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Mice to the Rescue NS 1 July
2000 Women may soon have a better way of saving their eggs
WITHIN the next year mice will be incubating the eggs of women who risk damaging their ovaries because of medical treatment, say Canadian scientists. The team has already successfully harvested human eggs from the back muscles of rodents, they told a meeting of the European Society of Human Reproduction and Embryology in Bologna. Ariel Revel of the Mount Sinal Hospital in Toronto, who leads the team developing the technology, says it "offers new hope" to young women who become infertile after vital medical intervention, such as cancer treatment. The development is sure to be controversial. There was an outcry last year when Italian embryologist Severino Antinori claimed to have produced four babies using sperm grown in rats' testes (New Scientist, 27 March 1999, p 5). Robert Casper, head of reproductive sciences at the University of Toronto and part of the research team, says: "We've been through all the proper channels and done everything ethically. Providing the process is safe and effective we don't anticipate problems in introducing this on ethical grounds." Many hospitals already freeze mature eggs from female patients. But freezing is difficult and can damage mature eggs, while attempts to transplant ovarian tissue back into patients have so far failed. In cancer patients, malignant cells might also be reintroduced in the transplant process. But now the Canadian researchers say they have successfully produced three viable, mature eggs from tissue grafted onto mice. The graft contained immature oocytes that had previously been frozen and stored. They think it should now be possible to take ovarian tissue from a girl undergoing treatment for leukaemia, and freeze the tissue until she is ready to have a family. At this time, the tissue containing immature eggs will be thawed and grafted onto the back muscles of the mice that can't reject human tissue because they have been genetically engineered to have weakened immune systems. The eggs will mature in the mouse for about nine weeks before being harvested, further matured in vitro and fertilised in the test tube. The fertilised eggs will then be implanted in the mother's womb. Casper says the next stage of the research will be to check that the first three mature eggs are normal. He says the researchers would be paying particular attention to the number and structure of the eggs' chromosomes, though he says, "There's no chance that mouse DNA could be mixed up with the human cells." But fVF expert Alan Handyside of St James Hospital in Leeds says people are bound to worry. 'This is very exciting stuff. But from a clinical viewpoint there are bound to be some safety concems. Clearly people are worried when you mix human and animal tissue." Michael Day, Bologna
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And you thought light moves fast NS 29 July 2000
SO MUCH for the ultimate speed limit. Scientists in Switzerland have measured how fast information can flow in the quantum world and have clocked it travelling 1500 times faster than light. The Swiss speed trap involved pairs of "entangled" photons. Once linked, the pair behave as one, even if the photons are on opposite sides of the Universe. Physicists don't think this flouts the light-speed limit enshrined in relativity. "You cannot use this effect to communicate, it's not like ordinary information," says Wolfgang Tittel of the University of Geneva. But the Swiss team wondered just how fast such communication could travel. So they created an entangled pair in their Geneva lab and sent the two photons in opposite directions along a 10-6-kilometre optical fibre. Because the two arms of the fibre are not exactly the same length, one photon will arrive first and will change its state when detected. This will change the state of the other which will be detected shortly after. Hence the researchers know they communicated in the short time between the first and second detection and can calculate the minimum speed of that communication. That speed was at least 4-5 x 1011 metres per second, enough to reach the nearest star, Alpha Centauri, in just over a day. Ordinary light would take 4-3 years. Justin Mullins
Source: Quantum Physics e-print 0007008 at hftp://xxx.lanl.gov
Sick to Death NS 5 Aug 2000 Extinction and Disease
