| RUNNERS UP 20-28 - | CHARLIE HAYTHORNWAITE, EMILY SCOTT,
HELEN PEARSON, JOHN PINNEGAR, KATHERINE PATERSON, MIKE SMART, MIKE GARDENER, MIKE SHANAHAN, SUSANNA LEON |
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With the number of users set to double annually until at least the turn of the century, the Internet's relentless growth is extraordinary. Empowering devotees, it delivers the World's largest library at the touch of a button and confers the great modern-day prize - information. As a commercial tool, the World Wide Web is still in its infancy yet business has been quick to seize upon the new opportunities, incorporating home shopping and personal banking within cyberspace, transforming these routine chores. The formidble advances in telecommunications extend far beyond the domain of the computer addict, exemplified by inventions such as the videophone, the fax and video conferencing. Even the simple telephone has made impressive strides forward in recent years where the clarity of today's transatlantic call can create the illusion of chatting to someone in the next room. As we are swept into this new era, I wonder how many of us have paused to draw breath and contemplated the technological quantum leap that is now stimulating an information explosion. Far from being just a simple matter of the increased processing power of modern computers, what is crucial is the ability to transmit colossal quantities of information rapidly, perhaps to the other side of the globe. Almost imperceptibly throughout the 1980's, an optical telecommunications revolution was taking place - quite literally under our feet - connecting together cities and the major continents. Digital information coded in the form of infra-red light pulses began to be sent along optical fibres with widths a mere fraction of a human hair. The new technology delivered a great deal but the World's insatiable demand for ever more information has posed new challenges as Prof Peter Cochrane (Head of the BT Research Labs) explains, "Despite there already being enough fibre to encompass the Earth over a thousand times, the existing network is close to full capacity - rather like M25 rush-hour traffic on a bad day!" The major complication arises due to the original signal, weakened through fibre loss, needing to be electronically reamplified every 30 miles. Even with today's lightning quick electronics, the speed of the amplifiers creates a processing bottleneck and imposes severe restrictions on the rate data can be transferred. "A very similar notion will be all too familiar for motorway drivers," says Prof Cochrane developing his analogy. "So often their progress is frustrated by road works which have the same effect of limiting the overall traffic flow." Towards the end of last year, the latest in a series of transatlantic undersea cables went into operation incorporating a remarkable breakthrough in amplifier design. With a data capacity of 10 billion bits per second, roughly equivalent to 156,000 simultaneous phone calls, the new cable is already alleviating the strain from this pivotal part of the system. Bypassing the bottlenecks of the constraining electronics, the Erbium Doped Fibre Amplifier - first demonstrated by Southampton University only a decade ago - is able to intensify light signals instantaneously by a purely optical process. The innovative device, simpler and more reliable than its electronic predecessors, is based upon many of the same fundamental principles as a laser. Power is derived from the absorption of light at a different wavelength from that of the signal, fed from a diode laser similar to those used in CD players. When signal photons (particles of light) pass through the device, they initiate a chain reaction releasing a cascade of identical photons, boosting the signal on its way. Whilst simply installing further fibre is in principle one solution to developing network capacity, the overwhelming rate of increase in demand does not make this a practical option. Certainly economically, the solution to the Information Superhighway lane extension problem lies in exploiting the new technology a point underlined by the speed at which the optical amplifier, fast becoming a billion dollar market, is being adopted in the telecom network. In as little as three years time, however, experts predict that once again demand will have overtaken the design limits of the current transatlantic link. Is there another technological leap on its way to the rescue? Prof David Payne from the University of Southampton is optimistic about the prospects of current research, "One of the beauties of the optical amplifier is that it's compatible with the idea of sending many independent signals along a fibre simultaneously. At the end of a link, individual messages with different wavelengths can be separated since they're effectively colour-coded." Whatever the future holds for the telecommunications network, one thing seems certain: research scientists face a continuous battle if they are to stay one step ahead of demand and avoid an almighty Information Super-traffic-jam. |
