaviour therapies, talking therapies, and study whether they work.  Determine whether they remove the markers in question."  This hints that future psychiatry could be a synergy of epigenetics, genetics, behaviour and therapy.  

There's also a scramble of entrepreneurship to make money out of genes and love.  GenePartner claims it can help you find your ideal social and biological partner.  To fall in love may lead to having children, and children are the combination of you and your partner's genes.  Do genes secretly steer our choices?  Can knowing our genes help us choose the best partners?  The enterprise is based on a few scraps of intriguing science.  Immune system is coded for by genes, and everyone (save clones and twins) has a unique set of immune genes, known as HLA genes.  Zoologist Claus Wedekind noticed that many animal species sniff out mating partners who have the biggest differences in HLA genes from their own.  The suggested reason is that such pairs produce offspring who have particularly varied immune systems, and are more likely to resist local germs.  This tendency has also been noted in humans, in a handful of studies, starting with Wedekind's own study in 1995.  Statistically speaking, women prefer the smell of men with the most different HLA genes, marriage choices in some communities appear based on this effect.  It's an exciting thing when pieces of scientific evidence can be tied together with evolutionary reasoning.  Once I explained to a boyfriend that our HLA genes were likely very different, ergo another reason why our relationship was destined to succeed.  I can't understand why he found this so amusing.

On the other hand, Craig Roberts, behavioural ecologist at University of Liverpool warns, "It's a scam.  We're not at the stage where we can say HLA genes make a practical difference."  There are other factors to consider here than the immune system, and a few other studies go against the varied HLA connection.  Again, statistically speaking, studies show that people tend to prefer faces of others who have similar HLA genes.  And has anyone studied if human children from varied HLA matches are actually better off?

Many people are afraid of genetic discrimination in the future.  This book goes a long way to explaining why this is unlikely to happen by describing the existing science and viewpoints.  Of course it remains a risk, which is why people need a gene lexicon containing terms like 'risk' and 'potential', rather than terms like 'good' and 'bad'.  Towards the end of the book, Lone discusses how it is thought both biology and sociology- a new 'biosociality'- needs to be a large part of the consciousness of the future.   Understanding of genetic difference may show where lifestyle changes could have the greatest impact.  Those with predispositions to stress from poorer backgrounds may benefit more from mentoring, or those at greater risks of certain illnesses will need more assistance avoid these things.  It will require a sensitivity of thought by any politicians passing legislation, and a malleability of 'nature vs. nurture' thinking on everyone's part.  Lone's view is that in understanding more about genomes, we will also come to understand and appreciate diversity.

So at the end of another enjoyable read, would I want my genome sequenced?  I certainly would not be afraid to have it done.  Will I have it done?  I'm in no hurry.  I don't think the science is well understood enough yet from an academic perspective to get any useful results.  I'm not yet inclined to approach a company to interpret my genes.  But it's getting closer, and I suppose, then, so am I.  One day, I'll learn more about myself.  It's nice to have such things to look forward to.

My Beautiful Genome - a TED talk by Lone Frank

I'm learning new things about Salvador Dali.  Earlier this year, I visited the Museum Boijmans Van Beuningen in Rotterdam, and discovered a room full of Dali paintings which I had never seen before.  When an artist is as famous and familiar, like Dali, they have assumed a public identity through their most famous and familiar paintings.  The distintegration of time, the fragile stem-legged elephants haunting desolate yet colourful deserts, tigers leaping after flowing cloth.  I've love the detail of Dali's Old Master-style, even and especially the way it slightly repulses me in its hyper-real depiction of unpleasant drooping textures and Surreal disturbia.  I'd never seen his painting of a vision of Africa, lushly dark in black and red, showing the painter poised in the corner, drawing up his vision like a magician gesturing magic.  Or his painting, 'The Great Paranoiac'.  Feverish, fainting figures stumble across the canvas, reaching out weakly for support.  A multitude of small bodies and stories make up the shape of Dali's own face, haunted and flickering.  Looking into the painting, my eyes flicked back and forth between the different ways of seeing, the shivering figures and the great bowed head.  It's a painting which personifies mental illness with ruthless clarity.

So, Salvador Dali, surrealist and psychologist.  But recently I found out that much more science permeates his work.  At the Kelvingrove Art Gallery and Museum hangs 'Christ of St John of the Cross'.  The painting is based on a 16th century drawing by St John of the Cross, a Spanish friar.  In the painting Christ is pressed against a cross, suspended in darkness over a stretch of shimmering clouds and skies, sculpted sandy horizon.  Dali based his painting on two dreams he had, and built physics and mathematics into its composition.  His first dream gave him an idea for the shape of the figure and perspective, based on his imagination of the nucleus of an atom.  Dali had studied physics and dreamt dreams of atoms in the wake of WWII.  The discovery of the atomic nature of the universe held a special meaning for him.

Picture yourself on a mountaintop.  The piercing cold temperature.  The unbarred views.  The thin air.

