Communicating science is tough without a common language (Image: lf Börjesson/Maskot/Plainpicture)

THE evening was warm, the beer was cold, and it was time to catch up. It was the last night of a scientific meeting and I spied three friends: Marie-Anne, whose lab is in Paris; Christian, who’s Swiss but works in Nice; and Thomas (also Swiss), based in Vienna. They were speaking French – the shoulder shrugs gave it away – but they are fluent in German too. As I joined them, they switched seamlessly to English. Well, of course: I’m British, so I only have a smattering of appalling French and German. But they also switched because English is the language of science.

It wasn’t always thus. Replay the scene 150 years earlier, and we would all have been able to communicate in the triumvirate of German, French and English, at least. A few centuries earlier, and it would have been Latin.

Michael Gordin’s excellent Scientific Babel asks what drives the languages science uses, and how English came to dominate. As he writes, “scientific languages are not born, they are made, and made with a good deal of effort”. Gordin uses chemistry to guide our tour because this was the key science during the transition to monolingualism. His story is insightful, engaging and based on superb scholarship, lightly worn.

What a lot of trouble language has caused. For example, after Dmitri Mendeleev first published a table in Russian showing the relationships of the then known elements, he realised he needed to tell a wider audience. So he wrote a short summary, translated into German for Zeitschrift fĂŒr Chemie.

Mendeleev discovered that the elements were periodic, but this was translated as stufenweise, or “phased”. It was the repeating feature of periodicity that was Mendeleev’s key insight. Reading the mistranslation, Mendeleev’s rival, Julius Lothar Meyer, who had also noticed the periodicity, thought the use of the word “phased” meant that he could therefore claim the discovery of periodicity. In the best tradition of science, an argument ensued. At its nub was that Mendeleev’s first papers were in Russian, which Meyer could not read. As Gordin says, “to count as a significant language of science, it was not enough
 to be written in, others had to be persuaded to read Ÿ±łÙ”.

It is the tension between mother tongue and a single language that has pulled and pushed at the languages of science. For example, as science uses a language, words diverge from their everyday meanings – take “compound” or “potential”. This divergence drives a positive feedback loop: as a word in language A acquires a scientific meaning, that makes it more likely that that word (still in language A) will be used.

The babel of languages used in science by the late 19th century was a good argument for a “universal, ideally neutral” language, writes Gordin. The first candidate was łŐŽÇ±ôČč±èĂŒ°ì, or “worldspeak”. Then came Esperanto and Ido. These were popular, but crashed with the first world war. Worse followed. Germany’s post-war penalty was severe: exclusion from a globalising science, with many conferences off limits. This led to the inevitable decline of German in science. The second world war accelerated this both by leaching scientists from Nazi Germany, largely to the Anglophone US, and by post-war restructuring.

With German increasingly forced out of the triumvirate, that left French and English. As English overtook German during both world wars, French was squeezed out. And as the “Fe Curtain” (a droll chapter heading) divided Europe, using Russian for science became politically important. Translating Russian into English was vital, so the West could see “what ‘Ivan’ was up to”. This focus on the English of the West versus the Russian of the East only squeezed French still further.

But geopolitics doesn’t entirely account for the hegemony of English. Nor, says Gordin, was there anything innately superior about the language. In fact, there is no one reason for its domination.

Will the dominance of English continue? We may revert from today’s monolingualism (as with Latin) to multiple languages, perhaps a modern triumvirate of Chinese, English and Spanish/Portuguese, as new world orders evolve. Meanwhile, we lucky native English speakers should remember that for everyone else, their scientific working language is no mother to them at all.

“We may revert to a modern triumvirate of Chinese, English and Spanish/Portuguese”

This article appeared in print under the headline “Speaking in one voice”

Our fear of insects has inspired countless horror movies (Image: Universal Pictures/Getty)

None of us is neutral about insects. The strong emotional reactions they provoke have deep roots, says Jeffrey A. Lockwood in The Infested Mind

FEAR + Disgust = Horror. That was the feeling that overcame Jeffrey Lockwood as he was engulfed by a plague of grasshoppers. The rub is that this happened while he was working as an entomologist at the University of Wyoming. What should have been a routine check of his field experiment became a moment when insects wormed their way into his psyche. “The experience of being buried alive by life challenged
 my mental health,” he writes in his latest book, and it catalysed his move into the arts. He now .