INDIA without vultures. It's hard to imagine. Since time immemorial they have lurked everywhere, in cities and the countryside, waiting for food to scavenge. Five thousand could live on one waste dump or around a single abattoir. A gang of vultures could pick a water buffalo carcass clean in 20 minutes. No more. In only a few years the onceubiquitous griffon vulture has all but disappeared from India. Other vulture species are not affected-but none of them is big enough or numerous enough to replace the griffons. The stench of rotting cattle carcasses pervades villages. And with plenty of meat on offer, packs of vicious, rabid dogs are multiplying. "All our reports and data show the vultures are dying of some viral disease," says Asad Rahmani, director of the Bombay Natural History Society. One species of the griffons, unique to India, even faces extinction. Why? Griffon vultures are merely the latest in a long line of wild animals that have fallen prey to "emerging diseases", caused by pathogens that may have been harmless in their original setting, but turned nasty when released among previously unexposed hosts. Rinderpest, a virus brought to Kenya with imported cattle in 1887, killed threequarters of the native antelope, kudu, wildebeest and other ungulates in southem Africa within ten years. VVhen distemper virus was brought to the North Sea in 1988 by hungry harp seals-driven from the Atlantic by overfishing-it killed threequarters of the local harbour seals. And when West Nile virus arrived in New York from Israel last September, the news reports focused on the seven people who died. But the virus also killed ten thousand crows in New York City alone. Migrating birds might now have spread the virus across North America (New Scientist, 8 July, p 4). Catastrophic epidemics among wild creatures used to be considered rare, one-off events. But animal pathogens are travelling the world with increasing ease as the global trade in food, plants and animals spirals upwards, and humans become increasingly mobile. All over the planet, lethal infections are killing off populations of creatures ranging from abalone to kangaroos, from coral to honeybees, and from pilchards to flamingoes. Yet ecologists, wildlife biologists and governments alike are ignoring the threat that emerging diseases pose to natural ecosystems, according to an intemational group of animal health experts. That complacency, they say, is based on the belief that pathogens and wild populations invariably reach a happy equifibrium, even though a spate of recent studies contradicts this assumption. The upshot is that virtually no precautions are being taken to prevent pathogens that are dangerous to native fauna from globetrotting. "Until the last three or four years, disease was scarcely on the radarscope as a potential cause of endangerment," says Ross McPhee of the American Museum of Natural History in New York City. "Forgetting disease was a big omission in our thinking about wild populations," agrees Andy Dobson of Princeton University in New Jersey. That omission has come about in part because there has been an apparently more sinister culprit to shoulder any blame: chemical pollution.
Frog fungus
"When there is a sudden die-off of wild animals, people usually suspect pollution," says Peter Daszak, a wildlife disease specialist at the University of Georgia at Athens, who helped to identify the fungal plague that is killing off the world's amphibians (New Scientist, 27 June 1998, p 4). "People spent an enormous amount of time pursuing environmental explanations for the amphibian deaths . . . but disease was the primary cause of the mass mortality." Pollution undoubtedly harms wildlife. Ever since the 1960s when DDT wiped out populations of eagles and other birds, inspiring Rachel Carson's book Silent Spring, generations of ecologists and environmentalists have been taught to see chemical pollutants as biodiversity's number one enemy. Infectious diseases, on the other hand, are usually seen as part of the natural order. Hence the widely held view that the damage is rarely permanent when wild populations are invaded by a new infection. Extreme virulence is not good for pathogens, it's true. They need their hosts to live at least long enough to pass the disease on. So most evolve a truce: the host develops immunity, the pathogen becomes less virulent, and the disease settles down at a tolerable level. The classic example is myxomatosis, introduced into western Europe and Australia in the 1950s to control rabbits. After a huge initial die-off, rabbits and virus adapted. They now coexist.