Hugh Montgomery presented the mountaintop to us as a natural laboratory space.  As Director of UCL Institute for Human Health and Performance, and Professor of Intensive Care Medicine, Hugh is interested in how the human body responds to exercise.  And the mountaintop presents an extreme environment for a particularly elite class of exercisers, the mountaineers.  Not only is mountain climbing a gruelling challenge for the body's muscles, but climbers must also tolerate low levels of oxygen in the air.  The higher they climb, the lower the oxygen levels fall.  But by studying the physical changes that mountain climbers undergo on a climb, and scrutinising the underlying genetic causes, Hugh's research group have produced some startling lessons for critical care of hospital patients.

Hugh Montgomery, smiling and fresh-faced, took to the stand at Bristol M-Shed to discuss his research.  He is the kind of researcher who deserves his own HBO television show, only this show would be about real scientific research rather than macho posturing and man vs. death escapades on the mountaintop.  The man's achievements and hobbies would make fiction unnecessary.  A diver, a record-breaking underwater piano player, an 'occasional' ultra-runner, a mountaineer, author, screenwriter, and a pioneering cardiovascular geneticist.  I could easily add more, but I am already lost in awe.

"Studying acute physiology can tell you really important things about yourself, and patients," said Hugh.  He began by outlining the key scientific tools that we needed to understand.  Angiotensin is an important hormone for your blood system, and the renin-angiotensin system (RAS) controls the blood pressure of the body.  It is a network of different hormones, including angiotensin, which tweak the size of blood vessels and the amount of water kept in the blood.  A key controlling element is angiotensin-converting-enzyme (ACE).  A high level of ACE in your RAS raises your blood pressure.

"That's where it stopped when I was in medical school," said Hugh.   "But it turns out, like most things I was taught at medical school, that wasn't half the story.  Because these systems are everywhere - in plants, in locusts, in fish, in jellyfish- all things that have been there for millions of years.  And jellyfish don't even have blood pressure!"

So RAS and ACE must affect more than blood pressure.  In fact, they are found in a huge range of human bodily tissues, from your brain to your eyeballs to your skin.  It is now understood that ACE also influences cell growth, inflammation, and metabolism in body tissues, even if the finer details of how it does this are still being uncovered.

In the 1980s, it was observed that increased amounts of ACE in rats leads them to develop bigger hearts.  Knockout the ACE gene, and hearts can't grow in size.  

In humans, the old romantic maxim is untrue.  Having a big heart is not a good thing, unless your heart is big due to exercise.  Otherwise, a large heart is associated with a higher likelihood of heart attack.  Therefore, it appears that whatever is making the heart increase in size is also damaging to heart tissues.

Based on the studies of ACE and heart size in animals, Hugh needed to see if the link between ACE levels and heart size applied in humans.  His group had found two different ACE gene variants - the I allele, and the D allele.  People with the I allele produced lower amounts of ACE.  People with the D allele produced more ACE.  And because everyone has two copies of each gene, any human could have II, ID, or DD.  But based on rules of inheritance, in a group of people 25% will have II, 50% will have ID, and the final 25% will have DD.

So if Hugh could take a group of humans, measure the differences in their heart size, and then correlate the heart size to the different genes, he would be able to prove ACE was affecting heart size in humans.  

But how could this be done, and more so, done ethically?  There could be many confounding factors affecting heart size.   Hugh found the perfect experimental subjects in the form of military recruits.  Military recruits all undergo the same strict regime of training and diet.  Exercise naturally causes heart growth.  So at the end of 8 weeks of training, Hugh would be able to measure differences in heart size, and link this to the I or D alleles.

After 8 weeks of training, the recruits with II alleles - producing the lowest levels of ACE - showed hearth growth of approximately 2%.  In DD recruits, who produced the highest levels of ACE, the heart growth was 6%.

Hugh sketched out the scientific reason that ACE caused heart growth.  In the RAS system, ACE breaks down kinins, proteins which are involved in blood vessel dilation.   High ACE equals low levels of kinin, which means greater growth in heart size.  As in most science, the chain of cause and effect was becoming a little long, but we were still with him.

So the military recruits proved the link between ACE and heart size.  And there was more.  Through a muscle fatigue test- a fancy way of saying, how long could each recruit hold a weight at arm's length without buckling - it was proved that II recruits have the best response to exercise.  ID recruits respond moderately to exercise, showing only small improvement in muscle fatigue after training.  DD, statistically speaking, showed no better improvement by end of their training.

Now, back to the mountains.  Mountain climbers with II are more likely to reach the peaks than DDs.  Similar trends can be seen in other oxygen-hungry sports, like marathon running, where runners are much more likely to have II alleles.  Hugh revealed another interesting tidbit.  Although gruelling endurance challenges like the Tour de France are dogged by doping scandals, where athletes use erythropoietin hormone to increase red blood cell loads, the ability to accumulate more oxygen on a mountaintop is not actually helpful to your body.  To put it more simply- if you put a Tibetan and a Westerner on a mountaintop, the Tibetan's body will generate less haemoglobin.  The genetic selection for successful living at high altitudes appears to be in keeping haemoglobin lower.

