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Grave expectations Rumours of a human clone pregnancy spark health fears and horror
IN NOVEMBER the world's first cloned baby could be born, if reports this week are to be believed. But cloning experts are horrified and say that even if the baby is healthy, the mother could be at a high risk of a rare invasive womb cancer.
Once more, Severino Antinori, the maverick Italian fertility expert, is at the centre of a controversy with his colleague Panos Zavos of the Andrology Institute of America in Lexington, Massachusetts. The pair vowed to clone a baby by the end of 2001.
Shock waves reverberated around the world last week at the report that one of Antinori's patients is pregnant with a clone. According to GuifNews, he told a meeting in the United Arab Emirates that "one woman among thousands of infertile couples in the programme is eight weeks pregnant".
Details are scarce, however. Neither Zavos nor Antinori would confirm or deny the news when New Scientist contacted them. But Giancarlo Calzolari, a journalist with Ii Tempo newspaper in Rome and a friend of Antinori's, claims Antinori told him that the news is true and the clone is of an "important, wealthy personality". Calzolari was also told that the cloning procedure was performed in a Muslim country.
Whatever the truth, condemnation came thick and fast in the wake of the news. Most of Antinori's critics warned that cloning is very inefficient only 1 to 6 per cent of cloned embryos survive to birth, and many die soon after, often from malformations.
"I am appalled that these people are attempting to produce cloned humans," says Rudolf Jaenisch, a cloning expert at the Massachusetts Institute of Technology. "All evidence indicates that most clones die early-the lucky ones-and the rare survivors may have serious abnormalities which may become apparent only later."
But amid fears for the clone itself, worries have emerged about the future health of the mother. Richard Gardner, an expert on early mammalian embryo development who chaired Britain's Royal Society's working group on cloning, says that the mother could be at risk from choriocarcinoma, an unusual form of cancer unique to humans.
The cancer develops from the trophoblast, the part of an embryo that invades the womb wall and develops into the placenta. Though the causes are unknown, poorly regulated genes controlling the growth of the placenta seem to be the key.
Animal experiments have shown that these genes remain switched on in cloned embryos when they should be silenced by a chemical masking process called 'imprinting". This means that important genes linked to the development of the placenta could go into overdrive, accelerating its growth and posing high risks to mothers. "The human has the most invasive placenta to start with," says Gardner, a zooloiogist at the University of Oxford. "If placental growth goes awry, there's a greater propensity for this problem to emerge in humans than in other animals." He admits that while the risk is only theoretical, people have paid far too little attention to it, focusing instead on the fate of the clone itself. Barry Hancock, director of a clinic at Weston Park Hospital in Sheffield that specialises in the treatment of trophoblastic cancers, agrees that abnormal imprinting in the genes of cloned human embryos may increase a mother's risk of the disease. 'But it's a theoretical risk," he says.
Whatever the dangers, many people doubt Antinori's claims and want to see some solid proof. 'It's very difficult to know what, if anything, is true," says Harry Griffin, head of communications at the Rostin Institute near Edinburgh where Dolly the sheep was cloned. Andy Coghlan and Emma Young
Cells do their stuff for Parkinson's patient
A MAN with Parkinson's disease seems to have recovered after cells grown from his own neural stem cells were implanted in his brain. If further transplants are equally successful, the technique could rival other cell-based therapies already under investigation.
Parkinson's disease involves damage to cells in the brain that produce the neurotransmitter dopamine. Doctors have long searched for a way to replace the damaged neurons. One option is to use neural cells from aborted fetuses. This alleviates the Parkinson's symptoms in some, but can cause serious side effects such as a worsening tremor. The patient's own neural stem cells-primitive cells that can develop into other types of brain cells-seem like an ideal alternative if they could be grown to produce the right sort of cells.
Now Michel Levesque, a neurosurgeon at Cedars-Sinal Medical Center in Los Angeles, claims his team has done just that. They extracted neural stem cells from the patient's brain and grew the cells in the lab for several months under conditions that favoured the development of neurons that make dopamine. They then implanted the cells back into the patient's brain.
