Category Archives: Science and Technology

HIV+ volunteers are bequeathing their organs to a new project

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MUCH of the medical research conducted on HIV, the virus that causes AIDS, looks at patients’ blood. This is no surprise. Blood is both easy to collect and easy to preserve. But HIV is not confined to the bloodstreams of those infected by it. It is found in almost all of their bodily tissues. In the view of Davey Smith, a virologist at the University of California, San Diego (UCSD), focusing only on the metaphorical “trees” of the blood is therefore a mistake. It misses the “forest” of the other organs.

Inspired by similar programmes in cancer research, Dr Smith therefore set up, in July 2017, a project called “Last Gift”. This seeks HIV-positive volunteers who are terminally ill for some other reason and asks them to bequeath their tissues for cryogenic preservation and subsequent study. So far, five people have signed up, two of whom have died. Dr Smith hopes for 20 more over the next four years.

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The crux of Last Gift’s operation is speed, because HIV’s genes and proteins start to degrade within four hours of a patient’s death. An autopsy team is therefore always on call to attend a volunteer’s deathbed, collect samples from his organs and bring them back to a laboratory at UCSD for cryogenic preservation. The team take specimens of brain, spinal cord, lungs, heart, kidneys, liver, spleen, muscle, bone marrow, adrenal glands, thyroid, lymph nodes, genital-tract tissues, foreskin and intestine.

That HIV can hide in such solid tissues has been known for years. It is a retrovirus, meaning that it integrates its genes into its host’s DNA. Once integrated in this way it can remain dormant indefinitely. The resulting reservoirs are the main barrier to eradicating it from someone’s system. Existing drugs control viral replication, but cannot affect dormant, integrated viral genes. If someone stops taking those drugs it requires only a small leak from one of the reservoirs to bring the infection roaring back. Dormancy, moreover, makes HIV invisible to the immune system. Understanding viral dormancy in solid tissues is thus important.

Even though they have only two sets of tissues to work with at the moment, Dr Smith and his colleagues have already made discoveries. They have, for example, recorded surprisingly high levels of live (as opposed to dormant) virus in the brain, the spleen and the liver. They have also documented disparities in the levels of live virus within and between these organs.

They are especially interested in epigenetic modifications of cells taken from their volunteers’ organs. Such modifications, which serve to regulate the activity of genes, are chemical alterations of a cell’s DNA and of the proteins in which that DNA is packed. The team hope to spot epigenetic patterns that will both give away those cells which are infected and help explain how HIV genes in a cell’s nucleus are activated and deactivated.

Another area of specific concern is how HIV replicates in the gut. Most new particles of the virus are produced in immune-system cells called T-lymphocytes. And most of the human immune system resides in the intestines, where it deals with pathogens ingested by mouth that have not succumbed to the acidity of the stomach. Understanding what is going on in the intestines is thus crucial to understanding the way the infection sustains itself once it has become established.

The need for speed means Last Gift is, at the moment, necessarily confined to volunteers living in, or close to, San Diego. But Dr Smith is hopeful that his method will be replicated elsewhere. His team are already sharing data with researchers at the University of California, San Francisco, who might one day start their own version of the operation. And scientists from three other American universities, and also the National Institutes of Health, have expressed interest in partnerships. That is to be welcomed. Any true cure for HIV infection will involve flushing the virus out of its solid-tissue hidey-holes. Knowing what is really going on in those hidey-holes is therefore essential.

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A rocket that devours itself

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IT TAKES a lot of oomph to launch a satellite into space. Typically, the payload represents only about 5% of the mass of a rocket as it leaves the launch pad. The rocket’s motors account for some of the rest, but the bulk of it consists of the propellants (the fuel and oxidant that react to produce the thrust required to reach orbit) and the gubbins needed to handle these propellants (tanks, pumps, valves, piping and the bodywork that contains them). The gubbins are not only expensive in themselves, but their mass also requires extra fuel to lift. Things would be more efficient if the gubbins could be dispensed with and a rocket designed that consists of only payload, motor and propellants.

