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Making Light Stand Still for Quantum Computing
New Scientist 27 Jan 2001

A PULSE of light can be stopped dead, and then sent on its way again at the flick of a switch, say two American research teams. Their achievement takes us a step closer to quantum computers, because it provides a way to pluck quantum information from a beam of light without having to keep individual atoms in a fragile quantum state. Light travels through empty space at 300,000 kilometres per second, or somewhat slower in a dense medium such as glass or water. In 1999, Lene Hau of Harvard University stunned physicists by slowing light to a few metres per second (New Scientist, 20 February 1999, p 10). Now Hau has gone one step further and brought light to a complete standstill in a specially prepared gas of cold sodium atoms. At the same time, a team at the Harvard-Smithsonian Center for Astrophysics has reported achieving similar results in a hot gas of rubidium atoms. According to Ron Walsworth of the Harvard-Smithsonian team, similar techniques could play a key role in future super-fast quantum computers. Such machines will need to transfer quantum information from light beams to atoms for processing. Previous attempts to do this have used light to push individual atoms into an excited state. But these states are so delicate they are liable to be destroyed by background noise. In the latest experiments, when the light stops, the information in its electromagnetic fields is stored in the arrangement of many gas atoms. "We have over 1012 atoms, which makes the state very robust," says David Phillips of the Harvard-Smithsonian team. This means the information can be retrieved with 100 per cent efficiency. The key to stopping light is to nudge the gas atoms into a "dark state" in which their electrons are unable to jump up to higher energy levels. This means-that the atoms cannot absorb light, so when the researchers shine a pulse of light into the gas it interacts with the "spin" of the gas nuclei instead. This is what slows the pulse down. Both groups used a second carefully tuned laser beam, known as the coupling beam, to create a gas in a dark state. The light pulse's speed depends on the intensity of the coupling beam. The dimmer the beam, the slower the pulse travels, and switching off the coupling beam brings the light to a complete stop. The researchers found that they could set the trapped light pulse moving again by restoring the coupling beam. T'he tricky part is switching off the coupling beam without destroying the dark state, says Mikhail Lukin of Harvard-Smithsonian, who led the theoretical work which inspired both experiments. But Hau says her team found that"'you can slam it on and off." Either way, "everybody thought it was pretty wild," says Seth Lloyd, a quantum computing engineer from the Massachusetts Institute of Technology who attended the Physics of Quantum Electronics conference in Utah last week where Lukin presented his experimental results. Engineers like Lloyd would prefer to be able to make their quantum computers out of a solid, rather than a gas. Phil Hemmer of the Air Force Research Laboratory at Hanscom in Massachusetts may have the answer. He has slowed light in a crystal of yttrium silicate, and is about to try stopping it completely using the new technique. "Now they've shown it's possible, the next step is to show it's practical," he says. Their success isn't guaranteed. In a solid, some atoms won't settle into a dark state and could absorb the pulse. Hemmer plans to use a third laser beam to dump the uncooperative atoms out of the way into a different energy level. Eugenie Samuel

More at: Naftire (vol 409, p490), Physical Review Letters (vol 86, p783)

We are all guilty! It's official, people are to blame for global warming New Scientist 27 Jan 2001

CLIMATE scientists from around the world have thrown aside their professional caution and admitted that humans are to blame for global warming. Their conclusions send a tough message to politicians who have reached a deadlock in negotiations on how to combat soaring temperatures and sea levels. This week, scientists met in Shanghai, China, to fine-tune the latest assessment from the UN's Intergovernmental Panel on Climate Change (IPCC). In their final text for policy makers, they toughened their language, saying "most of the warming is attributable to human activities". Drafts circulated last October said simply that human activities "have contributed substantially to the observed warming over the last 50 years". "There was no new science, but the scientists wanted to present a clear and strong message to policy makers," says Tim Higham of the UN Environment Programme. "The scientific consensus should sound alarm bells in every national capital," says Klaus Toepfer, director of UNEP. T'he IPCC's latest assessment of global warming is its first for five years. The report cites global melting as powerful evidence that the world really is warming. Since the 1960s, there has been a 20 per cent decrease in snow cover and a 40 per cent thinning of the Arctic ice cap. The scientists predict sea level will rise by between 9 and 88 centimetres by 2100, endangering millions of people in low-lying areas. The report also wams that temperatures will rise by between 1.4 and 5.8 'C in the 21st century, depending on emissions of greenhouse gases. This prediction is much worse than the 1996 warming estimate of between 1.0 and -3.5 'C. Fred Pearce

More at:

Drying bogs may release years of pollution New Scientist 27 Jan 2001

GLOBAL warming could release thousands of tonnes of toxic pollution trapped in Britain's peat bogs, poisoning rivers and threatening wildlife, say government scientists. Badly contaminated bogs in other parts of Europe, Russia and North America may present just as much of a threat. Over centuries, bogs have soaked up the heavy metals that industry releases into the atmosphere, combining them with organic materials in the peat. The danger now, according to a forthcoming report by the Centre for Ecology and Hydrology in Bangor, Gwynedd, and Windermere, Cumbria, is that climate change will dry out the bogs, letting the metals escape back into the environment. Researchers found levels of lead and cadmium in excess of Dutch and German safety limits, which are lower than those in England, in 7 out of 10 bogs in northern England and Scotland. Nickel levels in 8 bogs and zinc in all 10 exceeded stricter limits which the researchers believe are necessary to protect the environment. Heavy metals can interfere with soil microbes, kill insects, stunt the growth of plants and disable the gills of fish. The report, which Scottish Natural Heritage will publish in the spring, concludes that all of the bogs are likely to be damaged by the contamination. Ed Tipping from the Windermere centre says that the increase in droughts expected this century will oxidise sulphur pollution in the bogs, and as a result sulphuric acid will leach more metals from the peat. "Because of their sensitivity to climate change, bogs may stop storing pollution and start releasing it," he says. Rob Edwards