Before the operation, the man's condition had been deteriorating, despite drug treatment. But now, three years after the treatment, the patient has no symptoms, says Levesque, who is also principal investigator at Celmed B!oSciences in Canada. He revealed the work at the annual meeting of the American Association of Neurological Surgeons in Chicago, and is now moving the work into phase 2 trials.
But neurologist Arnold Kriegstein of Columbia University warns that it's too early to be sure the technique works. For instance, the neurons must be the kind that make dopamine, since other forms could cause seizures, he says. Sylvia Paghn Westphat, Boston
HAILED as the "natural" and healthy alternative to hormone replacement therapy, plant oestrogens are also said to help prevent cancer, strokes and bone loss following the menopause. But they could also pose a health risk, as evidence emerges that they act like "gender-bending" pollutants that may increase the risk of cancer.
Many foods, including soya, olives and onions, are rich in plant oestrogens, and extracts rich in these substances are marketed as a tonic for menopause symptoms. Some studies in rats have hinted that they protect women against breast cancer, an idea bolstered by the fact that Japanese women, who eat a lot of soya, have onesixth the Western incidence of breast cancer.
But some experts remain unconvinced of these benefits. "The evidence that plant oestrogens protect against cancer is very circumstantial," says Chris Kirk at the University of Birmingham. Genetic differences make populations difficult to compare, he points out. And people in japan eat much less fat, which is known to contribute to breast cancer.
In fact, far from keeping cancer at bay, Kirk has found evidence that plant oestrogens may actually encourage tumours to grow. He fears they may act in a similar way to pollutants, such as PCBS, insecticides and alkylphenols, which have been widely linked to hormone disruption and reproductive problems in animals. one effect of these pollutants is to block an enzyme involved in oestrogen metabolism called sulphotransferase. In breast cancer cells its activity is abnormally low, but injecting DNA that encodes the enzyme reduces the rate at which cancer cells divide. Kirk says this means these pollutants may contribute to the growth of breast tumours. This week, Kirk told a meeting of the Society for Experimental Biology in Swansea that plant oestrogens behave in exactly the same way. In experiments, his team has shown that some plant oestrogens reduce the activity of sulphotransferase in platelets and liver cells. Richard Sharpe at the Medical Research Council's Human Reproductive Sciences Unit in Edinburgh agrees that this is cause for concern. He fears plant oestrogens could also cause abnormalities during a fetus's development and says women should avoid consuming large amounts while pregnant. "We've got to get away from this idea that 'natural' is necessarily good," he says.
But Herman Adlercreutz of the University of Helsinki wants to see more evidence before we blame plant oestrogens. "Most of this is speculation," he says. James Randerson
Speed freak The Universe was coasting, until somebody hit the gas
SOMETHING in the Universe is speeding up its expansion and pushing the galaxies apart. But it wasn't always that way, according to a group of British physicists. They're suggesting that the accelerator may only have been pressed relatively recently, when the Universe was a few billion years old. If they're right, there's no reason why this mysterious repulsive force, dubbed "dark energy", couldn't change again or even switch off completely-meaning all bets about the future of the Universe are off.
The team, froir the University of Portsmouth and Oxford University, studied a range'oit4iosmological data sets, including -observations of the brightness of distant supernovae-key measurements which first revealed the existence of dark energy in 1998-as well as surveys of the distribution of galaxies and the cosmic background radiation, the dim "afterglow" of the big bang. "If the dark energy changed, it would change the curvature of space-time," says team member Carlo Ungarelli of the University of Portsmouth. "One way this would reveal itself is by changing the height of so-called peaks in the cosmic background radiation."
The researchers report in.. a paper submitted to Monthly Notices of the Royal Astronomical Society that they have found such changes. Their results suggest that the accelerating effect of dark energy kicked in when the Universe was a few billion years old, after most galaxies had formed. "Before this time, there was only gravity decelerating the expansion," says Ungarelli. "Afterwards, dark energy began to drive the acceleration of the Universe."