This is exactly what those behind what they call the “autophage” rocket hope to achieve. This team, a group of researchers led by Patrick Harkness of Glasgow University, in Britain, and Vitaly Yemets of Oles Honchar Dnipro National University, in Ukraine, is designing a rocket that has a body made of a rigid cylinder of fuel and oxidant. At launch, the engine will sit at the base of this cylinder, but by the time the craft reaches orbit, it will have gobbled its way up towards the top, consuming the rocket’s structure on the way. That will save on launch weight, and thus on fuel. And, as they report in the Journal of Spacecraft and Rockets, Dr Harkness and Dr Yemets have now carried out the first static test-firing of such a rocket’s motor.

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Self-evidently, the design they propose requires both fuel and oxidant to be solid. Solid-fuelled rockets are common in military applications, such as intercontinental ballistic missiles, but are less frequently employed for launching satellites because their thrust is hard to regulate. Like firework rockets (themselves solid-fuelled), once the metaphorical blue touchpaper has been lit, the fuel burns as it will. Liquid-fuelled rockets are preferred as satellite launchers because their thrust can be tuned by changing the flow of propellant to the motor. That makes it easier to position a payload into orbit correctly. But Dr Harkness and Dr Yemets think that their self-consuming design can overcome this difficulty, too.

The fuel for the motor is a hollow cylinder made from polypropylene, a plastic hard and strong enough to form a rocket’s outer casing. The middle of the cylinder is filled with a powdered mixture of ammonium perchlorate and ammonium nitrate, the oxidants. For their test firing, the researchers used a hydraulic ram to drive the cylinder into a preheated engine. Here, it made contact with a specially designed vaporisation surface, heated in order to turn both fuel and oxidants into gases and pierced by holes designed to collect the gases separately and channel them into a combustion chamber, where they mixed and burnt. To start the process, the vaporisation surface had to be warmed to its operating temperature by a gas burner (this would be done electrically in an operational model), but once the system was up and running, vaporisation and combustion became self sustaining. And, by varying the rate at which the propellant tube entered the engine, it was possible to control the amount of thrust developed.

A real rocket would, of course, have no ram to feed in the fuel. But Dr Harkness hopes Newton’s laws of motion will deal with that. Though the prototype under test is not yet powerful enough to make this work properly, the idea is that the acceleration of the motor will push constantly against the inertia of the propellant cylinder, forcing the cylinder against the vaporisation surface and causing it to be consumed. That process, moreover, is capable of regulation by using some sort of throttle to slow the cylinder’s feed-in speed, permitting control of the amount of thrust developed in a way not possible for a normal solid-fuelled rocket, in which the fuel burns in situ.

The autophage design Dr Harkness and Dr Yemets have come up with is not, in truth, likely to worry those who use large liquid-fuelled rockets to launch heavy satellites. The way rockets scale up means that freedom from gubbins is more valuable for small craft than big ones. But a small solid-fuel rocket fitted with an autophage engine might prove an ideal launcher for the growing number of small satellites being sent into space. Dr Harkness thinks such a vehicle could even be designed to launch an individual CubeSat, a type of satellite that has a volume of a litre and a maximum weight of 1.33kg.

At present, most CubeSats are taken up in batches alongside other payloads on big, liquid-fuelled rockets, and even Rocket Lab, a firm that has recently started offering dedicated CubeSat launches, uses liquid propulsion. A solid-fuel rocket would, though, be easier to handle than one full of liquid so, though a working autophage rocket is still several years from production, a launch vehicle that eats its way into space looks an attractive idea.

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Australia’s coral barrier reef keeps dying and coming back

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THE Great Barrier Reef, which runs for 2,300km along the coast of Queensland, is one of the icons of environmentalism. Conservationists constantly worry that human activity, particularly greenhouse-gas-induced global warming, will harm or even destroy it. Such fears are not foolish, but they do reflect a view of the reef’s permanence that is at variance with the truth. For, a mere 10,000 years ago, the coral-covered seabed that now forms the Great Barrier Reef was dry land—a fact lamented in the songs, tales and dances of indigenous people living along the coast, which speak of homelands being drowned by incoming waters.