Scientists will alter the very fabric of life - our genetic material - to cure the most common fatal inherited disease in the western world. The gripping tale of research into gene therapy for Cystic Fibrosis (CF) has found itself thrust into the media spotlight. Scientist and doctors are making rapid headway in their search for a life-saving treatment. But does the media's treatment of the subject benefit their cause by promoting public understanding and interest or is the rate of progress dangerously exaggerated giving false hope and misinformation? Recently ITV's GP drama, Peak Practice, ran a story line in which a doctor's baby daughter, born with CF, was apparently offered an increased chance of survival if she took part in a clinical trial for CF gene therapy. Producers were forced to issue an apology after a number of complaints that the story was misleading. Dr. Catherine Goddard, a scientist researching CF at Cambridge University, agrees. "It is very dangerous to suggest that you can take a CF baby to some magical trial and imply that this might save its life". Current trials are primarily designed to test safety rather than alleviate symptoms. Subjects are all over the age of 16. Of every 2500 babies born in the western world, one is born with CF. They have inherited a faulty gene, called the cftr gene. As a result they have an incomplete set of instructions for making a vital protein (CFTR) which acts as a tunnel connecting the inside of cells with the outside environment. Without CFTR, salt and water become incorrectly distributed in the linings of many major organs and a sticky mucus accumulates. In the lungs the thick mucus becomes hard to clear and makes breathing difficult. It also creates an ideal home for colonies of bacteria and it is these chronic lung infections that eventually kill over 95% of CF patients. Gene therapy will involve delivering the correct instructions for making CFTR to the cells that need it most; those lining the lungs. As a young research student in the field I am very optimistic about the prospects. In my group at Cambridge University we have hidden the gene in fatty droplets known as liposomes (better know for their appearance in adverts for skin creams). The gene can easily infiltrate the cells lining the lungs without alerting the body's defence systems because the liposomes are made of substances similar to the membranes that surround cells. Years of research by the Cambridge group, and others, to test this gene therapy system have produced such promising results that we have taken the next step and tested the treatment in patients with CF. The results were published in the scientific journal Gene Therapy. They show that a single dose of liposomes carrying the cftr gene can be safely applied to cells lining the nose and that a fully functional CFTR had been delivered to 6 out of 8 patients. The nose provides a safe, accessible place to test the therapy on cells very like those in the lungs. Progress is rapidly being made and our second trial has just been completed. While the results were being decoded (both patients and doctors are kept in the dark as to who is getting the real treatment) I met one of the patients. Matt is 23 and full of life. He sees the trial as an opportunity for him to learn more about the disease. "Being involved is really interesting", he explains. "Even if this research doesn't benefit me, it's bound to benefit someone in the future". Dr Bill Colledge,a senior researcher at Cambridge University, feels we are making good headway. "There are a lot of people doing a lot of research", he points out. However Colledge believes that the day when CF gene therapy reaches the clinic is still some way off. "10 years is optimistic; I5 years is realistic and 20 years is pessimistic", he states. He also emphasises the importance of being realistic with reports of progress. "Unfortunately media coverage of most scientific research is superficial; this tends to raise hopes. We need to be very careful." Gene therapy will be one of the great new technologies. Scientists and patients alike have every reason to feel positive. But it is not saving lives yet. The public deserves better of science jounalism than superficial hype. We owe it to readers to give them facts in plain language, as a basis for making their own judgements. |