In The Infested Mind, Lockwood takes us on a tour of our emotions surrounding insects and on to the wider world of mental health. These emotions aren’t specific to zoological taxonomy, so spiders and other arthropods – animals with external skeletons, segmented bodies and jointed limbs – are all included.

No one is neutral about insects. Most of us are slightly wary of them, a few have a debilitating horror, and a very few have a love for them, one that rarely speaks its name: entomophilia.

“No one is neutral about insects. A few of us have a debilitating horror of them, and a very few love them”

It’s perhaps because most of us aren’t that keen on them that Lockwood’s tour often struggles to engage the reader. The book does nicely clarify that where emotions are concerned, we are “culturally malleable creatures operating within evolutionary constraints”. It points out that negative emotions towards insects are getting more common, at a time in our history when we are probably least exposed to them.

The surrealist painter Salvador Dalí had a terror of grasshoppers, brought on in his boyhood after other children tormented him with them. In his art, grasshoppers became symbols of waste and destruction. Dalí also found ants crawling over his dead pet bat – no wonder surrealism beckoned – and ants came to symbolise mortality and decay.

We know that our emotions are irrational, but this doesn’t help where insects are concerned. Lockwood makes the point well; many people find it repulsive to eat arthropods such as grasshoppers, fed on fresh grass, but pay good money for other arthropods – lobsters – fed on sewage and decay. So why do insects get under our skin so much?

The evolutionary psychology answer is, to use Lockwood’s phrase, “survival of the scaredest”. In our history, those who quickly learned to be cautious about insects had greater evolutionary fitness and this, iterated over millennia, has got us to where we are now. This is why we are predisposed to be afraid of snakes. But none of these fears is very useful in our modern world. As Lockwood says – with a US perspective – it will be a while before we evolve the tendency to fear cars and guns in proportion to their likelihood of killing us.

Lockwood catalogues the central sources of our fears. What we really don’t like about insects is that they can invade, bite and sting us, that they have quick, slithering movements and quickly growing populations, that their bodies seem weird and alien, and that they defy our will and control. Chillingly, he shows how people use their fear of insects to dehumanise enemies. The Nazi leader Heinrich Himmler thought anti-Semitism the same as delousing. During the Rwandan genocide, a Hutu-run radio station referred to ethnic Tutsi as cockroaches that needed to be exterminated. “Bugsplat” is the name some in the US government use for civilians killed by drones.

“Sleep tight, don’t let the bedbugs bite” – remember that saying? You probably weren’t bitten at all, but did begin to have bugs crawling into your mind. That’s just part of being human.

This article appeared in print under the headline “Bugs on the brain”

Life partners: a woman waits to donate a kidney to her husband (Image: Tino Soriano/NGS)

Your compatibility genes make you unique as well as affecting all parts of your life, from your health to your choice in partner, finds Mark Viney

I AM me, and thou art thee. We are all individuals, and our individuality matters.

During the second world war, doctors tried to save severely burned pilots with grafts of donated skin. The grafted skin looked good for a few days, but then withered and died. Studies led by – found that grafts of an individual’s own skin did work, while those of a donor did not.

We now know that the donor skin grafts failed because the recipient’s immune system recognised the grafted skin as foreign and killed it. The same process leads to the rejection of donated organs. But how does our immune system learn what is self and what is foreign?

As explains in The Compatibility Gene, it is all down to specific genes – formally known as the major histocompatibility complex genes.

Although our appearance, lifestyle and career path may make us feel unique, we are actually always one of a group: it is only our compatibility genes that define us as true individuals. Davis provides a well-written and easy-to-read account of the sometimes complicated biology behind the crucial genes that affect our lives so profoundly.

From early on in the evolution of life, individual cells – and later multicellular organisms – developed the ability to recognise that which was the same as them, and that which was different.

Davis recounts how, when we are growing as fetuses, our compatibility genes train the immune system to recognise our own cells and tissues as “self” and so, in healthy people, they know what not to attack. Our cells are identified by the presence of unique surface molecules, coded for by the compatibility genes.

Meanwhile, our immune systems make antibodies. These are randomly generated in a kind of lottery, which means they will be able to attack a great diversity of molecules, especially those of pathogens.