The reality of the Great Barrier Reef’s existence is that it is a movable feast. Reef-forming corals prefer shallow water so, as the world’s sea levels have yo-yoed during the Ice Ages, the barrier reef has come and gone. The details of this have just been revealed in a paper published in Nature Geoscience by Jody Webster of the University of Sydney and her colleagues. The authors examined cores drilled through the reef in different places. They discovered, as the chart shows, that it has died and then been reborn five times during the past 30,000 years. Two early reefs were destroyed by exposure as sea levels fell. Three more recent ones were overwhelmed by water too deep for them to live in, and also smothered by sediment from the mainland. The current reef is therefore the sixth of the period.

The barrier reef’s ability to resurrect itself is encouraging. But whether it could rise from the dead a sixth time is moot. The threat now is different. It is called bleaching and involves the tiny animals, known as polyps, which are the living part of a reef, ejecting their symbiotic algae. These algae provide much of a polyp’s food, but also generate toxins if the temperature gets too high, in which case the polyp throws them out. That causes the coral to lose its colour.

Polyps can tolerate occasional bleaching, but if it goes on too long, then they die. In the short term, therefore, global warming really does look a serious threat to the reef. It would, no doubt, return if and when the sea temperature dropped again. But when that would be, who knows?

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A history of big-headedness

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“HOW the human got his brain” is probably the most important “Just So” story that Rudyard Kipling never wrote. Kipling did not ignore people in his quirky take on evolution. Two of his tales describe the invention of the alphabet and the invention of letter-writing. But he took for granted the human brains behind these inventions, which are three times the size of those of humanity’s closest living relatives, the great apes, and are thus as characteristic of people as trunks are of elephants or humps are of camels.

This week, though, sees the publication of two studies which, added together, form an important paragraph in the story of the human brain. Both concern a version of a gene called NOTCH2, which has been known for some time to be involved in embryonic development. Both point to an event in the past which changed the activity of this gene in the evolutionary line that leads to modern people. And both are supported by experiments which suggest that the change in question is crucial to the emergence of the big brains which distinguish human beings from all other living animal species.

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The two studies, which were carried out independently, are published in Cell. One was by a team led by David Haussler, a bioinformatician at the University of California, Santa Cruz. The other was directed by Pierre Vanderhaeghen, a developmental biologist at the Free University of Brussels, in Belgium.

Dr Haussler stumbled on his discovery while comparing the development of the brain’s cortex in human beings and in macaques, a type of monkey. He and his colleagues found in humans what appeared to be several previously undiscovered versions of NOTCH2, alongside the established one. The new genes, which they refer to as NOTCH2NLs, were absent from their macaques and—as a search of genetic databases showed—from all other living animals except chimpanzees and gorillas. In these two great apes there were two NOTCH2NL genes, but they seemed to be inactive. The difference between apes and humans is that in the human line one of these NOTCH2NLs has now become active, and has multiplied to create three versions, known as A, B and C.

Crucially, this A, B, C pattern is replicated in the DNA of two extinct species of human, Neanderthals and Denisovans. By looking at minor differences between the various NOTCH-related genes in the three human species and the two great apes, the researchers were able to estimate when the active NOTCH2NL arose: 3m-4m years ago. That is when, according to the fossil record, the craniums of mankind’s ancestors started expanding.

To follow up this discovery Dr Haussler created what are known as organoids (specifically, brainoids), which are in vitro replicas of developing brains, made in this case using mouse cells. He used these to test the effects of adding or deleting his newly discovered genes. In the absence of NOTCH2NL, the organoids developed normally. With it added, stem cells in the organoid which would otherwise have generated new neurons divided instead to create more stem cells. The result, when those stem cells did eventually turn into neurons, was more neurons than normal, and thus a bigger organoid. In effect, NOTCH2NL had generated a larger brain.