The eyes you are using to read this sentence produce pictures clearer than the most technologically advanced camera, yet they grew from a pin's head of cells in a few short weeks. Now scientists are opening our eyes to the genes which create the phenomenon of sight. It takes a long-winded instruction manual to tell us how to work a camera, let alone build one. Yet all the information needed to form the living camera of the eye is efficiently encoded in our cells, in the sections of DNA we call genes. Every human cell contains about 80,000 genes. Of these, a few decide whether your eyes are blue, brown or green, but around 2,500 are needed to form a perfect working eye in a growing embryo. One gene, called Pax6, is proving to be particularly eye-catching. Mutations, or mistakes, in the DNA of the Pax6 gene cause a rare disease called aniridia, in which the iris, the coloured ring of the eye, is missing. Amazingly, mice, fish, flies, even sea urchins and squid all have a Pax6 gene. More incredible still is that this same gene appears to direct the building of eyes in all these diverse creatures. Mice with a faulty Pax6 gene suffer a similar eye disease to aniridia and flies with mutations in their Pax6 are appropriately named eyeless. Using a bit of genetic cutting and pasting it has been possible to put a copy of the human Pax6 gene into the fly. The results are, literally, eye opening. If the gene is put into the part of the growing fly that normally becomes a leg, the leg instead forms an eye. This landmark experiment propelled Pax6 into the limelight of genetics with the title of a 'master gene' which controls eye formation in all animals. Such astonishing findings have led to a complete rethink of how eyes evolved. Evolution was creative in both eye design and position: while we find eyes useful in our heads, starfish have them on their arms and butterflies intriguingly find a use for eyes on their genitals. Humans and flies have such different eyes it was thought the genes involved in their formation would be different too. We have two spherical water-filled cameras whereas flies are well endowed with 800 light-sensitive cells fitted together like the patches of a football. Now it seems that the same gene, Pax6, is fundamental to development of such remarkably dissimilar eyes. Remember that in humans 2,500 genes are needed to form an eye - so where do they fit into the picture? Genes produce proteins, and it is these which carry out the gene's instructions in the cell. The protein produced by Pax6 is thought to act as a switch, switching on or off some of the other eye genes. Constructing an eye is really a team effort; although Pax6 may be high up in the eye gene team there are many echelons of power above and below it. Research at the MRC Human Genetics Unit in Edinburgh is now focusing on unravelling the complexities of these cell politics - who are the other key players in the Division of Eye Development? And what positions do they hold in the genetic hierarchy? One approach involves looking for genes which are not switched 'on' properly in cells with a defective Pax6 gene switch. In these cells the communication links have broken down - genes which are normally controlled by Pax6 will be acting oddly and can be identified. Ultimately this work might lead to identification of genes which cause other eye diseases, aiding the development of their diagnosis and treatment. Even glasses could eventually become a thing of the past. In the near future it will at least help us to position another piece of the enormous 80,000 part human gene jigsaw. The latest digital cameras require state-of-the-art technology whereas genes effortlessly produce two infinitely more sophisticated devices in the form of our eyes. We can put our sight to good use by scrutinising the genetic instructions in the eye manual - it will hopefully make repairs a little easier when our biological machinery fails. |
Douglas Adams, in his cult 1979, radio series 'The Hitch Hiker's Guide to the Galaxy', introduced us to the Babel fish, a small yellow leech-like creature which, inserted in the ear, allowed the wearer to understand anything said in any language. We read that "nothing so mindbogglingly useful could have evolved purely by chance", and that because of this "some thinkers chose to see it as a final and clinching proof of the non-existence of God". Although this is a work of fiction, Adams actually raises an interesting evolutionary paradox; one which has plagued scientists for over a century. That of "the incompetency of natural selection to account for the incipient stages of usefull characters." To understand this argument we must go back to its roots and the British Zoologist St. George Mivart who in 1871, challenged Darwin by arguing that for a bird to fly, a significant quantity of wing must have had to spring forth all at once, since part of a wing would confer little evolutionary benefit. Darwin fully appreciated the devastating implications of Mivart's critique and developed the principle of functional change as a result, arguing that wings have not always been used for flying, incipient stages originally performed a different function suited to their size. This principle is more poorly appreciated than any other in evolutionary theory, a fact which has become particularly evident in recent months with the discovery of what appears to be a flightless feathered dinosaur from the Liaoning province of China. Sinosauropteryx prima, as it has been named, is reported to exhibit a "halo" around the skeleton of what are assumed to be downy feathers. Its discoverers Chen Pei-Ji and Philip Currie believe that these were used for insulation, a