Adieu Amazon? New Scientist 27 Jan 2001
Clear away the trees, Brazil says it's time to get digging

BRAZIL will lose a quarter of its Amazon rainforest if a gigantic government development scheme goes ahead as planned, an international scientific team warned last week. "The fate of the greatest tropical rainforest on Earth is at stake," they say. Road networks, hydroelectric schemes, gas [email protected] and river channelling projects will be built under a $40 billion programme called Advance Brazil. Its goal is to expand mining, agricultural and timber industries across the Amazon region. "This is a huge scheme," says ecologist Philip Fearnside of INPA, Brazil's National Institute for Amazon Research in Manaus. Its budget dwarfs the $340 million that G7 countries recently allocated to protect Amazonian biodiversity. To gauge the scheme's impact, the researchers created computer models that combined the Advance Brazil plans with the environmental effects of smaller projects in the past. "We modelled impacts such as deforestation, fragmentation and vulnerability to wildfires," says Mark Cochrane from Michigan State University in East Lansing.

They predict that by 2020 deforestation will increase by up to 500,000 hectares per year, while degradation of pristine forest will increase by between 1.53 and 2.37 million hectares per year. Without human developments, scientists think it is likely that the Amazon rainforest will survive the effects of climate change (see p 36). "No serious environmental impact analysis has been attempted at any level," claims William Laurance of the Smithsonian Tropical Research Institute in Balboa, Panama. "Brazil's environmental agencies are now being consulted, but they were excluded from much of the planning process." The scheme will overwhelm existing conservation measures, the researchers say. In the past, it has been almost impossible for the government to control the logging, mining and land speculation that followed the building of new roads. Not all scientists accept that the model is valid, however. "I disagree with some of its most important assumptions," says ecologist Dan Nepstad of the Woods Hole Research Center in Massachusetts, who has modelled the effects of Amazonian wildfires. "We are still a few years away from really mathematically modelling the future of Amazonia. It's too early to predict with scientific rigour the effects of such infrastructural investments".

More at: Science (vol 291, p 439)

The Last of the North Sea Cod New Scientist 27 Jan 2001

EVERY nation has its comfort food. In Britain, it is a large chunk of white fish, battered and fried, with thick fried potatoes and a kind of sauce made of green peas, all wrapped in paper. This cheap, delicious meal-the nearest England gets to a national dish-should most definitely, say connoisseurs, be made of cod. Unfortunately, the latest evidence suggests Britain's favourite fish is, after umpteen wamings, really on the road to oblivion. "The stock is being harvested outside safe biological limits," concludes the latest annual report on North Sea cod (Gadus morhua) by the Copenhagen-based International Council for the Exploration of the Sea (ICES), released last November. Cod in neighbouring waters are in similar straits. Only the northern cod population, fished by Norway, seems healthy-so far. The crash of North Sea stocks has been spectacular. From a high of 277,000 tonnes in 1971, the spawning stock of cod has fallen steadily to 67,000 tonnes a year ago and now to 59,000 according to the latest figures. This is well below the level where the stock can survive continued fishing.