Encouraged by this discovery, Dr Haussler and his colleagues performed one further test, with the co-operation of real human beings. These were people with macro- or microcephaly (unusually large or small brains). After testing the DNA of each of these volunteers, the team found that NOTCH2NL, though present in people with larger than average brains, was absent from those whose brains were abnormally small—confirming the suspicion that it is involved in the hypertrophication of human brains.

Cogito ergo sum

Unlike Dr Haussler, who came across his initial result serendipitously, Dr Vanderhaeghen set out from the start to find genes that are unique to people, are directly responsible for creating new brain cells in the cortex, are active and are specifically working to encourage the development of stem cells into neurons. The needle that emerged from this haystack of demands was the same set of NOTCH2NLs that Dr Haussler’s team had lit upon. Seeking confirmation of the genes’ function, Dr Vanderhaeghen introduced them into mouse embryos and found that the number of stem cells in the embryos’ brains was thereby increased. He then repeated the experiment using stem cells taken from human fetuses and got the same results as Dr Haussler’s team had observed in their organoids. Sure enough, NOTCH2NLs encouraged stem cells to proliferate without turning into neurons, increasing the total number of neurons generated.

Taken together, these two studies suggest that NOTCH2NL has played a crucial role in the tale of “How the human got his brain”. They do not, however, answer the question of why this happened. Mutations occur all the time. It is improbable that this was the first occasion in history something like NOTCH2NL has arisen. For NOTCH2NL to have prospered in the way that it did, natural selection would have had to have favoured it. Big brains, in other words, must have been useful in the context in which the mutation occurred.

What that context was is unclear. Though it is hard for human beings to contemplate the idea that big brains could ever be undesirable, small-brained animals do perfectly well without them. And big brains are expensive to maintain. Some calculations suggest humans could not afford them calorifically without the invention of cooking—a process that liberates otherwise indigestible nutrients. Humans now dominate Earth, but that was not true for most of the 3m-4m years since active NOTCH2NL arose and brain hypertrophication began. Until 10,000 years or so ago, when agriculture was adopted, humans were rare.

The ultimate cause of human brain expansion thus remains unknown. Tool-making is one explanation. A more intriguing theory is that human brains are the equivalent of brightly coloured plumage in birds, permitting the sexes to show off to each other what good mates they would make. Yet another idea, the Machiavellian-intelligence hypothesis, is that big brains enable people to manipulate others to their own advantage—a trick that the invention of language would also assist. Nor need manipulation be malevolent. Collaboration is also a form of manipulation.

These ideas are not, of course, mutually exclusive. Any or all of them may be correct. Whether human beings are big-brained enough to decide between them and thus complete the missing “Just So” story remains to be seen.

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Another’s wasted investment is as disturbing as one’s own

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THAT human beings often continue to pour money into bad projects because they have already invested in them and cannot bring themselves to lose that investment is well known. Indeed the sunk-cost fallacy, as this phenomenon is called, is frequently cited as an example of people failing to behave in the “rational” way that classical economics suggests they should.

Though the exact psychological underpinning of the sunk-cost fallacy is debated, it might reasonably be expected to apply only when the person displaying it also made the original investment. However a study published recently in Psychological Science by Christopher Olivola of Carnegie Melon University suggests this is not true. In making decisions, people may also take into account the sunk costs of others.

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Dr Olivola was led into his investigation by a thought experiment of the sort sometimes conducted by physicists. His imagined experimental subject had just received, as a present from a well-intentioned aunt, a gaudy and uncomfortable jumper. He asked himself whether the putative subject would be more likely to wear the jumper if he also knew that his aunt had made significant sacrifices to buy it, and he suspected that the answer would be “yes”.

Having experimented reflectively on himself, he decided to try something like it on other people. He recruited volunteers and posed them similar hypothetical questions, though not involving aunts.