By chance, though, a few of these antibodies will also match the compatibility-gene molecules on our own cells. Leaving such antibodies around would be suicide – literally. To stop this, Darwinian-style selection comes into play within the immune system, eliminating any cells that produce antibodies matching “self”.

In this way, all of our cells are defined by compatibility genes, and our immune systems have been trained to recognise them as self, so that everything else is foreign and, thus, is attacked. All life on the planet – single-celled bacteria, plants and animals – consists of individuals differentiated by a compatibility gene system.

The pilots’ skin grafts failed, therefore, because a successful transplant of any tissue requires matching of donor and recipient compatibility genes. This is not an easy task, as Davis makes clear by a bit of self-study.

He recounts how he gained a measure of his individuality by having his compatibility genes analysed by an organ donation matching service, which immunologically mapped key parts of these genes. Out of 18 million people in an international database of potential organ donors, he is just one of four similar, but not identical, individuals. His wife comes in at one of 185 out of the 18 million – as he says, “not quite the one in a million I always thought she was”.

“Out of a database of 18 million people, Davis is just one of four similar, but not identical, individuals”

But compatibility genes affect many more aspects of our lives than just organ donation, says Davis. They are at work all the time, but their industry is largely silent to us.

Double-edged diversity

Think back to your last winter cold. When you caught it, viruses entered your cells and started to grow. These infected cells signalled the disease to your immune system by putting small pieces of virus on their own surface, attached to one of your compatibility gene products. As Davis explains, “a cell constantly ‘reports’ on its surface samples of all the proteins that it is making”, and the immune system goes looking for anything that is “non-self”. In this way, during that cold your immune system recognised the “infection flag” on those virus-infected cells, killed them, and killed the viruses too.

The sort of compatibility genes you are endowed with has a huge effect on the immune response you made to that infection, and so how ill you got. They define your disease susceptibility, or resistance. You are an individual and your immune response to an infection is individual too.

It is also possible to trace human history in the diversity of compatibility genes. Our African ancestral home has the greatest diversity of compatibility genes on the planet. In Africa, there is a correlation between compatibility gene types and language groups, reflecting how migration and interbreeding have simultaneously affected genetics and linguistics. Humans moved out of Africa, founding new populations from small groups of individuals. The further we are from Africa then, roughly, the less diverse our compatibility genes are because smaller groups of people – and fewer compatibility genes – founded more distant populations.

“In Africa there’s a correlation between compatibility gene types and language groups”

In the modern world, people are more mobile than ever, and many have moved away from their ancestral homes. As a result, most urban Western societies have planet-wide mixtures of compatibility genes, geographically rearranging our diversity. Although there may be a long-term effect on genetic diversity in these areas, it depends on who has a family with whom. But with this modern global shake-up, we have to take note of our compatibility genes – take note of our individuality.

Different compatibility genes cause different responses to vaccination, different disease susceptibility, and different responses to treatment, so recognising compatibility genes will ultimately give better health for all. Such an approach is not politically neutral, with its echoes of racism and segregation, but our compatibility gene individuality cannot be ignored. Although Davis gives an up-to-date account of the science, he steers clear of the wider societal implications that might lie ahead.

Where else might compatibility gene effects be felt? Possibly in that most individual of decisions – the choice of a mate. Davis recounts the flurry of studies, starting in the 1990s, that wondered whether human attractiveness – based on smell – was controlled by compatibility genes. Researchers asked women to rate how attractive they found the odour of T-shirts worn previously – and sweated in – by men. They then looked at whether there was a correlation in women’s responses and the relatedness of compatibility genes between the individual men and women.

The result from the first study was that women preferred the smell of men with compatibility genes dissimilar from their own. This answer was controversial; study and counter-study have followed since, with some finding these effects, others not.

Davis covers human compatibility genes well but a larger nod to compatibility systems in other animals and plants would not have gone amiss. These ubiquitous codes for uniqueness are a good reminder that we are just another species of animal. It is clear that other animals’ compatibility genes are involved in their choice of mate, perhaps to avoid inbreeding.

Humans are so closely related to all other mammals – different physical appearances belying the very close physiological similarity – that analogous effects must occur among us. Indeed, it would be startling if we didn’t use compatibility genes in some way when choosing our mates. Think of that next time you get intimate with the love of your life.