Hugh explained that I or D alleles affect how efficiently mitochondria use oxygen.  Mitochondria are the power plants of the cell, generating ATP energy from oxygen.  Low ACE levels make mitochondria better at generating ATP from oxygen, even low levels of oxygen.  D alleles are more like "leaky batteries" - they lead to a higher level of ACE in the body, which raises oxygen demand.

"So what genetics is telling us, is that when oxygen availability is low, we should try to increase the efficiency in which we use the oxygen," commented Hugh.  He recalled that the convention treatments for ICU patients in hospital is to try, forcibly, to put oxygen into their bodies.  But modern treatment needs to change, as studies have shown forcible oxygen transfusions can increase mortality.  Based on lessons from mountaineers, new modes of treatment are being introduced into hospitals to allow oxygen levels to reach lower levels than conventional treatment had allowed.  A normal person has an oxygen tension of 12 kPA.  On a ward, lower levels of 8 kPa is now being allowed.  A level of 6 kPA is still considered very worrisome.  However one experienced mountaineer has been able to reach 2 kPA.  This is conventionally considered terminal... but for him, it was not.  His body was attuned to that low level of oxygen.

Many animals adjust their body systems to withstand low oxygen environments.  These include a few fish with coincidentally interesting names - the epaulettes shark, the oscar fish, and the Crucian carp - who shut off unnecessary body functions when oxygen levels decline. With a wry grin, Hugh admitted that when he explained his research to his 6-year old son, he was told his research was "very obvious".  When a car is low on fuel, you don't leave all its systems running, you tune down to the bare essentials.  Why had it taken his father 20 years to work out that the human body does the same?

But the most startling and sobering impact of ACE was yet to come.  Hugh showed us the relationship between the ACE gene variants and medical conditions, especially in the ICU.  In premature babies with under-developed lungs, high ACE levels are associated with respiratory distress.  In patients who undergo bypass surgery, II patients with low ACE show better survival rates.  In meningitis patients, having the DD alleles is associated with the most severe examples of sudden meningococcal sepsis.   It was sobering to realise that survival, especially in the face of respiratory complications, could be so clearly linked to the ACE gene.

"In this audience, if we all came down with Adult Respiratory Distress Syndrome and ended up in Bristol ICU, the IIs could have a 90% chance of surviving.  Whereas DDs have an over 55% chance of dying.  That puts my job in perspective.  We like to congratulate ourselves as how good we are when someone lives - but a lot of that living and dying, is down to our genes."

Hugh moved onto another lesson of mountaineering - starvation.  Hypoxia, meaning low levels of oxygen, causes weight loss.  Mountaineers lose both fat and muscle in the hypoxic conditions of the mountain.  ICU patients, whose body tissues are low in oxygen, also show weight loss.  A key clue is that muscle is lost, along with fat, even in highly active and well-fed mountaineers.  A group of Hugh's mountaineers who scaled Everest lost 9 kg each, on average.  Hugh explained that the 90% of the body's energy goes into producing protein, to rebuild and renew the body.  It used to be thought that in low oxygen conditions, the body's regulation was simply thrown into disarray, causing inevitable weight loss.  But now it is shown that the body actually orchestrates sophisticated survival plans.  It tries to conserve oxygen by shutting down demanding systems.  Essentially, the body willingly creates a 'starvation' mode.

In starvation, a process known as ketosis occurs where fat is broken down for energy, producing chemicals known as ketones.  This is the fundamental concept of the Atkins diet.  Ketosis is also carried out by hibernating animals.  It appears likely that ketones have some kind of beneficial effect.  And this is true.  Ketones are an anticonvulsant, which is why the severity of epileptic fits can be reduced by putting patients on diets.  Ketones protect the brain from hypoxia and low levels of glucose.  Even sperm are more motile in ketones, and the heart increases its workload.

In short, starvation can actually be beneficial.  A synthetic ketone is being trialled in adults with heart failure in Belgium, and there are more studies which will test ketone compounds with patients and premature babies.  And astudies have shown that force-feeding of ICU patients in hospital can lead to muscle wasting, a new method of intermittent, low feeding may prove much more helpful.  Perhaps a more modern and effective treatment needs to accept starvation as one of the body's natural defence mechanisms.  There's some truth in granny's advice - 'feed a cold, starve a fever'.

Ketones, ACE, genes, and fitness.  I wondered what would my genotype be.  Did I respond to exercise well, like an II, or fall in between, as an ID?  I have only ever ventured up a bouldering slope, but I have dreams of climbing Kilimanjaro.  How much extra preparation would I need?

"Should I take ACE inhibitors to improve my chances of reaching the summit of Everest?" asked an audience member, a self-diagnosed DD.