In his first experiment he asked 602 people to imagine that they had obtained a front-row ticket to a basketball game but that a terrible storm on the day of the game meant travelling to watch it would be cold, slow and potentially hazardous. Participants were also told that it was too late to exchange the ticket or to give it to someone else. They were then asked to imagine either that they had obtained the ticket for themselves or that a friend had obtained it, but because of an unexpected work-related trip could not attend and had therefore given it to them. They were also asked to imagine either that they or their friend had obtained the ticket free, or had paid $200 for it. Armed with all this information they were then asked whether they would go to see the game live or stay at home and watch it on television.

As sunk-cost theory predicts, those told they had paid for the ticket themselves opted to attend the match, rather than watch it on TV, more often than those told they had obtained it free. Intriguingly, though, this was also true of those told they had been given the ticket, if they were told as well that the ticket had originally cost money rather than being a freebie. Moreover, similar results obtained in other experiments Dr Olivola conducted, involving imaginary tennis-club memberships, movie-watching and chocolate cake.

Oooo! It’s lovely!

A possible explanation for these results, and also for Dr Olivola’s own intuitive response to the aunt problem, is that social signalling is involved. In all cases the gift was supposed to have come from a close social connection (either a friend or a relative), so part of the act of using it was to show appreciation for its receipt. The costlier the gift, the more appreciation a donor might expect to be demonstrated, which was consistent with what he found.

To double-check the role of social connection, however, he decided to conduct one final round of experiments. In these the putative gift was supposed to have come not from a bosom buddy but rather from a casual acquaintance or a stranger. To his surprise, the effect was often stronger with these people than it was with friends and relatives.

What is going on here is obscure. Perhaps exaggerated gratitude towards acquaintances and strangers is a way of turning them into friends. All told, however, Dr Olivola believes he has demonstrated that the sunk-cost phenomenon shapes human behaviour much more broadly than was previously thought. Yet more evidence, then, that Homo sapiens and Homo economicus are different species.

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How stress echoes down the generations

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THE effects of child abuse can last a lifetime. Neglected or abused children have a higher risk of developing all sorts of ailments as adults, including mental illnesses such as depression but also physical ones like cancer and stroke. In fact, the effects may last even longer. Emerging evidence suggests that the consequences of mistreatment in childhood may persist down the generations, affecting a victim’s children or grand-children, even if they have experienced no abuse themselves.

Exactly how this happens is not well understood. Rigorous experiments on human subjects are difficult. Scientists have therefore turned to rats and mice. But now Larry Feig of Tufts University and his colleagues have shown that psychological stress seems to cause similar changes in the sperm of both mice and men. Their study is published this week in Translational Psychiatry.

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Biologists know that traits are carried down the generations by genes. Genes encode proteins, and proteins make up organisms. That is still true. But it has recently become clear that it is not the whole story. Organisms regulate the activity of their genes throughout their lives, switching different genes on and off as circumstances require. It is possible that such “epigenetic” phenomena can be passed, along with the genes themselves, to an animal’s descendants. They offer a mechanism by which an animal’s life experiences can have effects on its offspring.

Hunting for signs of this, Dr Feig and his colleagues asked 28 male volunteers to complete a questionnaire assessing the severity of any trauma they had experienced as youngsters. They also asked their volunteers to provide sperm samples. They then looked for evidence for a common epigenetic mechanism involving small molecules called micro-RNAs. Their job is to bind to another molecule called messenger RNA, whose task in turn is to ferry information read from a gene to the cellular factories that create the required protein. Micro-RNA renders messenger RNA inactive, reducing the activity of the gene in question—and it can travel in sperm alongside DNA.

Sure enough, upon screening the men’s sperm, the researchers found that concentrations of two types of micro-RNAs, miR-34 and miR-449, were as much as 100 times lower in samples from abused men.

The team then turned to their mice. A standard way to stress mice is to move them to new cages, with new mice, from time to time until they reach adulthood. When the team did this they found that the stressed males had lower levels of miR-34 and miR-449 in their sperm. They mated these males with unstressed females. The resulting embryos also had low levels of the two micro-RNAs. And so in turn did sperm produced by the male offspring of these unions.