theory championed by John Ofstrom, former professor of geology at Yale. Alan Feduccia of the University of North Carolina, however, reports in New Scientist that it is inconceivable how feathers, so well designed in aerodynamic terms, could have evolved to serve any purpose other than flight. This debate will continue until detailed microscopic studies show whether the Chinese dinosaur has completely modern feathers or not. In a striking parallel, it turns out that the wings of insects also developed as a means of temperature regulation. Kingsolver and Koehl demonstrated in 1985 that, the thoracic lobes (proto-wings) found on fossil insects would, even at the small sizes observed, have benefited in providing a surface for heating by the sun. Butterflies with wings cut to the size of those in fossil insects allowed a 55% greater increase in body temperature compared to butterflies with wings removed. Thermoregulatory benefits increase until at a threshold wing length, gains cease. By this size however, aerodynamic benefits become apparent allowing natural selection for even larger wings, although retaining the original function, particularly in the basal one third. In a paper published in February of this year, Michalis Averof and Stephen Chohen demonstrated, using molecular genetics, that insect wings evolved from gill-like appendages in aquatic ancestors. These authors showed that insect genes implicated in wing development, are homologous with genes associated with crustacean limb branches (epipods), known to have respiratory functions. Consequently, wings may have developed first for respiration, then thermoregulation and only later for flight. One of the most interesting changes of function to be found in any animal, are those of the human ear. When vertebrates first came ashore, hearing was a new problem. Air oscillations caused little vibration of the skull which might enable a land animal to hear in a fish-like fashion. Consequently our early ancestors needed to construct an amplifying device. With the disuse of the gills, the first gill slit (the spiracle), become the middle ear, and the ear drum, a membrane sensitive to even small air vibrations. Next, how to transmit vibrations to the braincase? In sharks, the upper jaw, is propped against the braincase (from which it is separate), by a bone which in jawless fishes was originally a gill-bar. This bone, with only a slight shift in position, was able, as the stapes, to transmit sound waves from drum to inner ear. This earbone is the only one present in amphibians, reptiles and birds. Furthermore, in reptiles there are normally seven bones in the lower jaw, whilst in mammals only one. Consequently the bones (quadrate and articular) which formed the old articulation became tiny and then useless. These old jaw bones, which lay close to the ear drum have joined the stapes to complete a chain of three ear ossicles. Breathing organs have become eating organs and then hearing organs. Therefore perhaps as the remnants of gill bars from jawless fishes, the
babel fish exists in all of us, converting vibrations of the air into comprehensible
language. |
A piece of bacon which is juicier, tastier and more tender than all the rest must come from a good home. Not such an absurd idea according to some new Scottish research suggesting that poor pig housing can yield a rotten rasher. It is already known that both the breed and feed of the Bacon Pig can substantially alter the status of the end product. Common breeds found in this country include the Landrace, Large White Boar and Yorkshire. Meat from the male pig (boar) is more likely to possess foul flavours which arise from deposits of pheromones into the meat. In some countries, boars are even castrated to reduce the incidence of this 'boar taint' as it is called. Stress of animals prior to slaughter has been the subject of much study in relation to the physical and chemical characteristics of the meat obtained. Relatively little attention, however, has been paid to bacon itself, especially with regards to the pig's habitat. Involved in a 3 year investigation, Steven Maw, an Animal Scientist based at the Scottish Agricultural College in Aberdeen has identified some of the farming factors which give rise to a first rate rasher. The study, which is funded by both Halls of Broxbun - renowned for their pigmeat products - and The Ministry of Agriculture Fisheries and Food, compared the farming practices of 23 commercial pig farms in the North East of Scotland in relation to the bacon they produce. "For a long while, the Food Industry has suspected that certain pig farms consistently produce bacon of an unacceptable standard hence the interest to find out why," reports Maw, who personally prefers his bacon smoky. His inspection provided intricate details concerning factors such as pig cleanliness, breed, feed and dust levels. Of special significance was the aerial ammonia level present in the pens and also the type of floor provided. The use of solid concrete and slatted floors came