Natural variation may have played a part in the decline, but the major culprit is too much fishing, says Paul Hagel, head of the Netherlands Institute for Fisheries Research in Ijmuiden. This week, EU fishing authorities gave cod some protection by banning catches in spawning grounds from February to April this year. But looming over their crisis meeting in Brussels was the spectre of the Grand Banks of Newfoundland. They have been closed to cod fishing since 1992 (New Scientist, 16 September 1995, p 24), yet the cod have not retumed. Some scientists warn that the same fate awaits the North Sea. Its cod may already be on an irreversible path to extinction. For decades, scientists have calculated how many fish there are in various fisheries, and how many may safely be caught without driving down the spawning stock that will produce the next generation. In the North Sea, ICES does the calculating and recommends limits on the cod catch. Then, every December, the European Union's fisheries ministers decide what limits to impose. Though the ministers are often accused of ignoring scientists' advice, four times in recent years they have actually set stricter limits than ICES recommended. But this year, despite dire wamings, the limits were more lenient. ICES calculated that only a total ban on cod fishing would restore the spawning stock to anything like safe levels. Yet ministers cut the catch by a mere 40 per cent from last year. The decision partly reflects a special difficulty of the North Sea: its mixed fish stocks. A netful of haddock wfll also contain some cod. A total ban on landing cod would mean it would have to be thrown overboard, and simply go to waste, says Hagel. Another real problem, according to Sarah Jones, a British-based representative of the conservation group WWF, is that calculations of the size of stocks is notoriously imprecise. For the past five years, fishing boats have failed to catch their full allowance of cod, and the same goes for five of the nine years from 1987 to 1995. This suggests, says Jones, that even the scientists' recommended catches were too high. And there are other lessons scientists have failed to leam when setting quotas. From 1997 to 1999, ICES overestimated the amount of cod in the North Sea by repeating a mistake made by Canadian fisheries scientists just before the Grand Banks collapsed. ICES wrongly assumed its estimates of fish numbers were too low when it saw that catches were higher than the estimates suggested. But this was because fishermen were concentrating their efforts where the few remaining fish were huddled. It was a serious mistake-the latest episode in what many scientists suspect is a general failure of quotas to protect stocks. Even in 1997, Robin Cook of the govemmentis Marine Laboratory in Aberdeen calculated that North Sea cod had for several years been fished at a level that was likely to force it into a downward spiral and crash. Reserves such as the no-fishing area agreed this week in the EU cod recovery plan are central to conservation strategies, says Dan Pauly of the University of Brifish Columbia in Vancouver. But "fisheries biologists don't think like conservationists", Pauly says, and have rarely set up reserves for commercial fish. "That must change," he says. Other scientists doubt whether this will work. "It n-dght restore the ecosystem in that area, and help other species," says Hagel. "But it will have no effect on fishing." He cites the so-called plaice box, a region along the Dutch and German coasts that has been closed to plaice fishing for a decade. "It has had no positive effect on the plaice at all." Hagel fears that a large fisheries exclusion zone would simply encourage boats to redouble their efforts elsewhere, and could even have a negative effect. But Jeff Hutchings of Dalhousie University in Halifax, Nova Scotia, says introducing reserves to ensure cod are not disturbed during spawning could help. His research, under way now, suggests that the fish have unexpectedly complicated rituals for mate selection. This implies it's important to allow them to reproduce undisturbed, he says. Doug Beveridge of Britain's National Federation of Fishermen's Organisations agrees that it's important to identify the cod's spawning grounds. But there doesn't seem to be much agreement on where they are. The European Commission wants to close an area halfway between Norway and Scotland. Beveridge says a scattering of smaller areas around the North Sea are where the cod are really spawning (see Map). Based on theoretical modelling studies in the North Sea, Pauly says that closing 40 per cent of the sea to fishing maximises both the fish population and profits to fishermen. But this only works if the number of fishing boats is also cut by 40 per cent. And that, says Beveridge, is the real problem: too many boats chasing too few fish. He says the industry knows it has to contract to have any future at all. "But small fisheries businesses cannot convert to something else, or just stop fishing for a while, without financial help." Such transitional support is normal for farmers, but for fishermen it is not even being discussed in Brussels, says Beveridge. Finding the political will to scrap or lay up more than a third of the North Sea fishing fleet, and close a third of its waters to fishing, is made even harder by fears that any subsequent recovery could be a long time coming. Hutchings tracked the recovery of 31 overfished stocks aromd the world of cod and its relatives. "If a spawning stock had fallen 65 per cent or more within 15 years," he says, "it was unlikely to have recovered even after another 15 years of little or no fishing." North Sea cod has fallen 50 per cent in the last 15 years-but nearly 80 per cent since 1971. It may recover within 15 years. But there's every chance it won't. A report by Britain's House of Lords EU Committee last week summed up the situation. The EU, it wrote, must "bring fishing activity down to sustainable levels. This requires a degree of political courage which has so far been lacking." If that will isn't found soon, it warns "the whole fishing industry could disappear". And with it will go Britain's cod and chips. Debora MacKenzie

Mirror Minds Mirror Neurons Alison Votluk New Scientist 27 Jan 2001

A CHILD watches her mother pick up a toy. The child smiles: Mum wants to play. A husband watches his wife pluck car keys from a table. He shivers: she really is leaving this time. A nurse watches a needle being jabbed into an elderly patient. She flinches: it must have hurt. How do these people know what the other person is thinking? How do they judge intentions and feelings, or assign goals or behefs to the other? It sounds simple, but the child could just as easily have decided that Mum was leaving or the husband that his wife wanted to play. Yet they didn't. They knew. "Reading" the minds of others is something we take for granted. Yet philosophers, psychologists and neuroscientists ahke have been baffled by our ability to anticipate other people's behaviour and empathise with their feelings. Now a team of Italian neurophysiologists may have stumbled on the key to this mystery. Vittorio Gallese, Giacomo Rizzolatti and their colleagues at the University of Parma have identified an entirely new class of neurons. These neurons are active when their owners perform a certain task, and in this respect are wholly unremarkable. But, more interestingly, the same neurons 'fire when their owner watches someone else perform that same task. The team has dubbed the novel nerve cells "mirror" umns, because they seem to be firing in sympathy, reflecting or perhaps simulating the actions of others. Many neuroscientists are starting to think that in higher primates, including humans, these neurons play a pivotal role in understanding the intentions of others. "Mirror neurons may be one important part of the mosaic that explains our social abilities," says Gallese. Vilayanur Ramachandran of the University of Cahfomia at San Diego goes further. He believes that mirror neurons will answer important questions about human evolution, language and culture-and may take us to the heart of what it means to be human. "I predict that mirror neurons will do for psychology what DNA did for biology," he says. "They will provide a unifying framework and help explain a host of mental abilities that have hitherto remained mysterious." Gailese and his colleagues didn't set out to find anything so radical when, in the early 1990s, they started recording the activity of neurons in a macaque's brain. They were tapping into the signals emitted from nerve cells in a part of the monkey's brain known as F5. This is part of a larger region called the premotor cortex, whose activity is linked to planning and making movements. Some years earlier, the same researchers had discovered that neurons in F5 fired when an animal performed certain goal-oriented motor tasks using its hands or mouth, such as picking things up, holding or biting them. They wanted to learn more about F5 neurons-how they responded to different objects with different shapes and sizes, for example. So they presented monkeys with things like raisins, slices of apple, paper clips, cubes and spheres. It wasn't long before they noficed something odd. As the monkey watched the experimenter's hand pick up the object and bring it close, a group of the F5 neurons leaped into action. But when the monkey looked at the same object lying on the tray, nothing happened. When it picked up the object, the same neurons fired again. Clearly their job wasn't just to recoose a parficular object.