But populations do not always bounce back. When a new strain of vibrio bacteria killed off starfish along the coastline of California in 1984, some species recovered faster than others, and maintained their advantage. VVhat used to be the most common species is now rare. And starfish are not alone in having their populations sculpted by disease. Since 1993, a team led by evolutionary biologist Andre Dhondt of Cornell University in Ithaca, New York, has followed the spread through songbird populations of a new strain of bacterium, Mycoplasma gallisepticum, that evolved in the crowded battery farms of the eastem US. Counts made by birdwatchers each winter showed that whether house finch populations were large or small before the infection arrived, they ended up at the same, low density afterwards. At this density, the disease is passed on just often enough to kill finches at the same rate at which the birds are reproducing (Proceedings of the National Academy of Sciences, vol 97, p 5303). In other words, disease determines numbers. "People thought large predators were the major control on numbers," says Dobson. "Or it was the availability of food." But it now seems that even ordinary pathogens-never mind virulent newcomers such as the finch infection-can dramatically alter wildlife populations. In 1998, Dobson helped to show that the cycle of boom and bust typical of many temperate species is, in British grouse, actually caused by cyclic variations in gut parasites. The observation may be a tuniing point in ecologists' thinking about disease. It makes sense that pathogens should play such an important role, says Dobson. For instance, they have far more opportunities to kill off the all-important breeding animals in a population than, say, wolves, which typically take out the old. Pathogens are much more important controls on wild populations than predators, he says, even when the pathogens are long established. Novel pathogens, to which the victims typically have no inununity, should have even more impact. Still, according to biological theory, even a new disease shouldn't be able to wipe a species out on its own. Once the host gets too scarce, the pathogen is no longer passed on frequently enough to keep in circulation. The disease wiu always die out before the host does. Or wiu it? Not according to a 1997 study by Mike Bonsall of Imperial College in Silwood Park, near Windsor. Two species of moth can, individually, coexist indefinitely in the lab with a wasp that lays her eggs in the moth's caterpillars. The wasp parasite, like any other infectious disease, needs a continual supply of fresh hosts to propagate itself. Wasp numbers plummet when caterpillars become scarce, so the two remain in balance.
Wasp waste
But if the wasp is allowed to attack both species at once, the moth that has the least resistance to the parasite dies out, fast. The more tolerant moth keeps wasp numbers up even when the other moths are too few to support the wasp population. The less tolerant moth goes "extinct". Similarly, North American grey squirrels have all but replaced native red squirrels in Europe, possibly because reds are more susceptible to a parapox virus that strikes both. But while some ecologists and wildlife biologists are coming around to the idea that pathogens can cause extinctions when there is a reservoir to top up the infecfion, few were prepared for just how many apparently innocuous fon-ns a reservoir can take. Burgeoning livestock populations and even pet animals are creating a multitude of artificial reservoirs. Domestic ducks harbour duck plague, a herpes virus that causes massive die-offs in wild ducks. African village dogs spread distemper and rabies to lions and wild canids (New Scientist, 19 April 1997, p 32). Even captive breeding programmes, the last hope for many endangered species, can be ffimatened by nearby artificial reservoirs for new diseases. A release of field crickets bred at London Zoo was delayed last year, says Andrew Cunningham of the Zoological Society of London, because the insects were infected with a protozoan possibly picked up from African crickets kept close by. The zoo now carries out pre-release screening for its captive-bred animals. But the most troubling development is the recent realisation that dead matter might act as a reservoir for potentially devastating emerging diseases. Take the catastrophic die-offs of the world's amphibians. In the Americas and Australia, the culprit tumed out to be a fungus that consumes keratin, a major protein in skin. Some species-the Central American golden toad and two species of Australian frogs that brood their young in their stomachs-have been driven to extinction, even though there are no obvious reservoir species for the fungus in their habitats. The problem, says Daszak, is that keratin is widespread in the environment in carcasses to shed skin. This means that the fungus might persist on dead tissue, until its hosts were well and truly extinct. Even so, Daszak and others are hopeful that there may be ways to limit the numbers of pathogen-induced die-offs in the future. Of prime importance, they say, is improving the ways animals are screened before they are transported across borders. "In Britain you have to declare any animal import that might be carrying a pathogen that could affect livestock, or