in with the introduction of the revolutionary intensive pig farming practices of the 1950s. Efficiency was high on the agenda as it still is today with slatted floors allowing pig urine and faeces to be drained away on a larger scale. Nowadays pigs kept on straw are in the minority, despite recognition by those in the field that bedding is beneficial for the welfare of this animal. Bacon from all 23 farms was subject to intense scrutiny by a trained food panel at The Robert Gordon University in Aberdeen with the help of Food Industry Consultant. Valerie Cheetham. Results from the 16 bacon traits analysed, such as the juiciness, crispiness, greasiness and the presence of unpleasant aromas or flavours, demonstrated that bacon from each farm was markedly distinct. More specifically, Maw discovered that pigs which were kept clean and which lived in pens with low concentrations of ammonia produced bacon of a fine quality. The dreaded 'boar taint' taste was found to be more prominent in pigs which were raised on solid floors. Conversely, pigs maintained in stys containing straw delivered a tender tasty and pleasantly cooked rasher. "After finding out what exactly are the housing factors which promote poor bacon quality, the next step would be to learn how precisely why," says Maw, who wishes to continue his study with pigs. For example, if poor air quality with high ammonia levels causes stunting of growth and hence an unfavourable influence on bacon properties, how might it exert this effect? "Perhaps via its irritating effects on the lung and nasal membranes which could lead to an infection. Ammonia in sufficient quantity can induce tears in man and also 'stick' to the back of the throat. In chickens it is known to damage the hypothalamus (the part of the brain which has many of the body's regulatory processes cut down to a fine art.)" It seems that the best way to prevent accumulation of ammonia is probably through cleanliness and good drainage. But before he can attempt to answer these hows and whys, Maw awaits results of a similar study, which will verify whether or not poor housing puts an adverse mark on the physical features of bacon as well. At any rate, it may be that everyone: industry, the 'pig conscious' and
the consumer alike will all eventually achieve a better bit of bacon, albeit
for different reasons. As for the average Landrace or White Boar Bacon 'Babe',
they could be in for some serious straw. |
Fifty years ago, Chuck Yeager became the first man to break the sound barrier in his Bell X-l plane. This year Richard Noble is hoping that his Thrust SSC car will break the world Land Speed Record which he himself set in 1983. Should his efforts be successful, Andy Green, the RAF fighter pilot who will drive the car, will be the first man to go faster than the speed of sound in a land vehicle. Breaking the sound barrier is not simply a matter of power. The two Rolls-Royce Spey engines on the car develop over 100000 honsepower (approximately equivalent to 1000 Ford Fiesta 1600's) which is more than enough to propel the car past 750 mph, the speed of sound at sea level. The problem is making sure that the driver can control it at that speed. As any student of aeronautics knows, and as many early test pilots found to their cost, weird and wonderful things happen when travelling at supersonic speeds. Any object moving through air forms sound waves, which are squashed together in front of the object and stretched out behind it. This explains why an ambulance siren changes pitch as it passes you by - the pitch of the sound depends on how close together the waves are. What happens if the object moves faster than the speed of sound? Basically, the waves in front are squashed together to form a shock wave - a cone shaped envelope of waves across which the air pressure changes dramatically. This wave is responsible for the "boom" caused when supersonic aircraft fly overhead, and was also responsible for the severe buffeting experienced by early test aircraft, resulting in many crashes and deaths. It is problems of this sort which have taxed the designers of Thrust SSC. The difficulties are made worse by the fact that the shock waves will interact with the ground, causing effects which have not been observed on aircraft. "The problem is that no-one knows for sure how the shock waves will behave when they are so close to the ground," says Professor Nigel Weatherill at the University of Wales Swansea. "Our calculations show that the waves will be reflected from the ground to car and back again along the car's length, which can cause handling problems." Weatherill was approached in 1994 by Thrust SSC's chief aerodynamicist Ron Ayers, to perform the complex computer simulations needed to predict the car's behaviour. Swansea has for many years had a strong research team investigating computer modelling of engineering problems using the Finite Element Method (FEM). This is a technique developed in the 1960's for solving complicated sets of equations like those which describe shockwaves. Although