"Yes... but we haven't done the study yet."  The study is in the planning stage, but they still don't know how ACE inhibitors will react with the body in hypoxic conditions.  This is too big a risk to take on a mountaintop.

And throughout his talk, Hugh pointed out that D alleles were not to be perceived as inferior.  This is the first gene that was discovered which was directly related to fitness.  It has some striking lessons for hospital care.  But it is not a case of genetic determinism, stating who is likely to be the best at keeping fit, or surviving overall.  The D allele confers its own benefits.  People with DD appear to be more resilient to haemorrhage.  And they are likely to be stronger, better at swimming and sprinting.  They tend to show greater muscle mass in old age which significantly reduces the problems of frailty and falls.  

I thought of my father, silver-haired and 70-something, still stomping round, still operating heavy machinery, still involved in the mysterious and never-ending movings of heavy objects.  For that matter, I also thought of my mother, thin, frail, and disabled, but who has been doggedly picking up an entire bulldozed bungalow, brick by brick, and assembling them into an array of neat stacked cubes in her garden.  I might never know my genotype for I or D and I might find it hard to predict, but it probably didn't matter anyway for my fitness.  What matters is the mind - willpower, determination.  For his part, Hugh was vehemently opposed to casual genotyping for these alleles.  The research needed to carry on, and it would be too easy for, say, medical insurance companies to jump the gun and draw broad - and expensive - conclusions.

After all, for all his incredible-sounding athleticism, Hugh himself is a DD.

You can listen to a recording of Hugh's talk here ...

And the following questions here ...

Hugh Montgomery also talks about his discovery of the first gene for fitness to Jim Al-Khalili, on the BBC's The Life Scientific

I like slime moulds, and so should you.

Let me convince you.

Slime moulds seem to bridge the gap between fungi and animals. In a nutshell, they are a glistening goop that spreads and develops in a webbed network of frilly fingers.  But this is an intelligent goop.  Slime moulds respond malleably to their environment. They can work out the most efficient shape to morph into in order to reach multiple food sources.  Scientists have shown this ability compares favourably to some of the most efficiently planned human transport systems. When times are hard, the slimes can change form to produce fruiting spores, sending its spores away to find better lands. When two slime moulds of the same species meet, they join forces into one large super-slime. Best of all, they seem pleasantly benevolent compared to many other microorganisms. No slime mould has yet proved itself to be a human pathogen. And they not only eat bacteria, they farm it.

So slime moulds are a wonderful piece of the biodiversity puzzle around us.  And we're slowly getting to know more about them.  They have cropped up in the 2010 Ig Nobels, for instance.  But there are some incredible combinations of man-made technology meeting nature, like fabulously weird experiments using slime moulds as living computing interfaces (quick translation: cyborg technology). Andrew Adamatzky's group at the University of West of England have almost given slime moulds a human face.

And on 27th January 2013, I attended an exhibition of slime moulds and 3D printing.  It was an interdisciplinary event hosted by the Waag Society, an arts-meets-sciences-meets-design sort of incident.  While the supposed schism of the arts and sciences has long been debated and reinvented to zombified death, introducing 'design' as part of interdisciplinary events has crept in on the tides of 21st century technology.

The exhibition showcased the results of a two-day workshop where participants designed with slime moulds and 3D printers.  This was to be my first visit to the Waag Society, institute for art, science and technology, and I'll admit, I was wary. I hardly knew much about 3D printing on a small-scale, and how could you design with a living organism?  To prepare myself for disappointment, my pessimistic mind conjured up images of an exhibition space containing conceptual sculptures splashed 'artistically' with slime mould goop. There might be a lot of dainty talk using inaccessible artspeak.  In short it could be all show, no engagement.

But there was no need for these pessimistic thoughts.  There was plenty of show and plenty of engagement.

The beautiful old Waag building is an excellent space for science-related public events. The winding staircase, curved walls and old architecture-style is fertile ground for imagining classical scientists pursuing their work.  For the Romantics, where else should you be bringing new creations to life, other than at the top of a wood-panelled, historical tower?  Indeed Rembrandt immortalised dissections carried out in the Waag.  

Inside there was a healthy mix of public, scientists, and designers.  A few small tables showed the results of the two-day Bio-Logic workshop.  A table held a couple of stewpots serving as simple incubators, and another held an array of petridishes containing yellowish agar and seeded with slime mould spores.  A few computers with coding programs.  A 3D printer in a modified box which served as a sterile cabinet.

Afterwards, scientists, designers and public mingled to discuss ideas and ask questions.  I loved thinking of the little flake of slime mould spore material in their dormant state.  Ostensibly dry and dead to the eye, but merely waiting.  Sensing their surroundings.  Unfurling, slowly, responding.  Molecular mechanisms begin to cascade, moisture is drawn up.  The machinery unfolds.  The mould becomes a mobile slime again and reaches for food.