All fired up

The neurons turned out to be quite fussy about what they reacted to. Those that responded to an experimenter plucking a raisin from a tray, for instance, failed to react when the experimenter dug the same raisin out of a small well with his finger. Some neurons fired when the experimenter held a few slices of apple, but not when he placed the apples on the tray-other neurons fired for that. Most importantly, the very same action that made a neuron fire when a monkey performed it would ahnost always make that neuron fire if the monkey saw the experimenter doing the same thing. It soon became clear that the motor system in the brain is not lin-dted to controlling movements. In some way it is also reading the actions of others. in 1998, Gallese gave a talk about mirror neurons at a meeting on the "Science of Consciousness" in Tucson, Arizona. Alvin Goldman, a philosopher from the University of Arizona, listened with interest. Afterwards, he approached Gallese and they spoke about the potential of these cells for reading the minds of others. "He wasn't familiar with the mind-reading literature in philosophy," says Goldman. Mind-reading, or theory of mind, is an ability that all healthy humans possess. We are particularly good at representing the specific mental states of others. These can be basic, such as seeing someone crying and understanding that they are sad, or realising that when someone is yelling and gesticulating wildly at you they may be angry and might even mean to harm you. But we intuitively understand more complex mental states too. When a mother loses a baby, other parents get lumps in their throats. When you hear that a colleague has been cheating on their spouse, you share the hurt and shame. A debate rages over whether other primates, such as chimps, can understand other minds, even in the simplest ways. And even in humans, while almost everybody agrees that some measure of n-tindreading goes on, there is little agreement on how it happens. One theory, sometimes calliZd "theory theory", holds that people build up common-sense hypotheses to explain why other people do what they do. Like physicists using rules and laws to explain observable phenomena, we all use our experiences to develop a set of explanatory laws for others' behaviour Another dominant theory, championed mainly by philosophers like Goldman, is known as simulation theory. It's based on the idea that people understand what is going through the minds of others by mentally mimicking what the other is thinking, feeling or doing-in essence, putting themselves in the other's shoes. The discovery of mirror neurons backs up this theory nicely. As the suspicion grew that these neurons might have something to do with the complexities of mind-reading, the bun-dng question became whether human brains had mirror neurons too. But finding out wasn't easy-humans aren't keen on having electrodes implanted into their brains, even for the lofty purposes of science. Luciano Fadiga, now at the University of Ferrara in Italy, was the first to find some evidence that humans may have a system analogous to that found in monkey brains, when he measured the excitability of particular muscles in the hand. He found that when the volunteers were watching grasping actions, the very muscles that would be needed to copy that movement seemed primed to act-as if they were preparing to make the same movement themselves. ,The interesting thing was that the pattem of activated muscles changed according to the observed actions," says Fadiga. But while this suggested that a mirror system n-dght exist in human brains too, it didn't yield any information about where it might reside Several brain-imaging studies followed, the first led by Rizzolatti, and another by Scott Grafton, then at the University of Southern Califon-da in Los Angeles. Both found that watching an experimenter pick up and handle objects activates two regions of the brain behind the temples on the left side: the superior temporal sulcus and, just above it, a part called Broca's area. An even more recent study by Marco Iacoboni at the Los Angeles School of Medicine confirmed that Broca's area was active while volunteers either watched images of someone drumming their fingers, and when they also tried to imitate the movement they saw (Science, vol 286, p 2526).