fish stocks," Cunningham points out. "No one checks for things that might threaten wildlife." The same applies in North America. Rabies, for example, was spread out of the southeastern US during the 1980s by hunters moving raccoons to boost their populations elsewhere. "They were moving them in truckloads," says Daszak. Some biologists are equally to blame. Conservationists often transport animals to reserves or reintroduce them into the wild. The World Conservation Union, based in Switzerland, recommends that such animals be checked for infection, and that any deaths after such moves be investigated. But a 1993 survey of 700 "terrestrial vertebrate translocations" in North America, Australia and New Zealand found that conservationists failed to screen for diseases in one-quarter of moves, and to investigate whether deaths had occurred in three-quarters. But new rules and regulations won't be enough without a better understanding of how diseases are spread through wild populations, which ones exist there naturally, and how environmental changes, such as crowding within dwindling habitats, can speed contagion. "We need to learn much more about wildlife pathogens, where they have been moved in the past, and which pose the most risk," says Daszak. Then, he hopes, it may be possible to prevent the accidental introduction of pathogens that are most likely to have an adverse impact on biodiversity. "We may never be able to predict everything," adds Cunningham. "But just because a mountain is high is no reason not to start climbing it." Gaining that understanding will also require more thorough investigations of animal die-offs. In India, for example, scientists looked for signs of chemical poisoning in the dead vultures, but until this year no one froze a carcass for pathological examination. It's about time, say Cunningham and his colleagues, that emerging diseases in wildlife got the same respect they do in humans. "Emerging diseases, such as AIDS and Ebola, have been recognised as a threat to humans for some time now," says Daszak. "The same conditions that apply to us also apply to wild animals." The difference, of course, is that for the time being, at least, we are unlikely to go extinct. F]
Further reading: "Emerging infectious diseases of wildlife-threats to biodiversity and human health" by Peter Daszak, Andrew Cunningham and Alex Hyatt, Science, vol 287, p 443 (2000) Article by Peter Daszak on amphibian population declines, in Emerging infectious Diseases online at www.cdc.gov/ncidod/eid/vol5no6/daszak.htm
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In the 1950s, Alice Stewart found that exposing pregnant mothers to X-rays doubled the risk of cancer in their children. Ever since, the physician and epidemiologist has argued that low doses of radiation might be harmful. It's a view that has put her at odds with governments, the military and the nuclear industry. This week, Stewart, who is 93, publishes new research supporting her claims. Michael Bond spoke to the maverick of radiation epidemiology and found her in fighting form.
What new evidence do you have to support your claims that lowlevel radiation could be dangerous?
Radiation safety standards are derived from studies of the A-bomb survivors of Hiroshima and Nagasaki. These studies were food for people supporting hormesis, the theory that a little bit of radiation can be good for you-that it stimulates the immune system. When it was found that a small number of the A-bomb survivors were living longer than they ought to, this was seen as proof that radiation had done them good. But we have new data that should put paid to that. We have proof that the A-bomb data have been wrongly interpreted. (See 'Radiation: how safe is safe?")
What does your research show?
It shows that cancer was not the only effect of the A-bomb radiation. People died from immune system damage as well. Our paper also shows that the A-bomb survivors were not a normal, homogenous population. They were the best athletes-the top 10 per cent-and did not include the young and the old. This means that we cannot base standards of radiation safety on such an elite cohort.
Do you think that the authorities will now reassess the idea that radiation at low doses is not harmful?
I think this new paper will do it. But I don't think it will lead to an immediate reaction.
Why do you think your findings always take so long to be taken seriously?
Take your work in the 1950s showing that a fetus exposed to X-rays has a higher risk of cancer. Or your findings in ihe 1970s that workers at the Hanford weapons complex in the US were getting cancer after supposedly safe levels of exposure. The trouble is that I've always had a very small set-up, with only just enough money to employ people to do the research. I've never had a department that's out selling the message to other people. So it's been a bit slower than usual. When it came to my work on X-rays, nobody wanted to believe it. X-rays were a favourite toy of the medical profession. But much more than that, it was just the moment when the nuclear industry was taking off. If we were right, the industry couldn't develop properly.
Your work has tended to attract a lot of criticism from scientists, one of whom is the leading epidemiologist Richard Doll. Why do you think he doesn't like your work?