I learned more about the slime mould being used, Physarum polycephalum.  It can move as quickly as one centimetre an hour.  The giant cells it forms are called plasmodia, and contain several nuclei.  As in any microbiology lab, contamination is an ever-present problem and can ruin carefully constructed petridishes, but sometimes slime moulds have used the invading growths of fungi as a scaffolding to climb out of the petridish.  

The moulds can also lay down a trail of physical 'memory'.  They can leave crystals behind as chemical signals, marking where they have explored.  They can also keep time.  When researchers exposed a slime mould to a pattern of regular temperature changes, it learned to anticipate these environmental changes.  One visitor asked if the slime moulds could be used to make a 'circuit switch'.  And the scientist's answer?  Yes!  See here for more information.

A hacked 3D printer designs structures out of organic material, and the slime moulds redefine these structures.  It's a start of a design exploration, bringing together technology and living matter.

So what do these slime moulds look like in action?  You can watch a beautiful time-lapse video here.

This is about why I went into science communication.  It's also about why I studied science.  And about why I feel so passionately about visual art.  It's all of those things, because I think they come from the same place.

On my birthday, I went to Hoge Veluwe National Park in the Netherlands.  The park is a beautiful amalgamation of rough green heathland and distant tree copses, red-barked pines and savannah grasslands, African desert dunes and twisted silvered trees.  I cycled through and marvelled at how the land changed as I went further in.  

And in one wing, the van Goghs.

The paintings are laid out chronologically,  and feature a lot of early van Gogh.  There are examples of the first still-life paintings he produced as he was first learning to use oil paint, in 1881.  And several works from 1882-1885, when he was dedicated to depicting peasant life and rural farming.  The museum has The Potato Eaters and Loom with Weaver.  There are also a few landscapes from this period.  Boggy-dark, muted green, obedient in their depiction of reality and technique.  What struck me is that, if you associate van Gogh with the most famous and reprinted works that came later, these paintings are remarkably boring.  Superficially attractive in their realism, with clues to his style of painting throughout.  But nothing that you might not already know about these landscapes, these scenes, these ideas.

The Sower, though.  I went in close to count how many shades of blue.  You can see the same shades hitting the canvas in strokes that might overlap, but which never blend.  He didn't smear the colours together, he laid them on.  There's a layer of grey-blue strokes, a layer of pale blue strokes, a layer of purplish-lilac-blue strokes.  Spattered throughout, shrill dabs of orange.  Orange and blue are opposites and so in terms of seeing colour, the contrast can't be greater.

And when I stepped back... everything changed.

It was then I realised there's an ideal viewing distance for van Gogh's most colourful paintings.  It's the point where contrast between blues and orange and yellow start working together.  They sink into the eyes.  And the effect is like music.  Every paintstroke a beat, a note, a particular sound.  Taken all together, the contrasts of colour work like a symphony.

And in this painting, against everything playing out of the foreground, in the background the linear motion of the sun rays blaze outwards and set a constant tempo.

Close up you see the notes, but from further away you can see the full music.  

And this.  Far more beautiful than his titular Sunflowers, that yellowish sunny painting I was first introduced to in primary school.  This is Four Sunflowers Gone to Seed.

Again, close up I saw the strokes.  Stepping away, I saw how everything came together to make four dying flowerheads come ablaze.

Contrast.  That's why I like Vincent van Gogh's style, his paintings.  I have been thinking a lot about the Sublime, since interviewing Anna Dumitriu about her artwork.  If we take the Sublime to mean an incredible beauty, it's something that can only be sharpened and highlighted by contrast.  Orange against blue, black against white, paint contrasts etched onto canvas, a symphony of something beautiful that van Gogh saw.

The painting was full of movement and direction and tempo.

Even van Gogh's life was about contrast.  Beauty and darkness, depression and mania.  He could see incredible visions of the Sublime in the scenes he painted, of the countryside, of objects, of people, of streets.  He painted his excitement and fervour into his works, striking out each piece into a moving orchestra of colours and brushstrokes and direction and tempo and blackness.  Then there were the times of horror, of nothingness, melancholia.  Perhaps the Sublime comes and goes.  Like the sun, you can't stare at it forever.  In between the beauty, the ordinariness, and beyond that, the complete lack of beauty.

I studied van Gogh in high school. The first time I saw an exhibition of his work was as a visiting exhibition at a modern art museum in Seoul, South Korea. What struck me then was the shininess of the colourful paint, which looked almost freshly applied. The chapped texture of the brushstrokes buttering the colours on. They were famous, and old, and alive. And I'd had no idea he had created so many paintings. Like most people, I grew up on a diet of Vincent van Gogh's Sunflowers. The same image turned out and appearing in textbooks, posters, school lesson photocopies, again and again, as though on a carousel.