Finding the words

The finding that Broca's area was activated was doubly intriguing. For one thing, F5 in monkeys is considered an analogue for Broca's area in humans. But even more suggestive was the fact that, while F5 is associated mainly with hand movement, Broca's area is traditionally thought of as a speech-production area. This raised questions about what a mirroring system might have to do with language-and language with mind-reading. Rizzolatti and Arbib think that mirror neurons may have provided the bridge from "doing" to 'communicating". The relationship between actor and observer may have developed into one involving the sending and receiving of a message. In all communication the sender and receiver have to have a common understanding about what's passing between them. Could mirror neurons explain how this is achieved? Rizzolatti and Arbib think the answer is yes. They suggest that it is probably no coincidence that the area which links action recognition and action production in the monkey brain is exactly the same area that in humans has been linked to speech production. They think that the development of human speech was made possible by the fact that F5, the precursor of Broca's area, was endowed with this mirroring mechanism for recognising actions made by others. This, they say, was a prerequisite for the development of conununication and ultimately of speech. It made us 'language-ready", says Arbib. Most of the time, a strong spinal cord inhibition prevents you from involving your own motor neurons in activity you are merely observing, according to work by Fadiga soon to be published in the European Journal ofneuroscience. But sometimes the premotor cortex allows a brief snippet of the movement-like the twitchy feeling you get when you're watching someone struggling to open a packet of crisps or untie a knot. This slight movement, says Arbib, tips off the person carrying out the action that the watcher knows what's going on, in a sort of primitive dialogue. "This dialogue forms the core of language," he says. "Perhaps we evolved some crude form of communication based in sign, then built speech," says Arbib. Imagine an early human chipping away at a stone, he says, and that this person wants to communicate something else while demonstrating this skill. Or perhaps he wants to communicate in the dark or at a distance. In both cases, using sign or gestures doesn't work so well. If the brain could allow the person to develop speech through the same neural apparatus earlier primates were already using to communicate manually or through lipsmacks, so much the better (New Scientist, 8 April 2000, p 30).

The exciting news is that mirror neurons may not be limited to these motor regions. Gallese, for one, suspects that they are found in other areas. "My behef is that this may apply also to other modalities, for instance sensory modalities," he says. Gallese points to recent work by William Hutchison, a physiologist at the University of Toronto. He and his colleagues studied humans who were conscious while undergoing brain surgery. They discovered neurons in the anterior cingulate cortex, a region thought to be involved in perceiving pain, which fired both in response to a finger being pricked and also when patients saw the experimenter prick himself (New Scientist, 8 May 1999, p 17). Gallese sees this as tantalising, preliminary evidence of a far-reaching neural mechanism. Could this explain how we are able to "feel" what others feel? Could it underpin the sensations behind empathy? Ramachandran also believes that mirror neurons play a bigger role than is generally appreciated. He thinks these exciting nerve cells don't just provide a missing link between gesture and language, but they go a great way towards explaining human learning, ingenuity, and culture in general. "Their emergence and further development in hominids was a decisive step," he says. He says mirror neurons and the way they facilitate imitative teaming help to explain why we only developed things like tool use, art and mathematics about 40,000 years ago, despite the fact that our brains had reached their full size some 150,000 years earher. These cultural inventions, he contends, probably popped up accidentally, but they were disseminated quickly because of our amazing, imitative, teaming brains-made possible by a more sophisticated version of the monkey mirror neuron system. He admits that mirror neurons probably aren't the whole story-necessary, but perhaps not sufficient-but insists they could be a big part of it. Language, imitative learning and mind-reading, seemingly unrelated human developments, may all be shown to be linked through these intriguing nerve cells. "These are all human qualities. All mysterious qualities," he says. "Mirror neurons may provide the key."

'Mirror neurons and the simulauon theory of mindreading' by Vittorio Gallese and Ajvin Goldman, in Trends in Cognitive Science. vol 2, p 493 (1998) 'Language within our grasp by Glacomo Rizzolatd and Michael Arbib, In Trends In Neurosiences vol 21, p 188 (1998)