the equations themselves have been well known for centuries, their solution has escaped generations of scientists and mathematicians, until the advent of the FEM. Firstly, the area of interest is subdivided into hundreds of thousands of little regions called elements. Although the way that the air flows over the car is unknown, it can be solved for over each element. By putting all the elements together an approximation to the total flow is achieved. Essentially, a problem that was insoluble reduces to one which involves millions of simple calculations, solvable on a computer, in this case a Cray supercomputer. The initial calculations performed by the Swansea team matched up very well with results from a scale model of the car - so well in fact that they helped persuade sponsors to provide further funding for the project. But the final predictions have not yet been verified. "Our predictions apply from about 650 mph to 850 mph, which so far the car has not reached" says Professor Weatherill. "Although we are confident of our results, we will only really know we are right after the car has gone supensonic." Like all great record attempts, being the first to go supersonic on the
ground means risk - which everyone in the Thrust SSC team understands. But
if they are successful, they will know that as in most areas of modern life,
computers had their part to play. |
The tabloid press continues to pontificate about teenagers running riot but the man in the street should be more worried about his own cells going on the rampage. Cell growth is normally a very closely regulated business Cancer arises when cells disregard their normal controls and repeatedly divide when they should be resting. However Dr Judah Folkman from Harvard Medical School says that most cancers "will not become larger than about the size of a pea" unless they develop a good blood supply. Dr Folkman has been working on blood vessel formation since the I970s and is investigating ways to control cancerous growths by cutting off their blood supply and literally strangling them to death. Philip Thorpe, from the University of Texas is also working towards producing an "avalanche of tumour cell death" by cutting off the blood supply to tumours. Both these groups have recently reported advances which may lead to new therapies to tame rampaging cancers. The development of a tumour begins when a single cell mutates and gains the ability to divide when it would normally be resting. The rogue cell and its progeny continue dividing until they form a small tumour. This benign tumour stops growing in size when the number of new cells produced is balanced by the number of cells dying. The next stage in a cancer's life, which may happen many months later, requires a better blood supply to deliver more nutrients to the tumour. The cancer can then become malignant and invade other parts of the body. It is only at this stage, when the invading cancer cells disrupt the tissue and organs of the body that cancers become lethal. The development of a blood supply is therefore a key step in the transition from a relatively harmless small group of mutated cells to a large malignant cancer which can go on the rampage. Dr Folkman's group have identified a molecule called endostatin that blocks the formation of new blood vessels. Bizarrely, this molecule was isolated from a tumour itself. Tumours produce chemicals which both encourage and inhibit blood vessel formation, and the production of new blood vessels is regulated by the balance of these chemicals. Endostatin stops the growth of tumours by preventing the replication of cells forming the walls of blood vessels, leaving other cell types unaffected. This is a good method of attack because most of the time blood vessel cells do not need to multiply, meaning that the blood supply to the tumour can be strangled without creating a negative impact on the rest of the body. In addition, endostatin should have fewer side effects than existing treatments, which often kill both cancerous and "normal" cells. It is also less likely to induce drug resistance in the cancerous cells, as it does not act directly upon them. Trials in mice showed that endostatin can shrink large tumours down to microscopic size. This dramatic reduction in tumour size demonstrates just how much tumours depend upon new blood vessel formation and illustrates just how effective strangling a cancer can be. Dr Thorpe's group have taken a different approach and used the formation of blood clots to block tumour blood vessels. This approach is an alternative way of cutting off the tumour's blood supply and thereby effectively strangling it. In these trials a fragment of tissue factor, the major initiating factor for blood coagulation, was linked to an antibody. The antibody only recognises markers on the outside of tumour blood vessel cells and thus specifically targets deadly clots to the tumours. During trials in mice blood clots formed in tumours within 30 minutes, and within 48 hours all the tumours were largely dead and had collapsed, whilst other organs were not affected. The identification of markers to target clots to human tumours is underway and several potential candidates have already been suggested. Human trials of these compounds may still be a few years off but other drugs which strangle tumours are being tested in clinical trials at the moment. Dr Thorpe says that this approach to tackling cancer "isn't pie in the sky" and sees exciting prospects for the continuing fight against cancer. |