The team decided to look for such a change simply because nobody knows anything about dark energy, so all possibilities are worth investigating. "Either it has remained constant throughout history or it has changed," says Ungareiii. "One possibility is that it has changed radically, undergoing what physicists call a phase transition." One example of a phase transition is when steam condenses into liquid water. Past a critical threshold, the substance, in this case H20, starts behaving in a completely different way. Similarly, Ungarelli and his colleagues suggest that the Universe might contain a type of unknown matter that underwent a phase transition from a fluid with no gravitational effect into one with repulsive gravity. But the researchers admit they have no idea how or why this change could have happened. "What is missing is a fundamental physical phenomenon which could cause such a phase transition," says Ungarelli. "All we have done is look for evidence in the data for a change in the dark energy. If it holds up, it's up to us theorists to come up with an explanation." The team knows it will need better data to convince the sceptics. "What they are saying would be tremendously important if true," says Max Tegmark of the University of Pennsylvania. But he says that, for now, he's sticking to the idea that dark energy has always been around. Marcus Chown More at: wwwarxivorg/abs/astro-ph/0203383
Nasty neighbours In a warmer world will species survive new predators?
MANY ecosystems face meltdown as global warming gathers pace. A new study suggests that fewer species than expected will become extinct-but they are set for a turbulent time as the ecosystems they live in become unrecognisable. Conventional models of warming assume that most species and ecosystems will migrate gradually towards the poles or up mountainsides. "That is too simplistic," says A. Townsend Peterson of the University of Kansas, who has investigated the likely effects in MexiCO2 a major centre of biological diversity. "The e?fects will be a lot more complicated, and often a lot more drastic."
In reality, complex communities of species with intimate relationships with each other will be blown apart, with highly unpredictable results. Climate change will "bring together new hosts and parasites, new predators and prey", says Peterson. Under such circumstances, the actual changes in temperature could be the least concern for many species. Peterson's conclusions are based on a detailed analysis of what climate change could hold for some 1800 species of birds, mammals and butterflies in Mexico. He has mapped the current geographical range of each by combining records from collections held in natural history museums around the world with software that can identify the species' ecological niches. And he has used simulations of likely climate change to plot where species might end up in 50 years' time.
The result is a lot more complicated than conventional predictions based on climate alone. The greatest disruption to individual species, he says, may come from the "reshuffling" of ecosystems rather than the warming itself.
Take one species, an endemic Mexican bird called the West Mexican chachalaca, which is something like a cross between a turkey and a pheasant and is named after the sound of its loud cry. If climate were all that mattered the bird might expand its range by up to 75 per cent, says Peterson. But in the real world, the bird will probably lose about a quarter of its habitat and be holed up in the foothills of the Sierra Madre del Sur.
The good news is that, while up to a fifth of Mexico's endemic species may lose most of their range, many fewer are likely to become extinct than had been feared. The bad news is that the eco logical changes in many places could be catastrophic. As old ecosystems disappear, new ones with unknown properties will emerge, says Peterson.
In some places in MexiCO2 the 'turnover" of species will exceed 40 per cent, as dozens disappear or are displaced by invaders. This kind of ecological meltdown is likely in the Chihuahua desert and the Baia California penin sula in the north, he says. Mean while, some mountain areas could become "refugee camps" for displaced species.
The findings raise questions about the effectiveness of plans being devised by conservation ists to protect wildlife during climate change by creating nat tiral "corridors" through which animals and plants can migrate as temperatures change. If Peter son is right, then the corridors will be chaotic places full of unexpected perils. Fred Pearce
A Natural mistake? The jury's still out on whether Mexico's wild maize has modified genes
A REPORT saying genetically modified maize is polluting wild maize in a remote part of Mexico is severely flawed, critics say, prompting the journal Nature to retract the article. But the report's authors say their main conclusion has not been disproven.