Ice Age Amazon New Scientist 27 Jan 2001

ONCE it was a lush green forest, but now it stretches out, yellow and bare, an endless savannah. Only a few clumps of trees remain as a sad reminder of what the Amazon rainforest used to be. No, this isn't a pessimist's view of the future. It's how a long-held theory describes what happened to the region during the ice ages. And it's a theory that's been widely accepted for decades, simply because it explains one of the greatest mysteries of ecology: why the tropical forests are so amazingly diverse. According to this theory, every time the world is plunged into an ice age, the tropics take a beating. Cold air from the poles alters the pattems of the prevailing winds and sucks all the moisture out of the equatorial region. The tropical forests die back, and the parrots and the monkeys run screeching for the few trees that remain. That creates isolated refuges where plants and animals evolve away from their fellows. When the forest eventually grows back, it is full of new species-creating the diverse Amazon rainforest that we know today. It's a simple, compelling explanation. No wonder ecologists have put all their faith in it. The problem is, it's probably wrong. For decades, one man has been digging holes in the jungle to find ancient pollen and test the theory. He concludes that the Amazon region has been trees, trees and more trees as far back as he can see. No grasslands, no savannah. Just forest. Now at last the world is starting to listen to his message. It leaves researchers hunting for a different explanation for tropical diversity It also implies that the rainforest is a lot more resistant to climate change than anyone ever imagined. The Amazon rainforest is the most biologically diverse place on Earth. Around 80,000 different kinds of plants and 30 million species of animal live there. And back in 1969, German geologist Jijrgen Hatter suggested his idea of ice age dieback and islands of forest to explain this extraordinary abundance. At the time, the theory fitted nicely with studies showing that Africa appeared to have dried out during the last ice age. But the evidence of drought in the Amazon wasn't nearly so clear-cut. Paul Colinvaux, a palaeoecologist based at the Marine Biological Laboratory in Woods Hole, Massachusetts, decided to test the theory, so he picked up his drilling equipment and headed for the rainforest. Colinvaux's idea was simple. If he could find a spot in the Amazon where soil had been laid down over the n-dllennia, he could drill a core and see whether it contained pollen from grass or trees. If there was a drop in tree pollen and a large rise in pollen from grass that coincided with an ice age Haffer's theory would be proved true. The hard part was finding the soil. Most of the forest floor is a deep mass of overlapping tree roots, while threading through the Amazon basin is a vast network of rivers which have washed away most of the fresh soil. Much of the rest is weathered into hard red clay that is devoid of pollen. Colinvaux needed a lake that had been around for hundreds of thousands of years, where sediments and pollen grains could have settled undisturbed onto its floor. Lake Patai on a hill lying 300 metres above the jungles of northwestem Brazil looked promising. Rain washes debris into Lake Pata almost constantly and water then seeps out through pores in the rock. There is no outgoing river to flush away the soil, and the hill is made of hard rock, suggesting the lake has been there for some time. The only trouble was getting there. "You take a river boat as far as the river boats will go, which is about three days," says Mark Bush, an ecologist from the Florida Institute of Technology and one of Colinvaux's companions on the 1990 trek to Pata. "Then you go into a bus and you drive as far as the bus can drive, which is about another half a day. And then you get into a small canoe, and you paddle up as far as you can take a canoe. And then you get dumped out and you're left standing at the bottom of this huge hill with no trails up it." It took Colinvaux and his team three days just to get their equipment to the top of the hill. The forest floor was a slippery path of tree roots with potholes a metre deep. Not to mention the mosquitoes. "We were up there for about two weeks. It was miserable," says Bush. But it was worth it. The researchers bagged a core 6.5 metres long, and carbon dating showed that the first metre alone held 30,000 years of history, going right into the heart of the last ice age. Cofinvaux and his colleagues spent painstaking months picking through the mud for pollen grains, sorting them into some 450 different families. What they found made the refuge hypothesis look very shaky. Throughout the core, there was plenty of evidence of trees and no increase in the amount of grass pollen. And, says Colinvaux, since wind-blown pollen can travel a long way, his sediment didn't just represent the vegetafion of the hifl. "There are places on that climb where you can see the forest stretching out before you until it disappears into the haze of the horizon,' says Colinvaux. "Now if any of that within view had been savannah, I'll bet anything we would have seen it in our record." T'he results, published in Science in 1996, put a dent in the refuge hypothesis, but they didn't disprove it. It was just possible that by some extraordinary coincidence Lake Pata might have been smack in the middle of a refuge. Trees could have remained there while the rest of the forest shrank. So Colinvaux set out for another lake, 1500 kilometres from the first. The logistics for this trip were even worse, with a helicopter needed to get in, no landing site closer than a three-day machete-hack through the jungle, and malaria running rampant in the nearest village. But Colinvaux eventually bagged another core. Again, he found nothing but trees going back more than 30,000 years. The results have yet to be published, but from his conference talks Colinvaux ah-eady knows what the critics wifl say: "Wow, how odd. You've found another refuge.' "It's ridiculous," he says. "They move the refuge boundaries after our work." Areas that were once charted as savannah under the refuge theory are simply re-inked green to represent forest, he says. But he's got yet another, more convincing piece of evidence from the ultimate drainage site of the forest: the sea floor at the mouth of the Amazon. In 1994, the Ocean Drilling Program sent a ship to sink a drill into sediment some 400 kilometres from the river mouth. One core they pulled up was more than 35 metres long, and held sedi-inent more than 50,000 years old. But again it revealed no increase in grass pollen-just more trees. Says Colinvaux, "even if this is only draining the lowland basin, that's exactly where the refugists said there was most likely to be savannah. So just how far back did the forest exist? At first, Colinvaux couldn't tell. He had five more metres of mud from the bottom of Lake Pata, but he couldn't date it with radiocarbon since that's only effective to about 50,000 years ago. Then Bush noticed something strange about the core. Chemical analysis of the deep mud had revealed that its concentration of potassium varied in a complex and peculiar zigzag pattern. After years of puzzling over it, Bush finally realised that this zigzag was marking out a well-known pattem of climate change. The more recent ice ages and many other major changes in the Earth's climate are generally attributed to wobbles in the Earth's orbit around the Sun. This complicated celestial ballet adds up to a wiggly line known as the Milankovitch cycle, which describes the amount of sunlight reaching the Earth at various latitudes over time. Bush spotted that the Amazonian potassium data followed the Milankovitch cycle for the equator. Why should potassium levels act as a climate marker? The answer, says Bush, appears to lie in algae. Lake Pata is generally black with dissolved organics, and light can only penetrate a few cenfimetres into the water. When the water is deep that stops any life from growing, since it needs both nutrients from the bottom of the lake and light from the top. But when the lake levels are low enough, both light and food come together and the water turns pea green with algae. Bush believes that the algae take up potassium from the water, and that this is preserved in the sediment when the algae die. "It's a peculiarity of this particular system, it isn't universal," says Colinvaux. "We were lucky." Since the Milankovitch cycle is so well documented, the correlation means the researchers can date the sediments from their entire core. It tums out that it goes back 170,000 years-long enough to see into a previous ice age. "We've spotted samples from all the way down the core, and it's all forested," says Bush. "You will not find savannah interludes in it. I'll go to the bank on that one." For Colinvaux, that clinches it. The refuge theory is dead. Others have yet to be persuaded. Colin Pendry, a botanist from the Royal Botanical Garden in Edinburgh, is sceptical about the pollen data. "Palynology is a bit of a blunt tool," he says, pointing out that trees can't be identified at the species level. And even two good sites hardly constitute an extensive look at an area the size of the continental US. "Paul would make out that everything's sewn up and he's got it right," says Pendry. "But everything is still very much up in the air." Even so, Pendry, along with some of Colinvaux's other crifics, is beginning to doubt that the Amazon basin dried up into grassland. "The pendulum has really swung against the refuge theory," he says. This group is taking a middle road, believing that the rainforest became a seasonally dry forest full of legumes like the Brazil tree. The most serious objection to Colinvaux's conclusions comes from an earlier study of an area called Carajis in the north Brazilian plateau. In 1991, Maria Lucia Absy and her colleagues found a strong grass pollen signal there from 24,000 to 11,000 years ago, a period that covers the height of the last ice age. But Colinvaux dismisses the idea that this was an area of savannah between refuges. The grass pollen, he claims, is consistent with the marshy plant life that lives on that high, relafively dry plateau even today. Generally, it seems, the tide is starting to turn against the refuge theory. "I really don't think that is too much in vogue now," says Joel Cracraft, an omithologist at the American Museum of Natural History in New York, who has written several books about biodiversity in the Amazon. As far as he's concerned, shifts in river location could very well explain the clumping of animal and plant species in the jungle. Though it isn't obvious, he says, a river can be a pretty big barrier, even to a bird. In the end, Colinvaux finds himself coming back to the theory that was pretty much accepted before Haffer came along-that the Amazon is a generally pleasant place to live, so species just don't die out. Given time, he thinks, the jungle simply accumulates new species. Does this mean that any future climate change will leave the rainforest intact? Though researchers are still figuring out the details of tropical climate during the ice ages, it seems that the forest survived temperature drops of around 5 'C, and a serious reduction in rainfall (see "Cold and dry"). Surely, then, with this degree of adaptability, it should be nice and cosy if things get just a little warmer. "It can take a hell of a lot," agrees Colinvaux. "I think the Amazon will almost certainly survive any warming we throw at it-as long as we don't chop it down." But, he wams, that might be the wrong way to think about things. The ice ages aren't really difficult or unusual times. The planet has spent about four-fifths of the past million years in a deep freeze, making that the normal state of affairs. "The awful time is now," he says. "Nature took a normal glacial period and heated it up and made it horrible. And global warming will just make it worse." Just because the Amazon can handle the cold doesn't mean it will be able to take the heat. "It may be close to its limit, we just don't know."