Colour has always been what I like best in paintings.  Colour and contrast.  Colour played against blackness to bring it out and make it breathe.  Sitting in the museum, staring into a van Gogh painting, I felt an odd feeling, like a brief psychological disjunction.  I was reading a message written out in paintstrokes and paintings by another long-passed artist's work.  Did I feel as he had felt?  Did he know what it was that he created in his work?

Feeling how another person feels, seeing how they see.  I thought about this a lot as the museum closed and I started pedalling back through the park.  Along with visual art, I have always liked science.  I like to know the names of things, and why things happen.  I like to see in closer and closer detail how something works, from learning about a leaf, to the cell, to the mitochondrion inside and beyond to where you can no longer see, in the diagrammatic sketching of the visualised electron transport chain.  School had always been about progressing in greater and greater levels, so it's not entirely unsurprising that I studied Biology at university.  Knowing these things gives me a sense of similar excitement to looking at a beautiful contrast of colours in a painting.  And to step back from the details, to try and hold everything in your head at the same time as you look at the bigger picture- how the machinery of the genes moves the molecules that connect up the proteins that altogether animate the entire organism... it's bewildering, and it's incredibly difficult.  That's science.  But it seemed to me that trying to hold everything together like that is not so different from stepping back from a van Gogh, and finding the point where everything begins to move and work together as one.

And that was why I'd become interested in science communication, too.  Science communication can have many roles and they are best explored in another article.  I'll define two major types of science communication here, though.  One reason is to communicate clearly, to rearrange a piece of complex jargon-filled research into something legible to a non-specialist.  The second reason is to make you feel as I feel.  There's a beauty in science communication, because it is an art form.  The way an idea is expressed, whether through words, a picture, a book, a sentence, an article, a concept.  If I could create something that communicates that flash of beauty, fascination, of that Sublime in science, then I will have shared what I see in it.  And that's the true point of science communication and science engagement to me.  If I ever achieve that then it will mean, like van Gogh to his viewers, that I succeeded.

What is the romantic disease?  Watch the film below to see artist Anna Dumitriu talking about her exhibition.

Anna Dumitriu explains the stories behind her exhibition here

I’m in a room with humanity's biggest killer.  It began eating away at us over 9000 years ago, and has never really stopped.  

The marks of our relationship surround me in an array of medical leaflets and dyed fabrics.  Mysterious objects sit on stands.  A glistening set of metal needles and devices inside a spongy wooden case.  There's a tiny, bare bed, and a ghostly pale dress. A collection of tiny felted grey lungs that resemble a group of settled moths on a wall.

This is an exhibition on tuberculosis. 'The Romantic Disease' has been created by Anna Dumitriu, a British artist with a taste for microbiology and emerging technologies. She is the artist-in-residence for the Modernising Medical Microbiology project, a collaboration between Oxford University and Public Health England, and she was inspired to create this exhibition by their research into bacterial diseases. The exhibition is on tour through Europe, and is currently hosted in the Theatrum Anatomicum at Waag Society in Amsterdam. 

What caused tuberculosis? 

On one side of the room I see an animated black dog circling and pacing endlessly. It represents one early interpretation, the 'demon dog'. This dog would enter the bodies of sufferers and bark, making them cough. Later, people thought tuberculosis could be inherited. On another wall I read an old medical text warning of the 'tubercular taint' that could be passed on through risky marriage. I find out that the pale dress hanging on its stand is a Romantic era maternity dress, representing how some pregnant women with tuberculosis were forced to have abortions. It was a long time before the real cause was found. Bacteria were only seen for the first time in 1676 by Anton van Leeuwenhoek, and in 1882 the microbiologist Robert Koch proved that tuberculosis was caused by bacteria. 

At the entrance to the exhibition I spy a quote from the Romantic poet, Lord Byron. 

' “How pale I look! – I should like, I think, to die of a consumption –because then the women would all say, 'see that poor Byron- how interesting he looks in dying!” '

Ah, the vanity of poets. I wonder how tuberculosis could ever be thought of as 'romantic'. The disease was called 'consumption' from the 14th century because of its vampire-like effect on sufferers. It mainly eats away at the lungs, causing hacking coughs and bloody sputum, sweaty fever, the body weakening and wasting away. The statistics for tuberculosis are shocking. One third of the world's population are infected with Mycobacterium tuberculosis, the bacterium responsible for causing the disease. Of those, ten percent will develop the disease. Of those, around five percent would die of it without treatment. It is currently the second most deadly infectious disease after HIV and has killed far more people overall. While it is curable with modern antibiotics, in the right conditions extremely drug-resistant tuberculosis can evolve. So what's romantic about all of this?

But I'm looking at this wrong. 

Nowadays, we know about tuberculosis. We know about bacteria. We have antibiotics and medical advice. We have scientists with gene sequencers and electron microscopes. But for most of our history, people did not know what caused, spread, or cured tuberculosis. Forced to live alongside this mysterious and widespread disease, unpicking its mystery with slow science, people also responded with myth, imagination, and art. After all, anyone could get tuberculosis, from famous figures to the unknown. Many Romantic Era artists like Keats had it. Perhaps Byron spoke tongue-in-cheek, since his own father died of the disease. And unlike other common diseases of the time, like smallpox, tuberculosis was less devastating on the appearance. A waifish, pale appearance was even considered fashionable, tuberculosis or not. This is not so different from today's unchanging fashions of the catwalk, or tastes for sparkly skinny vampires, then.