Ignacio Chapela and David Quist from the University of California at Berkeley wrote the original report last year. In it they said they had found three genes typically used in GM corn in samples of wild corn from the Mexican state of Oaxaca (Nature, vol 414, p 541).
They also concluded that the introduced genes were scattered throughout the wild maize genome. This suggests the genes might be passing from generation to generation, rather than appearing only in firstgeneration hybrids.
But now critics say they're sceptical of both claims, especially the evidence of gene scattering through the genome. They say the results would imply that the genes were jumping around the genome in an unprecedented way, and they take issue with the methods the researchers used to reach their conclusion.
Chapela used a technique called inverse polymerase chain reaction (i-PCR) to pinpoint the modified gene by finding DNA sequences flanking it. But the critics say what they probably found was not a modified gene but a similar, natural chunk of maize DNA.
Quist and Chapela admit there were problems with some of their I-PCR results. But they stand by their finding that GM crop genes jumped into wild plants. They also report new results from a third test, which they say confirms that 1 in 100 kernels of wild corn contains the rogue genes. One critic, however, objects to their methods in this test as well. Kurt Kleiner More at: Nature (DOI: 10.1038/nature738, 739, 740)
No easy answer Trees aren't going to solve the problem of global warming
FORESTS will be less effective at slowing climate change than scientists thought, because they'll mop up less carbon dioxide than expected. That verdict follows a fouryear experiment to see how much CO2 trees will absorb from the atmosphere when pollution has raised levels of the gas.
The results should hammer home the message that the world can't rely on trees to solve the problem of C02 emissions, according to William Schlesinger at Duke University in North Carolina, whose team carried out the work. "It throws doubt on nations such as the US who have carbon sequestration as their only strategy for dealing with the problem," he says.
Global C02 emissions from sources such as car exhausts and industry are predicted to double between now and 2050. More C02 means that trees will grow faster and lock up more carbon. This led some to hope that plants might mop up all the extra gas, says Schiesinger. But earlier experiments to find out how much CO2 plants can absorb have been inconclusive because they took place in sealed environments such as greenhouses. These can't maintain realistic outdoor climate conditions of temperature, humidity and rain.
To find out more, Schlesinger and his colleagues have monitored growth of mature trees in Duke Forest, North Carolina. They staked out six plots of trees with rings of 32 vertical pipes. Each plot is 30 metres in diameter. At three sites, the pipes pump out air enriched with C02 to mimic conditions predicted for 2050; at the other three sites, they pump out normal turn-of-thecentury air. The system monitors C02 levels within the ring and adjusts delivery to maintain the right mix.
The team found that the trees in the 2050 atmosphere converted more carbon dioxide into plant matter, locking up 27 per cent more carbon than at control sites. However, even if this extra growth occurs in existing temperate forests all over the world in 2050, the trees will only absorb 10 per cent of human-generated CO2. "They will soak up carbon, but the study contradicts those who say they will soak up large amounts," says Schlesinger.
"The effect is not as large as people had expected," agrees Peter Cox at Britain's Meteorological Office in Bracknell, Berkshire. He says Schlesinger's results warn us that forests cannot solve the problem of global warming, and emissions need to be reduced. "Eventually you have to deal with the root cause," he says. Will Steffen at the Royal Swedish Academy of Sciences adds that there are still uncertainties as to how much carbon forests can mop up. As CO2 levels rise, the atmosphere will warm, causing more fires in forests and releasing more carbon. The warmer climate could'also speed up breakdown of leaf litter by microbes, releasing yet more CO2 into the atmosphere.
In this week's Nature (vol 416, p 617), Jeffery Richey of the University of Washington in Seattle and his colleagues say the breakdown of leaf litter is already releasing large amounts of carbon in the rivers and wetlands of the Amazon rainforest. This means the forest may be releasing as much C02 as it absorbs, if not more.