I moved to Birmingham University for that reason. I knew that if I stayed at Oxford I would always be under the thumb of Doll. But that is the extraordinary thing. I can have reason to be angry with him because he was powerful and I was weak. He can have no reason at all to be angry at me, and yet he must resent me for some reason. Something irks him about me, and I'm conceited enough to think he suspects I'm a better epidemiologist than him. Now, he will tell you he has never had any quarrel with me at all.
Doll has criticised your methodology on the Hanford Studies. Why?
He's criticised my methodology from the word go. I don't know why. He's even criticised the mathematics of George Kneale, my statistician. But Doll doesn't know a fraction of the mathematics that George knows. I don't know what he means when he says our method is wrong, but he should be called to account.
The main objections to my X-rays study was that the mothers were lay informants -that they weren't scientists, and they could have made up stories. We always knew there were weaknesses in our story. But we'd done our best to check this through the hospitals where they had their X-rays.
You've been described as 'an avowed opponent of the nuclear industry' Are you?
Well, I've never avowed it to anybody. But if by the nuclear industry you mean the war and energy industries, then yes I'm against it. If you mean, do I think we should stop using X-rays, then no, but you must use them knowing they are a dangerous toy. I think the medical profession has quite a lot of uses for it. Take, for example, irradiated food. If this was going to prolong the life of food that you could send to a country to save it from starving, it would be excellent. But what you've got to be careful of is not to allow industry to indiscriminately use this radiation and to find it's going down your back drains. I'm automatically against it for war, and you have to remember that the nuclear military and energy industries have always been far more intimately connected than most people realise.
The discovery that made your name in 1956 was that a fetus exposed to an X-ray is twice as likely to develop cancer within 10 years as one that is not. Did this finding come as a complete surprise to you?
Yes. We weren't particularly looking for a link between cancer and X-rays. We were comparing the medical records of children who had died from leukaemia with those of healthy children from the same regions. And in the questionnaire, we had asked mothers if they'd been X-rayed. lt looked to me as if there had been something before birth that produced a little epidemic at a certain age group that never repeated itself. But the risk was so small that if we'd tackled it any other way we'd never have discovered it. We were lucky, but it wouldn't have been thought of by someone who hadn't had some experience of medicine, and it might have been wrongly interpreted.
So if you hadn't found the link it might have been another 20 years before someone else did?
No, not 20 years. To this day we would be thinking X-rays were safe. This is because, as I've indicated, the A-bomb survivor studies from Hiroshima and Nagasaki, which was the only other study on this, was saying it was safe, and this would have been considered satisfactory to the point where everybody would have been quite happy about X-rays.
How much do you think being a woman helped or hindered your career?
When you first walked into the lecture hall as a medical student at Cambridge in 1925 you were met with 200 male students stamping their feet at you. I'm sure my sex made a tremendous difference. But thanks to my family-my mother was a doctor-and thanks to the war, rather than being a crippling difficulty it actually proved to be rather a helpful one. I found I was constantly thinking of things in an unusual way. I didn't expect to be allowed to get to the top rung, which is something a man would expect, and so perhaps that made it easier to stay with a subject that wasn't very popular.
Has that bothered you?
Not at the time, but in retrospect I think it's the one thing I rather regret ... that I should have pressed for something more. But I was stuck, I could only do one or other of two things: I could either be fighting the battle for women or I could be getting on with my job. I couldn't win both. And I chose to go on with my job. But I think a braver person might have done something about it.
Were you ever bitter about being sidelined?
No, I think I personally had everything to gain by it. It's always worked in my favour. An element of uncertainty is always a good thing. It's been a constant help. You need some resistance and criticism to bring out the good work. One of the reasons it's been so interesting for me is that no one has ever lost interest in what I've said about radiation. They may despise me, they may hate me, but the problem is there and will stay there if nobody's solved it.
Most people think about cutting back on work when they reach seventy. Did you miss out on anything by carrying on in your nineties?
I stayed working because I was enjoying it, and it was all voluntary. lt became obvious early on that we had hit on something that was going to take more than a lifetime to resolve. It wasn't just the radiation thing that interested me. I was really interested in where the other cancers were coming from. You need to follow it for a long time.