Unfit for humans New Scientist 2nd Dec 2000

Corn has been contaminated with a potentially harmful protein

A PESTICIDE gene only approved for use in maize for animal feed may have jumped into a com variety destined for people. The discovery comes just two months after StarLink corn, which was engineered to contain the gene, turned up in foods such as taco shells, sparking a recall of about 800 different products in the US. The gene's product, Cry9C, makes maize more resistant to the European com borer. Because of concems that the protein might cause an allergic reaction in humans, StarLink can only be fed to animals. But Aventis CropScience, which developed StarLink, has now found traces in another variety "Aventis CropScience does not know how Cry9C protein came to be present in a variety other than StarLink brand seeds," the company says in a press release. Aventis found the protein in maize produced by Garst Seed of Slater, Iowa. Garst also pro- duces StarLink corn for Aventis, but it isn't supposed to use Cry9C in any other variety. Jeff Lacina, a spokesman for Garst Seed, says his company discovered traces of Cry9C in a seed sample from 1998. The company doesn't yet know how much of the maize was pro- duced, he says, or where it was sold. "First, we have to see which lots were affected. Then we have to track [them] through the system," Lacina says. It's not clear if the sample was simply contaminated with seeds of StarLink corn, or if the gene for Cry9C has actually jumped into the other corn variety. Earlier this year, a GM sugar beet being developed by Aventis in Europe accidentally gained resistance to two kinds of herbicide when one variety pollinated another in a seed company's greenhouse (New Scientist, 21 October, p 6). Kurt Kleiner

Generation game New Scientist 2nd Dec 2000

FOCUS If gene therapy in the womb could cure common diseases, what's the problem?

'The earlier you put genes into a fetus, the more likely they are to reach developing eggs or sperm causing "germline" changes'