It is a myth that in tropical forests the bounty of nature's larder is available year round to support fruit-eating animals. In reality they experience alternating episodes of feast and famine with fig-eating possibly making the difference between survival and extinction. Most tropical fruit-bearing plants share distinctly seasonal fruiting patterns, with one or two peaks of ripening at the same time each year. Fig plants though can fruit at any time of year (regardless of other members of their species or population) and so may sustain fruit-eaters through lean times. As well as providing for the vertebrates, figs may ensure the survival of more rarely-fruiting species by maintaining animals which disperse their seeds. By attracting seed dispersing animals figs can be instrumental in the recolonisation of deforested areas, or volcanic islands like Krakatau. For these reasons ecologists have described figs as keystone species in tropical forests. Just as the removal of the keystone of an arch is quickly followed by the structure's collapse, loss of ecologically important keystone species can trigger a cascade of local extinction. With some 750 diverse species, fig plants (genus Fictis) exhibit great variety in growth forms including trees, scrambling climbers, shrubs, bushes and tree-stranglers. More so than any other wild tropical fruit, figs provide a large dietary contribution for a veritable Noah's Ark of animal species, varying in fig design and position to attract different types of vertebrates. Essentially the diversity of fig species is mirrored by that of the vertebrates feeding on them. The weird and wonderful mix of fig-eaters include birds, fruitbats, monkeys, rodents, bearded pigs, spectacled bears and the oddly-named olingos, kinkajous and binturongs. All feed on figs with preferred groups of characteristics (together classed as syndromes) varying depending on the feeders. Birds are attracted to small, bright red figs in the canopy whilst bats prefer dull, green or brown figs more easily accessible growing from trunks or hanging on pendulous branches. Year-round fruiting is good news for the fruit-eaters, especially when combined with the facts that fig trees produce superabundant crops (up to one million figs) and have only short intervals between fruiting episodes. These facts highlight the importance of figs to a wide diversity of fruit-eaters in times of fruit shortage. The best documented tropical fruit shortage is the 1970-71 famine on Barro Colorado Island, Panama, where in the eight months from July 1970, under 50% of potentially productive plant species bore fruit. Intense hunger stress among fruit-eaters resulted, culminating in deaths to the extent that vultures could not cope with the supply of corpses (by December 1970, mammal carcasses could be found every 300 metres along forest trails). Starvation levels declined suddenly when figs came to the rescue with peak fruiting in January and February 1971. More recent research has identified a possible keystone role of figs in Peninsular Malaysia, Borneo and Peru's Amazon basin where Princeton University's John Terborgh suggests that loss of figs could lead to the ecosystem's collapse. However, at other sites in Gabon and India figs are apparently less important - being present at low densities and feeding only a small proportion of fruit-eaters. The importance of fig species evidently varies (to misquote George Orwell, '"some figs are more equal than others") either due to their distribution, density and crop size, or as a consequence of animals' abilities to locate and utilise the fig resource. Because of this variability, it is the job of field biologists to act as 'keystone-cops' in order to identity which fig species are disproportionately important in tropical forests with rollercoaster fruit economies. This requires exhaustive fieldwork encompassing studies of fruiting patterns of figs and other species and behavioural studies of the fruit-eating animals. In Shakespeare's Antony and Cleopatra, one of the queen's attendants declares "I love long life better than figs". Tropical fruit-eaters may be able to enjoy both, living longer through their love of figs. If some fig species are shown to have keystone importance their protection may be vital to threatened tropical communities. This conservation goal is not too far out of reach as to be unrealistic. Without protection, loss of keystone-figs could cause what Henry Howe
of the University of Iowa calls "a widening circle of extinctions precipitated