And while many artists had tuberculosis, could tuberculosis actually create the artist? Some people have theorised that tuberculosis enhanced creativity by inducing spes phthisica, a state of euphoric creativity before death. While it's likely that this state was only based on romantic anecdotes, perhaps a feverish delirium could inspire strange and artistic ideas.

Anna showed me around the exhibition, inside the softly lit circular room of the Theatrum Anatomicum. Her artworks tell the story of how we have long tried to understand tuberculosis.

“Because it's had such an impact on humanity, there are a lot of myths around tuberculosis,” Anna says. “And there's a lot of different areas of medical research that have changed over time. There's this fascinating cultural story alongside the microbiological side.”

How was it transmitted? 

“Where there's dust there's danger,” warns a 1902 guide by the National Society for the Prevention of Consumption. At this time, tuberculosis was thought to be spread mainly by infected spit that dried on specks of dust. Invite a few tuberculosis sufferers into your home, let them spit on the floor, neglect to sweep for a few weeks, and eventually you could be stirring up clouds of death with your broom. Close up, I see the moth-like objects on the wall are actually tiny grey lungs. These are made from felt and dust, by Anna and people who have attended her interactive workshops. The advice was almost right in that tuberculosis can be spread by sputum, sprayed into the air by coughing, but dust could not spread tuberculosis. Drying out sputum droplets tends to kill the bacterium.

Today, thanks to whole genome sequencing, transmission of a disease can be more precisely mapped. I learn about this by examining a stand holding an old 'pocket-bottle for coughers'. The Blue Henry is an attractive blue glass bottle with a silver lid, intended to provide a safe and fashionable receptacle for sufferers to cough up blood in public. 

Like many of the artworks on display here, Anna has combined the past and present of tuberculosis on this object. The top is engraved with a patient transmission map, produced by the research of the Modernising Medical Microbiology (MMM) project. 

Today, the MMM scientists investigate deadly bacterial diseases by sequencing the genomes of the bacteria responsible. Using the sequences, they can identify which strains are responsible for disease outbreaks, and they can also map the transmission of an outbreak back to its source. The diagram on the lid of the Blue Henry shows how multiple people were infected by one person, who was in turn infected by Patient Zero, the first person to get the disease. Prior to whole-genome sequencing, unravelling the spread of a disease would have relied on a laborious process of interviews and piecing together likely infection scenarios.

How was tuberculosis treated? 

There are fascinating items showing how tuberculosis treatments were marketed. 'REST... to beat TB' one medical poster declares, showing an improbably merry man as he lies in bed, resting off his tuberculosis. Resting was supposed to help recovery by lowering the breathing rate and giving the lungs of sufferers less work to do. Patients would also be shuttled off to sanatoriums in mountainous regions, where the air was thinner and thought to be better for the body. Anna tells me about an infamous Welsh mountain sanatorium, Craig-y-nos, where children were forced to sleep outside in fresh yet painfully frosty air, since this was thought to be another benefit. A jaunty magazine poses an attractive young couple under the headline, 'I had TB!'. Below this, Anna has arranged an innocuous little microscope slide of stained M. tuberculosis from sputum, the foe in question. 

But there are also works based on more sinister tools. Anna explains that artificial pneumothorax- collapsing a lung- was once a common treatment. The idea was that collapsing the lung would 'rest' it, giving the lung a break to tackle its tuberculosis infection, and also starving the tuberculosis bacteria of oxygen. Around one third of tuberculosis patients were treated to this between the 1930s to 1950s, including the writer George Orwell. It's a toe-curlingly unpleasant idea, but Anna tells me that some small, recent trials suggest this antiquated treatment might help fight the modern rise of extremely-drug resistant tuberculosis. Sometimes medicine, like history, turns in cycles.

Textiles and dyes also play a large part in the history of tuberculosis. The maternity dress has been dyed with walnut husks, madder root and safflower.  All common natural dyes, and all early treatments for tuberculosis. There's a vial and fabric-stains of Prontosil, the world's first 'sulfonamide' drug which could slow the growth of bacteria. It was produced by Bayer, today known as a chemical pharmaceutical giant, but who began as a dye manufacturer. 

Bayer's large chemical laboratories for producing dyes were perfect playgrounds to test out new chemical combinations. With ready supplies of coal tar, a by-product of coal production, a base for many dyes, and the bane of my childhood thanks to my dad's inexplicable fondness for coal-tar soap, many scientists tried to produce dyes to specifically target bacteria. Along with other useful products like aspirin, Bayer eventually produced Prontosil, and medicines derived from this bright red substance were widely used in bandages during WWII. It also had the side effect of dyeing the skin red. 