To get vital medicines to children in need throughout Zambia, entrepreneur Simon Berry started taking cues from Coca-Cola

How did you get the idea for ColaLife?
I was working in a remote part of Zambia and I could always get a Coca-Cola but, at the same time, one in five children didn’t make it to their fifth birthday because there weren’t medicines for them. After respiratory disease, the second biggest killer was dehydration – from diarrhoea – which can be stopped with oral rehydration salts (ORS) and zinc. Both are very stable at normal temperatures, as is Coca-Cola, so in principle they can go through the same supply chain.

How did you go from that realisation to a fully fledged business plan?
I put the bare bones of my idea on Facebook. Soon thousands of people were egging us on, so in 2011 my wife and I gave up our day jobs to dedicate a year to get it going. Then, last year, we began a trial with 2500 households.

What was the first thing you did?
We designed the Kit Yamoyo, or “kit of life”. It is a plastic container designed to fit between bottles in drinks crates. Each kit has ORS sachets and zinc tablets. The container is also a water measurer to make the ORS solution, and a cup from which a child can drink the rehydration solution.

How did you come up with the kit design?
We went out and asked people what their problems were in treating diarrhoea. I don’t think anyone had ever done that before; the kits are designed not for poor people, but with them. Some NGOs sit in their ivory towers thinking they are doing good, but how many of them give people the dignity of attention and choice?

Is delivering the kits in drinks crates working?
In the end, hardly any of our kits have been put into crates. Instead, what has worked is copying Coca-Cola’s business techniques: create a desirable product, market it like mad, and put the product in a distribution system at a price so that everyone can make a profit. If there is demand and retailers can make a profit, then they will do anything to meet that demand.

But aren’t the people you are trying to help some of the poorest in the world?
Our kits don’t cost a lot of money: about 60p, or the price of five bananas. People can find the odd bit of cash if they need it. As it is, children get sick and parents have to find money to get them to the health centre, but when they arrive there are often no medicines.

Has the trial saved children’s lives?
We have gone from a standing start – essentially zero use of ORS and zinc – to about 40 per cent of the test population using our kits. We reckon we have saved about 60 lives in six months.

What’s next?
Now we are looking to scale up. There is a lot of interest from the private sector. I think there is huge potential for the ColaLife concept in public health. You could imagine a “tough toddlers kit” containing vitamins, nutritional supplements and deworming tablets. A parent could buy it for their child’s third birthday.

This article appeared in print under the headline “One minute with
 Simon Berry”

Peacocks are the dandies of the bird world, investing a huge amount of energy into growing their elaborate coloured tails. Now we have the first idea of just what a peahen looks for in a peacock’s tail – and for such an icon of evolutionary biology, the answer is surprisingly little.

Peacocks display their large iridescent, shimmering tails to advertise what good mates they will be. Peahens then choose from among competing peacocks, the preferred males father most offspring, and evolution trundles on. A tail can have up to 175 eyespots to try and attract females – but are they paying any attention?

To find out, and colleagues at Duke University in Durham, North Carolina, tracked peahens’ eye movements by fitting them with head cams. The results are discouraging from a male’s point of view.

Even when a peacock’s tail is raised, the peahens ignore him almost two-thirds of the time. When they do look at him, they focus on the bottom edge of the male’s tails, ignoring the vast majority of what is on display.

“This shows just how much effort the males put into getting the females’ attention,” says of the University of St Andrews, UK, who was not involved in the work. “They think they’ve done it with their tails, but no wonder males constantly rustle their tails, because otherwise there would be so little attention.”

What, then, is the point of the rest of the peacock’s tail? “We think the upper portion is used by peahens to locate peacocks in dense vegetation,” says Yorzinski. But once they’re close up, the focus shifts down, she says.

Journal reference:

The Jubilee line is the youngest and smartest of all London Underground lines, but it is mouldier than the much older Central and Bakerloo lines.

, now at the University of Bath, UK, and colleagues collected fungal cells lurking on the platforms at 12 stations across the three lines. They then compared these levels with those in a London hospital and in one of the city’s parks.

People travelling on the Jubilee line – which opened in 1979 and was extended in 1999 – breathe in fractionally more fungal cells than those on the Central line, which opened in 1900. In both cases, it was just over 1 fungal cell per minute. This is twice as much as you would get in the park and, reassuringly, four times as much as in the hospital. On the Bakerloo line, which opened in 1906, people take in 0.75 cells a minute.