GENE therapy has proved one of medical research's greatest disappointments. Not only has it failed to make many people bet- ter, it's made a significant number worse. And following the exposure of activities at the University of Pennsylvania, we now know that unethical use of gene therapy has killed at least one patient. But researchers haven't given up hope of finding ways to treat inherited diseases. "We were frustrated that not much was happening, that it was short-term, and that even if we succeeded we would not be able to reverse the disease," says Charles Coutelle, a leading researcher in gene ther- apy at London's Imperial College School of Medicine. So Coutelle, and a handful of groups in the US, are pinning their hopes on using gene therapy to treat some- one before they're born. This was a hot topic among delegates to the Millennium Festival of Medicine in London last month. Treating the baby in the womb has sev- eral advantages. First, because it's small there's a better chance of getting the genes to all the cells that need to be corrected. Going in early, before the immune system is fully developed, also avoids an immune reaction to the products of the introduced genes, and the systems that deliver them. And finally, in utero therapy for disorders such as cystic fibrosis would prevent them causing lasting damage. Animal tests are already showing success. In a recent trial, Coutelle and his colleagues used non-infective virus-like particles to carry the gene for the human blood clotting agent factor IX into sheep embryos. The added genes produce the protein for as long as they remain in the animals' cells, but they are not incorpo- rated into the cells' DNA. When the lambs were born, their levels of human factor IX were 80 per cent of the normal human level-which in people would be enough to keep haemophilia at bay. The lambs only made factor IX for around 40 days after birth, highlighting a problem with any form of gene therapy that doesn't integrate the introduced genes into the patient's own DNA. Eventually, Coutelle and his team are hoping to find ways of doing this, allowing fetal gene therapy to introduce genes that will remain active for life. Coutelle says that his therapy could eventually be simple and safe enough to treat genetic risk factors for even common conditions such as raised cholesterol. "You could treat it with a single shot during pregnancy." Already, Janet Larson from the Ochsner Medical Foundation in New Orleans and her colleagues have used gene therapy on unborn mice carrying the genes for cystic fibrosis. The treatment com- pletely and permanently prevented the disease appearing in the animals. It's a rosy vision, but there's a problem.

The earlier you put genes into a fetus or an embryo, the better the chances that they get where they are supposed to go. But this also makes it more likely that the DNA will reach developing eggs or sperm, introduc- ing "germline" changes-genes that will be passed on to future generations. Because of this risk, gene therapy on fetuses is effectively banned in Britain. "With in utero gene therapy, you are dealing with a much smaller target," says Norman Nevin, chair of the govermnent's Gene Therapy Advisory Committee, which decided in 1998 that it would not approve any proposals for this type of treatment. "At this point in time, if a proposal is submitted for in utero gene therapy, it is unlikely to be approved, because of the risk of accidentally introducing germline changes. We don't know what the conse- quences of that would be," Nevin said. According to Coutelle, this is unfair, as it applies more stringent standards to gene therapy than to other treatments. "It is a well known fact that medically we are creating mutations by chemotherapy,' he says. "No one seems to worry about that." Because the mutations are random, it is impossible to trace any damage to the germline, he says. "We should try to avoid germline gene transfer, but if it happens, it has to be balanced against the benefits. And that holds for all gene therapy trials.' According to Coutelle, his team could be ready for human clinical trials of fetal gene therapy in four or five years' time. But will they be allowed permission? "When we are in a position to apply for it, then we'll return to the issue," he says. There is similar pressure to push for- ward fetal gene therapy in the US too. In 1998, French Anderson, director of the gene therapy laboratories at the University of Southern California, submitted two pro- posals to the National Institutes of Health for carrying out gene transfer into human fetuses which would have a "distinct pos- sibility" of leading to germline changes. He submitted the proposals with the aim of stimulating debate in the area. But soon the question could be of more than academic interest. Anderson says that after more than a decade of research on fetal gene therapy in animals, he could be ready for human trials in as little as three years. Other researchers think the regulators are right to be cautious. Cell biologist Stuart Newman from New York Medical College agrees. "Somatic modification in embryos is a grey area because there is a greater likelihood of germline modifica- tion. If it is ever going to be done, it has to be done right. We would have to be assured that there was a vanishingly small chance of affecting the germline." "My concem is that we don't know what we're doing," says John Bell, head of clinical medicine at Oxford University. "Maybe it will be acceptable in a thousand years' time, but not today." A report by the American Association for the Advancement of Science entitled Human Inheritable Genetic Modifications, published in September, concludes that it is I very likely" that some of the adult gene therapy trials authorised in the US have had unintentional impacts on the germline. It adds that the possibility of genetic prob- lems occurring because of these germline side effects seem "at least as great or greater" than problems that might arise from altering the germline intentionally. With such unintentional changes already taking place, some feel that it is only a matter of time before in utero gene therapy is endorsed, and perhaps germline genetherapy too. In fact, Newman suspects that some people may be deliberately down- playing concerns about in utero gene therapy inorder to soften up public opinion and pave the way for germline therapy. Most researchers, however, think delib- erate germline modification is some way off, not least because its medical uses are limited. For carriers of recessive disorders such as cystic fibrosis, for example, IVF procedures would be needed to correct an embryo's DNA. And if you're going to per- form IVF, then other techniques such as prenatal genetic diagnosis (PGD) could be used to select embryos for implantation that did not have CF. While the AAAS concludes that germ-line therapy cannot yet be carried out safely in people, it looks ahead to the day when it might be used. The report suggests, though, that the first use of the technique will not be aimed at introducing genes that will be passed down the generations, but will simply be to correct motility defects in sperm. And while the debate over in vitro gene therapy rages, other developments are causing constemation. Babies are already being made in the US with mitochondria from a donor, meaning that they have DNA from three different individuals. "It is start- ing to blur the question, 'who are the par- ents of the child?'" says Newman. "Society has not worked out what the implications of children having three, four or ten parents might be. It's a whole mess.' The regulators argue that the risks of modifying the DNA our grandchildren will inherit are too great for fetal gene therapy to be allowed. But Coutelle sees another point of view. The technique, he says, could enable us to cure many inherited diseases before birth. And that, he says, must make it worth pursuing. Joanna Marchant