Anna has also found staining effects in modern treatments for tuberculosis, and she used the growth media for Bacillus Calmette-Guerin (BCG) (an attenuated strain of Mycobacterium bovis used as a vaccine for TB) to add striking touches of pale blue to some of her artworks.

I also find out that Byron's vain wish to be pale and interesting would get a colourful update. Anna reveals that a modern antibiotic used to treat tuberculosis, rifampicin, can cause the tears and sweat to turn orange. “In a way, they look like they have a nice tan,” she commented wryly. “So it's interesting how that link between fashion, appearances and tuberculosis has come about again.”

Stories and the Sublime

Anna is fascinated by objects that are tainted with the story of the disease, and has added more subtle combinations of old and new stories. The dress and tiny lungs are infused with the extracted DNA of M. tuberculosis. There is no danger that the DNA can harm anybody. But the DNA's presence in objects so close to me make me feel face-to-face with the bacterium itself, laid open before me. It is an intimate and respectful meeting, one without infection, disease, or pain. 

“My research into this exhibition began with conversations with scientists, and reading about the disease, and the more I did the more stories I found. The strangeness of everything, the stories, it's not really what people expect,” reflected Anna. “I'm definitely planning to take the work further, I think there's many more stories to be told.” She also runs hands-on workshops to explore the history of tuberculosis further, and sometimes people attend who have experienced old tuberculosis treatments first-hand.

Looking round the exhibition, I'm struck by how much it has filled in the cultural side of tuberculosis to me, something which was entirely missing when I studied the disease at university. In modern times we might easily think that only the scientific view remains now. With sophisticated technologies or new drugs, scientists work towards understanding cause, transmission, and treatment in ever closer detail. But cultural understanding of the disease is something uniquely human. And inspiration and appreciation of the microbiological world play a vital role in pushing scientific discoveries. 

Anna points out that microbiology is still a relatively new science. It was only a few hundred years ago that Anton van Leeuwenhoek, a textiles dealer, first saw microbes under his homemade microscopes. Van Leeuwenhoek was not a scientist, he was a textiles dealer used to examining thread counts under magnifying glasses. Yet he was inspired to explore the microscopic world after seeing pictures from Robert Hooke's 1665 book, Micrographia, with its detailed illustrations of textiles in the microscopic world. Van Leeuwenhoek went on to make a number of groundbreaking discoveries in science, and was always guided by his interest and appreciation in what he saw.

“We're at a fascinating time when new technology is available and revealing more about the microbial world,” Anna said. She is also looking forward to exploring our relationship with other infamous bacteria, including artworks based on Staphylococcus aureus, the agent responsible for MRSA. 

I asked Anna what she wanted people to go away from the exhibition with a sense of. 

“To me bacteria have this effect of the sublime. With all the effect they've had on humanity, but the fact that they're fascinating and beautiful too. Ideally I'd like people to come away from the exhibition with a sense of the bacterial sublime, to understand the sea of bacteria they're a part of, and that they're super-organisms containing bacteria. I'd like people to understand that.”

Additional Information

Anna Dumitriu explains more about her artwork and inspiration in this film.

Anna Dumitriu received a Leverhulme Trust Artist in Residence Award in 2011 to work with the Modernising Medical Microbiology project led by the University of Oxford, Nuffield Centre for Clinical Medicine, in conjunction with Public Health England. 'The Romantic Disease' exhibition is funded by the Wellcome Trust. The exhibition will be shown at the Waag Society until 27th July, and the Art Laboratory in Berlin from 26th September - November 2014. 

Links

Anna Dumitriu's website: http://normalflora.co.uk/ 
Modernising Medical Microbiology website: http://modmedmicro.nsms.ox.ac.uk/ 
Waag Society: http://waag.org/en/event/romantic-disease-exhibition 

Further reading

• WHO factsheet on tuberculosis
• Hershkovitz et al. (2008) Detection and Molecular Characterization of 9000-Year-Old Mycobacterium tuberculosis from a Neolithic Settlement in the Eastern Mediterranean. PLOSOne DOI: 10.1371/journal.pone.0003426 
• Rene Jules Dubos & Jean Dubos. The White Plague: Tuberculosis, Man, and Society. Pg 60: Consumption and the Romantic Age
• Chalke, H.D. (1962) The Impact of Tuberculosis on History, Literature and Art. Med Hist. Oct 1962; 6(4): 301–318.
• Warren P. (2006) The evolution of the sanatorium: the first half-century, 1854-1904. Can Bull Med Hist. 2006;23(2):457-76.
• Welsh sanatorium Craig-y-nos – Ann Shaw's blog
• Ann Shaw and Carole Reeves. The children of Craig-y-nos: Life in a Welsh Tuberculosis Sanatorium. London: Wellcome Trust Centre for the History of Medicine at UCL, 2009