Strangely, the Jubilee line had the fewest Penicillium cells – from which penicillin is produced – though it is one of the most common fungal species in the outside air.

Why the differences among the lines? “It’s an open question,” says Henk, but it’s likely to be down temperature, humidity, the influence of other microbes, and how the underground stations are connected to the outside.

Most fungal spores are harmless to healthy people, says Catherine Pashley at the University of Leicester, UK, who was not involved in the work. Many of these will be filtered out by the hairs that line our noses. Any that do get to the lungs will be dealt with by the immune system.

The London Underground is also home to its own species of mosquito, the aptly named , which has evolved to be genetically separate from the species living on the surface.

Journal reference:

It’s often said that in a city, you’re never far from a rat. Today’s in England, Scotland and Wales reveals the extent to which researchers, too, are surrounded by rats and other rodents. In all 4 million animals were used, a 9 per cent increase on 2011. Most of these – 3.3 million – were rodents. Some 2200 primates were used, mainly in pharmaceutical safety tests.

The majority of the rodents – 1.77 million mice – were mutant, “knockout” mice: animals with a specific gene turned off, helping scientists to understand what that gene does. “It’s a bit like trying to understand a car engine without a plan – piece by piece you pull parts out and then see how this contributes to the car not working,” says of the Wellcome Trust Sanger Institute in Cambridge, UK.

Supplying these lab animals is a large and lucrative global industry. Around 100 scientists in North America and Europe are involved in (IKMC) – a group working to knock out each of the 20,000 mouse genes by 2016. The IKMC has been funded to the tune of $150 million by the US National Institutes of Health and the European Union.

“We’re doing this to really understand human biology and disease,” said , one of the leaders of IKMC, which supplies animals to labs at cost price.

“Mice are small and furry – we’re large and not very furry, but inside we are very similar,” says Steve Brown of the UK’s . Despite advances in cell culture, animals remain an important part of research, he says. “If you think of glucose metabolism, this involves the pancreas, liver and muscle, which you can’t replicate in a culture dish.”

Making a knockout mouse

When a researcher wants a mouse with a particular gene turned off, the IKMC suppliers turn to a gene library of embryonic stem cells, each carrying a known mutation. The relevant mutant stem cells are selected, and injected into the embryo of a normal mouse, which is then implanted into a surrogate mouse mother. Her pups are chimeras because they are a mixture of normal and mutant cells. Mice bred from these chimeras eventually end up with one whose germ line is founded from a mutant cell. From these you can breed mice that are made only of mutant cells: knockout mice.

It’s a fairly routine process, but it’s not cheap. A bespoke knockout mouse will cost around $45,000, says Doron Shmerling of near Zurich, Switzerland. Phil Simmons of , St Louis, Missouri, another commercial supplier of knockout animals, estimates that the industry’s annual turnover is $50 million, worldwide. “There’s room for both academic and commercial partners, and in fact we often work together very closely,” he says.

The larger research centres house more than 100,000 mice at any one time. Knockout mice are also kept in frozen storage as sperm or embryos. żìĂš¶ÌÊÓÆ”s can get these frozen stocks to use as they want.

Although individual research teams will have specific experiments in mind for their knockout mice, the idea is that all such mice will also be profiled in a standard way to determine how they are affected by having a gene knocked out.

This is where the (IMPC) comes in. “Each knocked-out mouse is put through a full medical and health screen for up to 16 weeks,” says Adams – well into a mouse’s middle age.

Most knocked-out mice appear normal. “It’s very, very unusual to see any deformities,” says Adams.

Like the IKMC, the IMPC is a major undertaking. It cost $200 million to set up, and another $300-400 million will be needed to analyse all knockout mice, Brown says.

THREE times in the last decade Earth’s spin has missed a beat. These seemingly random blips cause days to temporarily stretch and shrink. They have emerged from the clearest ever view of how long a day is.

Earth’s spin fluctuates as the oceans and the atmosphere push and tug on the planet’s spin But these small daily variations hide longer-term patterns, some well known, some not.

Richard Holme of the University of Liverpool, UK, looked at 50 years of GPS and astronomical data to see how day length varied during that time. The analysis threw up a well-known cycle due to slow changes at the Earth’s core, which lengthen days by a few milliseconds over roughly a decade, then shrink them down again.