Dr Feig and others have shown that the female offspring of stressed male mice tend to be more anxious and less sociable. Furthermore, the sons of stressed fathers themselves produce stressed daughters. The effects of cage-shuffling, in other words, seem to last for at least three generations. The researchers have not demonstrated conclusively that miR-34 and miR-449 are responsible. But their results are suggestive.

To try to nail their case, the researchers plan to carry out a bigger study. This time, they will give questionnaires to their human subjects’ fathers, to tease out whether any epigenetic changes they observe arise from the childhood experiences of the subject or his father. Sisters and daughters may be included in the study, too. That is an ambitious goal. It is also a worthy one. Unless genetic engineering can one day be perfected, changes in genes are hard-wired. But epigenetic effects might be treatable, by boosting levels of particular micro-RNAs in sperm, for example. That could mean the legacy of abuse is no longer passed to future generations.

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A planetary census puts humans in their place

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BILLIONS of years ago a star began to die. In the process, it created something new: 65,500 billion tonnes of carbon that would later be incorporated into the nascent planet Earth. That carbon is still there, and nowadays a fair chunk of it makes up the bodies of living beings. A new study, published this week by Yinon Bar-On and others from the Weizmann Institute of Science, in Israel, provides a comprehensive estimate of how the Earth’s carbon stock is distributed among its inhabitants.

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By estimating the amount of carbon stored in organisms, otherwise known as biomass, the scientists were able to compare the relative abundance of different kinds of Earth’s life, weighing both the microbes beneath the soil and the giraffes walking above it on the same scale. The mammals known as human beings like to imagine themselves the lords of the planet. But in terms of raw biomass, the results—published in Proceedings of the National Academy of Sciences—tell a different story.

No animal comes remotely close to the domination of plants, which account for 80% of the planet’s biomass (see chart). That makes sense: plants convert sunlight into food, and thus lie at the base of almost every food chain. Land plants account for the majority of that total, despite the fact that water covers almost three-quarters of the planet’s surface. Bacteria take second place, with approximately 13%. The remainder is distributed among fungi, archaea, protists, animals and viruses, in that order. Even within the animal count itself, there is little for humans to boast of. There is about as much biomass in one species of Antarctic krill, tiny shrimp-like crustaceans eaten by blue whales, as there is in all 7.6 billion human beings.

But size is not everything. Humans have had a profound impact on the prevalence of other species. Dr Bar-On’s research indicates that over the short span of human history on Earth (specifically after a large period of extinction that began 50,000 years ago) the biomass of wild mammals has decreased to a sixth of its previous value. Meanwhile, the carbon count of domesticated poultry grew to three times higher than that of every species of wild bird combined. Humans and their livestock have come to outweigh all other vertebrates on the planet with the exception of fish. That is not to say fish were spared. The biomass of fish is thought to have decreased by around 100m tonnes during humanity’s tenure. And the dominance of plants, although it is still overwhelming, was far greater before the start of human civilisation. Dr Bar-On suggests that the total biomass of plants has fallen to just half its previous level.

Of course, these numbers are estimates. Dr Bar-On and his team could not individually count each organism they reported. They relied on collating information from hundreds of other studies, public data when they were available, and their own analysis of the likelihood of a certain thing being in a certain place. They were able to be a lot more confident about visible organisms in well-explored ecosystems than they were about microscopic ones in the Earth’s deep subsurface or the ocean’s deep water, such as bacteria.

Future research may therefore change these numbers, possibly dramatically. But Dr Bar-On’s portrait of the planet is an impressive achievement—and a welcome dose of perspective.

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Another way to recycle plastic

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PLASTIC production has tripled over the past 25 years, and the mess it causes has risen commensurately. Recycling is one option. Another is biology, and with that in mind researchers have been hunting for creatures that can digest plastics. Several species of fungi and bacteria can do the job, but only slowly. Now Anja Brandon, a student at Stanford University, and her research supervisor, Craig Criddle, have found that bacteria in the guts of mealworms can break down polymers much more quickly.