On the other hand, woody species might colonise semi-arid areas of land in future because plants can retain water more efficiently in high-CO2 atmospheres. They would then help take CO2 out of the atmosphere. "We really must look at the whole ecosystem," says Steffen. James Randerson More at: Oecologia (DOI 10.1007/sOO442-002-0884-x)
All the World's a Net
ALL researchers dream of making a discovery that will transform their field. Albert-Laszlo Barabasi can go one better. In just three years, his discovery has started making waves in fields as diverse as ecology, molecular biology, computer science and quantum physics. It all began when he found that sites on the Web form a network with unique mathematical properties. In itself, this may not seem very profound, but it soon emerged that these properties were not unique to the Web. We are surrounded by networks: social, sexual and professional. Ecosystems are networks, and even our bodies-and the pathogens that lay us low-are kept alive by networks of chemicals. Barabasi and others have found that many of these networks have the same architecture as the Web. They grow in much the same way and have the same strengths and weaknesses: understand one and you start to understand them all. Universal mathematical laws are rare in biology but, without meaning to, Barabasi seems to have uncovered one.
Born in Romania and educated in Hungary, Barabasi is now a professor of physics at the University of Notre Dame in Indiana. Until a few years ago, he was preoccupied with arcane fields such as the fractal nature of surfaces and the dynamics of granular materials such as sand. To understand all these fields needs a heavy dose of statistics, which is Barabasi's forte. He also had a long interest in complex networks, but information about them was sparse. By 1998, however, the tools for interrogating the Web had reached alevel of sophistication that enabled Barabasi to go exploring.
For theoreticians, the established way to model complex networks is with a random network. Make some dots on-a page and start drawing lines between them at random. You end up with a network in which, on average, all the dots-or "nodes"-have the same number of links. Now count the number of nodes with one link, two links and so on, and plot these numbers on a graph. You end up with a well-known distribution-a bell curve (see Graph below).
This is whlt BarabAsi expected to find when he and his colleagues Reka Albert and Hawoong jeong started studying the Web. They sent a software robot crawling around the Web to analyse the links between websites. But when they looked ai the architecture of the Web and plotted the distribution of sites and the numbers of links to them, something strange happened. "It became clear we were looking at a more complex situation than that described by random networks," Barabasi says.
There was no bell curve. Instead, the Web had lots of sites with a few links, a few sites with a medium number of links and a very few sites with loads of connections. This produced an ever-decreasing curve characteristic of what physicists call a power law (New Scientist, 8 November 1997, p 30). Gone was the average number of links-or scale-of the bell curve. Instead, announced Barabasi, the Web was a "scale-free" network.
"This distribution," says Barabasi, "points to the fact that the Web's structure is dominated by a few, highly connected sites." He calls these sites "hubs"-classic examples are Yahoo and Napster-which have developed because they offer short cuts to the information we want.
A curious property of this architecture is that it takes only a few clicks to get from one site to any other on the Web. 'On average, the journey from one Web page to any other can be made in just 19 clicks,' he says. This shows that the Web is a type of "small world", a concept made popular by John Guare in his play Six Degrees of Separation. In turn, Guare based his work on the idea that a message between any two individuals on the planet would only need to pass through an average of six intermediaries (New Scientist, 4 December 1999, p 24). This small-world property is essential to future growth because it means that as more sites come online, the Web will stay easy to navigate. Even if it grows by 1000 per cent, Barabasi calculates that websites would still be separated by an average of only 21 clicks.
At first, Barabasi thought his scale-free structure was unique to the Web. But he soon discovered the same pattern in other networks, such as the Kevin Bacon game (www.cs.virginia.edu/oracle). Picture all the world's actors as nodes with links between them when they've appeared together in a movie. The aim is to link an actor to Bacon through the smallest number of other actors. Barabgsi found that the actors' network is dominated by a few, usually famous actors, such as Bacon, who appear as hubs because they've made so many films.
Since then, numerous other networks have been added to the list of the scale-free, not least the network of computers that underlies the Web itself-the Internet. In biology, the grids of interacting proteins and chemicals that keep cells in good working order are scale-free. Food webs-the networks of who eats whom in various ecosystems-are built around 'hub species" that eat large numbers of different prey species (New Scientist, 18 August 2001, p 30). And in human society, the network of scientists who've worked together is scale-free, as is the way they cite each other's research. Even the web of human sexual contacts turns out to be scale-free.