There’s also a 5.9-year cycle, due to a persistent wobble between the fluid outer core and surrounding mantle, which changes day length by fractions of milliseconds a year.

When Holme stripped away both of these regular cycles, sudden unexpected jumps in day length emerged from the calculations. Three times in recent years – in 2003, 2004, and 2007 – our planet’s spin has stuttered. The jumps interrupt the longer-term changes by a fraction of a millisecond, and last several months before going back to normal ().

Satellite readings of the planet’s magnetic field over the last 20 years show that the field also undergoes sudden jerks, and Holmes found that they coincide with the jumps in the Earth’s spin. He says the sudden changes probably occur when a patch of molten outer core temporarily sticks to the mantle, causing a step change in angular velocity.

“The planet’s magnetic field also undergoes sudden jerks that coincide with jumps in Earth’s spin”

Jon Mound of the University of Leeds, UK, says we need to rethink the dynamics of the Earth’s core in the light of these findings.

This article appeared in print under the headline “The beat that Earth’s heart skipped”

(Image: Indiana University)

Eternal flames mark only our most important shrines – but nature has them aplenty. This one, burning behind a waterfall veil in Erie county, New York, has now been studied in detail.

Team leader Giuseppe Etiope of the National Institute of Geophysics and Volcanology in Rome, Italy, says he has studied many eternal flames, but never one so beautiful.

The flames can arise in places where natural gas seeps continually from underground rocks. When the flow concentrates into a strong “macroseep” and ignites, the resulting flame need never go out.

The one in Erie County is 20 centimetres tall and burns about a kilogram of gas a day – mostly methane, although it also contains the highest proportions of ethane and propane ever recorded in a natural seep. The chemistry of the gas revealed that its source is a known shale formation about 400 metres down.

Local tectonic events have “naturally fracked” the underlying rocks. The researchers suggest that such sites might present good opportunities for hydrocarbon exploration without resorting to artificial fracking.

Seepage of natural gas has important implications for the atmosphere too. Almost a third of the methane in air comes from natural sources: natural gas seeps and wetlands are the biggest.

Not all eternal flames are what they seem, though. The team investigated a flame in Pennsylvania that proved not natural at all – it is probably an abandoned gas or oil well.

Journal reference:

Making babies isn’t what it once was. Around 1 in 50 children are now conceived through IVF, and 5 million “test tube babies” have been born worldwide since 1978.

The growing numbers of IVF births has prompted some to question whether the procedure leads to any health problems. For example, the IVF embryo transfer procedure is more likely to lead to twin births, which can lead to health problems in babies.

Others wonder whether children born through IVF procedures . The evidence to date has been ambiguous.

Sperm strength

In an effort to resolve the question, a research team including Karl-Gösta Nygren at the Karolinska Institute in Stockholm, Sweden, looked at the health of 2.5 million children born in Sweden between 1982 and 2007, following them for an average of 10 years. Of these children, about 31,000 were born following an IVF procedure.

Some 19,500 of these IVF births followed simple mixing of sperm and egg in a dish, but in 10,500 cases, the sperm were unable to penetrate and fertilise the egg under their own steam, and were instead artificially injected into the egg. For the remaining cases – fewer than 1000 in total – there were no sperm in the prospective fathers’ ejaculate, so the sperm were extracted from their testicles through a surgical procedure before being injected into the egg.

Once they had taken into account the fact that IVF is more likely than natural conception to lead to a risky multiple birth, Nygren and his colleagues found that the 31,000 IVF-born children were at no greater risk of developing autism than the 2.47 million children in the study who were conceived naturally. “This is reassuring,” says Nygren.

Tiny risk

However, they found that the IVF procedures which involved injecting sperm into eggs do increase by 50 per cent the risk of intellectual disability – defined as an IQ lower than 70 together with limitations in adaptive behaviour. The absolute risk of intellectual disability is still tiny though.

This study does not explain why these effects occur. It could be something to do with these IVF procedures themselves – the egg may be damaged by the injection, for instance – or alternatively, it might be related to the fathers’ infertility.

Allan Pacey of the says the study highlights the importance of using standard IVF rather than sperm injection where possible, and also using ejaculated sperm rather than those recovered surgically.

Nevertheless, he recommends that concerned people considering the procedure “should not worry and should discuss any concerns about their treatment plan with the team responsible for their care”.

Journal reference: , vol 310, p 42