Other researchers had already found that mealworms can digest a particular plastic called polystyrene. Ms Brandon and Dr Criddle wondered whether polystyrene was uniquely palatable, or whether the bacteria in the worms’ guts might be able to eat other sorts of plastic, too. To check, they turned to polyethylene, which is both more common than polystyrene and very different in chemical terms. If the worms found it nutritious as well, that would suggest their tastes might be usefully wide-ranging.

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As they describe in Environmental Science & Technology, the researchers divided their worms into groups. Some were given 1.8 grams of either polyethylene or polystyrene. Some were given both. Others had their plastic meals supplemented with wheat bran. (Wheat bran had been found to increase the rate at which mealworms could digest polystyrene). A control group of worms was fed only bran.

More than 90% of the worms survived the 32-day experiment. Those fed only polyethylene found it very agreeable, polishing off 0.87 of their 1.8-gram helping. That was significantly more than the worms eating polystyrene, who managed just 0.57 grams of the stuff. Best of all were the worms that were given bran with their plastic. They chewed through 1.1 grams of polyethylene and 0.98 grams of polystyrene.

Nor were the insects merely chewing up the plastics and then passing them in their faeces. Instead, chemical reactions in their guts were converting them into carbon dioxide. The conversion rate was low at first, but by the end of the experiment the worms fed polyethylene were converting 50% of it into gas and those fed polystyrene were converting 45%.

Ms Brandon and Dr Criddle theorised that the bacterial ecosystems inside the insects’ guts were changing to fit their unusual diets. They dissected the worms at the end of the experiment and compared the gut fauna of those that had been eating plastics with the fauna found in the control group. They found big differences, with several types of bacteria being more common in the guts of mealworms that had been fed plastic.

The researchers argue that not only are mealworms probably capable of digesting a wide range of plastics, but that the protean nature of their gut bacteria should allow them to specialise in a particular sort relatively quickly. A small population of a thousand worms, they reckon, might manage to devour 0.32 grams of polyethylene or 0.28 grams of polystyrene in a day. That is still not lightning fast. But it is quicker than waiting for it to break down in a landfill.

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Germ-free children may be more prone to leukaemia

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THE long struggle to cure acute lymphoblastic leukaemia (ALL), a childhood blood cancer, is a stand-out tale in the history of medicine. It was a massive endeavour, over decades, with many toxic drugs being tested in different combinations on dying children. It succeeded in the end. Half a century ago, survival rates were less than 0.1%. Today they are about 90%. Yet the cure brings unpleasant side effects, including problems with memory and concentration, and sometimes even other cancers. Globally, rates of ALL seem to be rising by about 1% a year. Yet it is almost non-existent in the poorest countries.

Its causes remain unclear and even controversial. A charity called Children with Cancer UK, for instance, still suggests the disease is connected to electromagnetic radiation from power lines. Into this debate comes Mel Greaves, of the Institute of Cancer Research in London. In a paper in Nature Reviews Cancer, Dr Greaves has marshalled decades of research into ALL alongside some new lab work, and created a comprehensive theory about its origins.

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His theory involves three steps. First is a genetic mutation. Then there is an infectious illness. Lastly, the child’s immune system reacts badly to that infection. And this chain of events is more likely in those who had little exposure to germs and bacteria in early childhood.

The first part of Dr Greaves’s theory dates back to 1988. Studies on twins showed that, where both suffered from ALL, the cause could often be traced back to a mutation in just one. Specifically, if they had shared a placenta, then genetic errors in the bone marrow, where blood cells are made, would result in one twin producing mutant cells. Those cells could then spread through the placenta into the other twin, even if his genes were free from the error. Such mutant cells are necessary, but not sufficient, for the later development of ALL.

Bugs are a feature

Lab work by Dr Greaves suggests that the genetic error that produces these pre-leukaemia cells is much more common than ALL itself. When he screened blood from umbilical cords in British hospitals, he found that six babies among 567 had pre-leukaemia cells. But the disease occurs in just 1 in 2,000 British children.