by the disappearance of one pivotal species". Rather than investing
limited resources only in the protection of rare, poorly understood species,
managing more common keystone-species with known importance in maintaining
community stability may result in greater overall conservation of biodiversity. |
Chemists are reinventing the lottery in the quest for new drugs Susanna Leon reports Time is money, particulany if you are hoping to win the lottery. It could be you next week, but only with a great deal of luck. Realistically, if you buy one ticket for every draw, chance is more likely to come your way once only in 135,000 years. You might well grow weary of waiting. Until recently, chemists have been treading a path all too similar to that of the lottery player. Drug discovery is big business yet has often involved rather a gamble, with chemists spending years designing and hand-crafting each new target molecule only for it to fail to make the grade as the sought after new wonder drug. Tired of just waiting for the winning combination to appear, chemists are finally losing their patience. They are reinventing the numbers garne in a way which promises to turn chance in their favour. Why risk with a single lottery ticket when you can play all the possible combinations for the sarne price? The catchword is "combinatorial chemistry" and the aim is to save time by making as many different molecules as possible in a single pot. Researchers are achieving this by taking a number of small building blocks and putting them together in all the possible combinations. The original idea was devised by Arpad Furka in 1988 at the University of Budapest, or so he argues, though at the time was ridiculed by his colleagues who did not see the point. Mixtures of compounds have always been a taboo to any chemist. The idea was simply an extension of Bruce Merriflelds work, who in 1963 pioneered a technique for the Synthesis of peptides (small proteins) which later won him the Nobel prize. Peptides consist of amino acids linked together in chain-like sequences. By attaching the first amino acid onto tiny polymer beads, Merrifield was able to connect on each consecutive building block to create a peptide in a fraction of the time and effort. Furka's twist was simply to shuffle the building blocks at each step so that the beads carried not one but a mixture of peptides in the same pot. Quick to realise the potential of Furka's approach, rival chemists in America were soon laying their own claims and developing the idea towards biological screening. Tethering the molecules to beads bypasses lengthy, laborious purification, since any impurities can be simply rinsed from the beads. Another advantage is that despite the molecules being jumbled in a mixture, each bead carries molecules of only one structure and so can still be picked out from the rest with ease. Vast mixtures, termed "combinatorial libraries" containing up to several million molecular structures can thus be screened in one single test, unlike previously where each compound would be assayed separately. Not surprisingly, the field has become hot on the agenda of all the major pharmaceutical companies. Stephen Kaldor, head of combinatorial chemistry at Eli Lilly in Indianapolis says that it is now used in over 75 per cent of the firm's drug discovery programmes. Instead of relying on existing compounds from their ageing databases, companies are now able to generate vast new collections of drug candidates in a matter of days - unthinkable ten years ago. The whole process is becoming highly automated with robots carrying out most of the chemistry, and libraries can be tailored specifically towards a particular drug target. Since the early work with peptides, all kinds of chemical structures from antibiotics to industrial catalysts have been conceived. Moreover, combinatorial chemistry does not stop at beads. Molecules have been synthesised on cotton, paper, plastic pins and even microchips with a view to extending the chemist's repertoire. It seems that researchers have found a new way of letting their hair down, and having now shattered the bottleneck in drug discovery many are being swept away by this new chemical superhighway. Nevertheless, the method is still very much in its infancey and many scientists remain sceptical about its long-term usefulness. Derek Hudson, director of research and development at Biosearch Technologies in California, is cautious in his enthusiasm. "Combinatorial chemistry is accelerating drug discovery", he agrees, "but many have overemphasised its impact''. Rather thin replacing well-established techniques, his view is one of "just more tools in the tool chest" for researchers. With such high stakes, pharmaceutical companies are keeping many of their latest projects under wraps. Understandably they are reluctant to divulge too much and with drug licensing taking at least five years to complete, a successful drug has yet to be marketed. Nevertheless, judging by companies' huge investments, they certainly seem confident of hitting the jackpot. |