So Barabasi's work has begun to expose a pattern of organisation that crops up time and again in natural and artificial worlds. Somehow, the collective actions of individual agents-be they websites or proteinsgenerate networks that conform to a single, well-defined mathematical formula. And every agent iri all tbese systems seems to share the same behaviours.
It didn't take Barabasi and his team long to pin down these shared features. They found two vital ingredients. First, a scalefree network must be growing-so the Web needs new pages to be added every day, and the actors' network needs a constant supply of raw talent. Second, these new recruits must show some form of preference as they attach to the network. So, for example, new websites want to be picked up by popular sites, such as Yahoo, to increase their traffic. And ambitious ac4)rs want to appear in films with established stars, rather than unknown B-movi ' actors. In general, then, the highly connecte*d tend to become even more connected or, if you like, "the rich get richer".
For some scale-free networks, the preferences at work are not clear. It's absurd, for example, to think that prey species choose to be eaten by a predator with a particularly varied diet. Nonetheless, solving this puzzle will undoubtedly improve our understanding of how ecosystems evolve. With proteins, one candidate for this "preference" mechanism is gene duplication-a rare occurrence during cell division when genes are copied twice. Every time this happens, all the proteins that interact with the duplicated protein gain another Ifnk.
Robust yet vulnerable
If the discovery that scale-free networks are everywhere is presenting us with new answers and questions about the world, so too are their properties. These networks are robust and vulnerable at the same time. Barabasi, Albert and jeong subjected a scalefree network to two types of attack. In one, they hit individual nodes at random, while in the other they only took out the hubsthe highly connected nodes in the network.
Random networks are highly susceptible to indiscriminate attacks. As more and more nodes are destroyed, the number of steps needed to get from one node to another increases steadily. By contrast, scale-free networks are robust in the face of such attacks. Even with 5 per cent of the nodes obliterated, the performance of the network is unaffected.
With highly targeted attacks, random networks decay in the same way as with indiscriminate attacks, but scale-free networks fare much worse. Once 5 per cent of the hubs have been removed, the number of steps needed to cross the network doubles. "This shows that scale-free networks, in general, are highly vulnerable to intelligent attack," says Barabasi. It exposes the Internet's Achilles's heel-the hubs. "If hackers wanted to, they could probably bring down the Internet very easily," he adds.
The same vulnerability may also show up in protein networks-with disastrous results. In 1979, p53 was the first gene to be identified as suppressing the development of tumours. To do this, it codes for a protein that controls the activity of a large number of other proteins. "It seems p53 is a hub," says Bert Vogelstein of Johns Hopkins University in Baltimore. "It is one of the few genes whose failure causes such catastrophic results in the cell." In a paper in Nature (vol 408, p 307), Vogelstein, David Lane of the University of Dundee and Arnold Levine from Rockefeller University in New York likened the failure of p53 in a cell-and the development of cancer-to the collapse of a hub on the Web and the subsequent crash. Viewing protein networks as scale-free could help develop more realistic approaches to treatment for cancer, says Vogelstein. But he stresses it's still early days. "We're far away from understanding all the biochemical interactions in a cell," he says.
For any disease, seeing proteins as actors within a larger play will help drug designers to aim their chemicals in such a way that they don't disrupt the whole performance.
Blocking a hub protein, for example, would be very risky because of the large number of potential side effects it could cause, not to mention the possibility of destroying cells. Conversely, there may be times when you want to wipe out cells. Barabasi and his colleagues have shown that the protein network in Helicobacter pylori, the bacterium thought to cause peptic ulcers, is scale-free. Knocking out hub proteins in this bug could be a good way to disable or even kill it.
At the evolutionary level, scale-free networks may have succeeded not only because they are robust in the face of random errors, but also because they allow variation to take place. Proteins with only a few connections could mutate or be lost entirely without damaging the health of the organism. Some of these mutations could give it an advantage, allowing it to outcompete its rivals.