This is where the second and third steps of the theory come in. For those pre-leukaemia cells to develop into a full-blown blood cancer, a child has to be exposed to an infectious disease, and his immune system must then overreact to the threat. And there is substantial, albeit circumstantial, evidence to suggest that the risk of such an overreaction is raised by a lack of exposure to infections and microbes in the first year of a child’s life.

In the 1990s the UK Children’s Cancer Study Group found that babies who had been sent to child care in the first year of their lives were less likely to develop childhood leukaemia. That finding has since been replicated around the world. It is bolstered by a separate and fairly well-established inverse relationship between common diseases in early life and the risk of developing ALL.

More suggestive evidence comes from the fact that childhood leukaemia rates are higher in children born by Caesarean section, which avoids exposing them to microbes in the vagina. Dr Greaves’s theory also offers an explanation for rare but puzzling geographical clusters of ALL. An infection might sweep through a community and pick out the children who are over-reactive carriers of pre-leukaemia cells.

In Milan in 2009, for instance, seven children developed ALL in rapid succession. All had been infected with swine flu three to six months before. None had been to nursery before the age of one. There is no reason to think that one infection is more likely than another to trigger ALL. But flu is common enough that researchers have been able to detect an uptick of ALL a few months after the virus sweeps through a country. Work in mice has proved that early stimulation of their immune systems protects against a murine version of ALL.

That is the evidence. So far, though, the precise mechanism remains mysterious. One candidate is a type of inflammatory molecule known as a cytokine—specifically, one called transforming growth factor-β , which seems to selectively boost the growth of pre-leukaemia cells. It is also known to promote other cancers.

Breastfeeding, which helps to calibrate a baby’s immune system, can help. But if Dr Greaves is right, then another message for parents is to encourage early social contact with other infants, which encourages the swapping of germs.

Dr Greaves is not the first to have such ideas. The theory that modern humans are under-exposed to micro-organisms and parasites is known as the “hygiene hypothesis”. It has been invoked as an explanation for rising rates in the rich world of autoimmune disorders such as type-1 diabetes, multiple sclerosis and allergies. And ALL may not be the only cancer implicated. A malfunctioning immune system can cause chronic inflammation. That has been suggested as a risk factor in the development of oesophageal cancer, colon cancer and some cancers of the pancreas.

The hygiene hypothesis is a striking idea. But it is not yet proved. And even if it were, balancing the risks could be tricky, says Donna Lancaster, a paediatric oncologist at the Royal Marsden NHS Foundation Trust in London. Hygiene has benefits as well as drawbacks. Exposing children to germs means that many will become ill, and a few will become seriously so. One idea for squaring the circle—albeit a very speculative one—is a carefully designed vaccine that gives just the right nudge to an infant’s immune system without the risk of making them properly ill.

If Dr Greaves’s theory stands the test of time then the reputation of the hygiene hypothesis will rise. It even offers a possible explanation for the statistical link between power lines and leukaemia. Parents who fret about their children playing near power lines might keep them indoors—away from dirt, germs and each other.

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Shoemakers bring bespoke footwear to the high street

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AMONG the boutiques in the canal district of Amsterdam is a shoe shop, called W-21, that has a selection of stylish footwear in the window. A select group of customers were recently invited there to have their feet scanned by a laser, and then to spend 30 seconds walking on a modified treadmill in a special pair of shoes stuffed with accelerometers, pressure gauges, thermometers and hygrometers. All this generated a wealth of data, which was displayed on a large screen along with a model of how the walker’s feet were moving.

From these data an algorithm determined the ideal soles for the customer’s shoes. Upstairs, a couple of 3D printers began humming away to make those soles. In about two hours they were ready to be fitted to a new pair of shoes, uniquely tailored to each person’s feet.

Some level of customisation is nothing new for buyers of apparel. But there is a big difference between clothes, which are relatively straightforward to tailor and alter, and shoes,…

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