Who will carry on your fight in the radiation debate?
I've got a voice in the next generation in Steve Wing and his department at the University of North Carolina at Chapel Hill. Mind you, they're going to make life difficult for them, with grants and everything. People in the nuclear industry will do their very best to stop it. But I'm a great believer that in the end, they'll get caught up in their own machinations and the truth will emerge from an unexpected quarter.
Further reading: "A bomb survivors: factors that may lead to a re-assessment of the radiation hazard", lntemational Journal of Epidemiology, volume 29, no 4 (4 August 2000)
The Woman Who Knew Too Much by Gayle Greene, University of Michigan Press, E1 9-99, ISBN 0472111078
Cloning without embryos NS 29 Jan 2000
IT'S the acceptable face of human cloning: creating new cells and tissues to replace those lost to disease. But even the prospect of this "therapeutic cloning" has a troubling side. Every time a patient is treated, a cloned human embryo would be destroyed-a tiny ball of cells admittedly, but a potential human life nonetheless. Now a company linked to the team that created Dolly the sheep plans to overcome this ethical obstacle by removing the embryo step. It claims already to have promising results. And the technique wouldn't need to use human egg cel6, whidi are scarce and in demand for IVF patients. Therapeutic cloning could revolutionise the treatment of conditions such as Parkinson's disease. Doctors would take a healthy cell from the patient and fuse it with a human egg stripped of its own chromosomes to create a cloned embryo. A few days later, when the embryo has grown in a culture dish into a ball of cells called a blastocyst, they would remove the embryonic stem cells, which can develop into any of the body's tissues. Once biologists have discovered the triggers that will persuade stem cells to turn into the brain cells a Parkinson's patient needs, it should be possible to grow cells that are a perfect match for each patient. But Geron BioMed, a company launched by the team that cloned Dolly at the Roslin Institute near Edinburgh, is now working on cloning techniques that dispense with human eggs. In conventional cloning, the gutted egg reprograms the genes of the donor cell, winding back their developmental clock. But Simon Best, Geron BioMed's managing director, thinks it will be possible to achieve this trick using embryonic stem cells, rather than eggs. In this case, the reprogrammed cells wouldn't form an embryo, but instead develop directly into the cells or tissues the patient needs. Ardent pro-life groups may still object to scientists using embryonic stem cells because they are derived from a human embryo. But it would greatly reduce the number of embryos sacrificed, because limitless supplies of embryonic stem cells can be grown in culture. Significantly, British patents on cloning awarded to the Roslin team last week are worded to include the new technique. Rather than specifying eggs, the patents describe the fusion of a donor cell with "a suitable rer-ipient cell". The research that inspired Geron BioMed's new approach was published with little fanfare around the time that Dolly arrived on the scene. In 1997, researchers led by Azim Surani of the Wellcome/ CRC Institute of Cancer Research and Developmental Biology in., Cambridge revealed in The EMBO journal (vol 16, p 6510) that they had merged mouse thymocytes, a type of white blood cell, with mouse embryonic germ cells-stem cells that ultimately develop into sperm or eggs. After each merger, the white blood cell's genetic slate was unexpectedly wiped clean. What's more, the resulting hybrid cells could develop into a wide variety of different tissues, just like embryonic stem cans. Surani has agreed to collaborate with Geron BioMed, but warns of difficulties using the Dolly technique on stem cells instead of eggs. To obtain cells and tissues that match a patient, you would need to fuse one of the patient's cells with a gutted embryonic stem cell. Surani fears that, unlike eggs, gutted stem cells won't make all the substances needed for reprogramming. But Best remains optimistic. 'We're trying it with mouse cells and sheep cells. We have some completely novel ideas which we can't disclose now. Once we confirm the hypothesis in sheep, we might be able to try it in people three years later." If so, Geron BioMed would be in pole position to exploit therapeutic cloning. Its parent company, Geron of Menlo Park, Califomia, has an exclusive licence to commercialise human embryonic stem cell technology. Andy Coghlan
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