Perhaps the most surprising property of scale-free networks emerged last year and is changing our understanding of the way diseases spread among humans. Once again the story begins with the Net, when Alessandro Vespignani of the International Centre for Theoretical Physics in Trieste and Romualdo Pastor-Satorras of the Technical University of Catatonia in Barcelona decided to look at how computer viruses spread across the Net. According to epidemiologists, a virus must reach a certain level of virulence for an outbreak to occur. Below this "epidemic threshold", the virus is not infectious enough to spread quickly and dies out. The higher above the threshold it is, the faster it will spread. But when Vespingnani charted the movement of his software virus across the Internet, he got a shock. "There is no such threshold for an outbreak to occur," he says. "The hubs propagate viruses so efficiently that even a weak virus will spread rapidly through these nodes." This discovery has profound implications not only for the Net, but also for human disease. "It is a breakthrough in the understanding of a certain class of epidemics," Vespignaiii says (Physical Review Letters, vol 86, p 3200). ,
This discovery gave Fredrik Liljeros, a sociologist at the University of Stockholm, the impetus to look at how human diseases spread. Studies by Vespignani and Barabasi had concluded that the way HIV spreads through populations is similar to the spread of viruses on the Net. So Liljeros chose to look at sexually transmitted diseases.
He and his colleagues studied the sexual habits of 2900 Swedes. It came as no surprise that a few "hubs" had lots more sexual partners than the rest. But Liljeros also recognised this distribution of partners as a mark of a scale-free network. 'Maybe people become more attractive the more partners they get," he says. If so, it looks strangely like the preference mechanism needed to create a scale-free network.
Normally with a new vaccine, public health officials aim for blanket immunisation of at-risk people, setting a target for the percentage to be immunised. That percentage depends on the epidemic threshold of the disease-causing microbe. Liljeros's findings suggest that this approach could have little or no impact. "In diseases such as AIDS, targeting the most promiscuous individuals is the crucial factor," says Liljeros. "We can attempt to stop the spread of a virus by blindly vaccinating huge groups, but without treating these key individuals we may never bring it under control.'
It's common sense that a programme of vaccination against sexually transmitted diseases should try to reach the most promiscuous individuals first. But the idea that health campaigns may be utterly worthless if they miss these people is a shock. For Vespignani, this mixture of the obvious and the unexpected shows the real value of the scale-free revolution. It gives a mathematical form to common-sense concepts-which means theories can be tested and results understood. And it leads to important, nonobvious results. "Nobody would have thought that there is no immunisation threshold in such networks," he says.
We can expect more surprises like this in future. How significant those surprises will be is hard to say: the concept of scale-free networks is only three years old, after all. Yet it's difficult to conceive that a theory which predicts the behaviours of both a collection of inanimate chemicals and a group of thinking humans is not telling us something profound about nature.
The idea has already been jumped upon by AIDS researchers, computer network designers and ecologists. For Barabasi it's this pervasiveness that gives scale-free networks their significance. "It is not that they are creating a revolution in any single field," he says. 'Rather, they prompt us to use the same tools, methods and approach to study very disparate systems.They allow us to see in a new and very similar perspective all the nodes and links around us."
If there is one way that scale-free networks are destined to make their mark, it could be in helping us to understanding emergence: the idea that many interacting agents following simple rules can collectively produce complex behaviours. So thousands of ants can produce a thriving colony that behaves like a single organism.
The challenge facing scientists now is to work out how the rules governing individual agents relate to large-scale behaviours. Scale-free networks give us the beginnings of a mathematical way to study that relationship. They are unlikely to be the whole answer, but they are at least a start. El
David Cohen is a writer based in London
Further reading: Linked by Albert-L6sz[6 Barabisi
Nexus by Mark Buchanan is published in the US
is published in the US this month by Perseus
in May by W. W. Norton. In Britain, it's called Small Worlds and is published in June by Weidenfeld & Nicolson