A stroke occurs when a clot forms in a blood vessel in the brain or when a vessel ruptures and leaks blood. This causes brain cells to die. In about 20 per cent of stroke patients, the cell death happens in areas important for language and speaking.

Amphetamine boosts levels of noradrenaline, a neurotransmitter, which scientists think encourages new brain cell connections.

Lead researcher Dalaina Walker-Batson of Texas Woman’s University, Dallas, says that speech therapy also works by enhancing nerve growth and connections. She suspects that amphetamine speeds this process. “It’s not just the drug, it’s the drug paired with very focused practise,” she told New ĐÓ°ÉÔ­´´.

Eoin Redahan of the Stroke Association for England and Wales says: “To someone who retains their other mental abilities, it is extremely frustrating to know what you want to say but be unable to say it. This is an interesting study and any treatment that could potentially help stroke patients is worth developing further.”

Long-term improvement

The researchers gave 21 stroke victims either a placebo or an amphetamine called dexedrine half an hour before speech and language therapy. This took place twice a week for five weeks.

Seven days after the treatment stopped, the patients were asked to recognise and name objects, and speak, read and write simple sentences. Their performance was compared to what they could do before treatment.

Ten of the 12 amphetamine-treated subjects showed a high level of improvement, but only two of the nine placebo treated patients performed so well.

“We tested them again 180 days later and the differences were maintained and even increased,” Walker-Batson told New ĐÓ°ÉÔ­´´. “Now we need to explore the results in a larger number of patients.”

She points out that the low dose of amphetamine caused no side effects. But she warns that the drug is probably only useful if it is given within a certain window of time after the stroke. Exactly what that time window might be is not yet clear. “We have given it to a small number of chronic patients after six months and we did not get an effect,” she says.

Journal reference: Stroke (vol 32, p 2093)

Every time a strain of bacteria becomes resistant to an antibiotic, or a weed mutates so it can thrive after being sprayed with a herbicide, there is a financial cost to humankind, Stephen Palumbi points out. He estimates that cost to be at least $100 billion every year in the US alone.

“And that’s got to be an underestimate,” Palumbi told New ĐÓ°ÉÔ­´´. “We are paying a lot for these arms races.”

Decision-makers need to anticipate evolution and build it into public policy, he says.

Lord Robert May of the Royal Society, London agrees. “So many of the triumphialist claims that we can eradicate something like infectious disease could only be made by someone who didn’t appreciate the moving nature of the target,” he told New ĐÓ°ÉÔ­´´.

Last resort

Palumbi highlights several of the most costly results of human evolutionary pressure. The emergence of antibiotic-resistant strains of the bug Staphylococcus aureus, and the loss of crops due to herbicide and pesticide resistance are two key problems, he says.

But HIV is the fastest-evolving, says Palumbi. It evolves so quickly, it forms a new “quasi-species” inside every person it infects, he says.

He thinks humans must implement strategies to slow evolution down as a matter of urgency.

Interspersing the use of one herbicide with another is one option. Another ploy is to withhold a powerful treatment as a last resort, to prevent resistance developing.

Vancomycin, a powerful antibiotic, is now used as a treatment of last resort in many hospitals around the world. It is the only option for use against superbugs such as MRSA (methicillin-resistant S. aureus).

But although the principles of strategies to slow evolution are well known, Palumbi believes that they have been re-invented from scratch several times. “If they realised that other people had blazed that trail, it might be far easier,” he says.

“In the US more than half the people don’t believe in evolution. We have to train people about it – we can’t afford not to.”

The new study, using data from the San Francisco gay community, suggests that by 2005, at least 42 percent of HIV cases could be drug resistant. In 1997, the figure was less than five percent.

The researchers found that unprotected sex is unlikely to be the cause of an epidemic of drug resistant strains. Instead, resistance appears primarily to be caused by patients who are taking the drug cocktails not sticking to a strict pill-popping regime. Any deviation from the treatment programme can allow the virus the opportunity to replicate and develop resistance.

This presents a serious problem as the health of people infected with HIV has been vastly improved by the drugs. Resistant strains can multiply unchecked, suppressing their host’s immune system so that illness and death follow.

Stop before you start

“The emphasis needs to be on stopping drug resistance in the first place,” rather than preventing transmission of resistant strains, said lead researcher Sally Blower, from the AIDS Institute at the University of California, Los Angeles. She pointed out that doctors need to be as vigilant as patients in making sure correct treatment programmes are followed. She recommends creating specialist treatment centres for the disease.

The results have serious implications for developing countries, where it may be even more difficult to ensure medication is taken correctly.

“For resistance to occur you need the virus to evolve,” says HIV specialist Andrew Phillips from the Royal Free Hospital, London. He told New ĐÓ°ÉÔ­´´ that if patients follow an intensive regime that includes three different classes of drugs, the virus cannot replicate enough to evolve.

Resistant strains take hold when patients continue to take drugs that are unsuccessful at lowering the viral load. “If it evolves in the presence of drugs then it gets a chance to out compete the drug-sensitive virus,” says Phillips. This can be prevented if patients quickly switch to different drugs.

On target

The study predicted the transmission of drug-sensitive and drug-resistant cases of HIV between 1996 to 2005. The rate depended on the number of infections, the level of drug treatment and the rate at which resistant strains evolve within a person.

The study showed that if fewer people are treated for HIV, resistance will not become such a problem. However, not only is it unethical to withhold treatment, but treatment reduces the chance that the infection will be passed to a sexual partner. The researchers estimate that for every case of resistance caused by treatment, one other infection will be prevented.

Computer modelling tools are not perfect, says Phillips, because they rely on uncertain assumptions. But he adds that they are the only real tools we have for predicting the future of HIV.

The model predicted that 28.5 percent of HIV cases would be drug resistant in 1999, and this was almost exactly correct.

Journal reference: Nature Medicine (vol 7, p 1016)

A torrent swept through Lynmouth, Devon and remains the worst flood on record for the UK, drowning 35 people. “I’d never seen a sky that colour – yellowy, greeny, purple – it was uncanny,” one eye-witness said.

Government defence officials have always denied that cloud seeding experiments were carried out before 1955. But now documents have been unearthed showing that scientists had teamed up with the RAF to try to make rain in the week of the disaster.

De-classified War Office documents also suggest that the military had been interested in using rain to cause downpours to hamper enemy movements, clear fog from airfields, and even increase the fallout range of atomic weapons.

Control measures

The Lynmouth flood might serve as a warning to those seeking to coax rain from the skies today, but they claim to be able to control the amount of rain they produce.

“We use the latest technology in radar systems to tell us how much moisture is in the air, so we can figure out how much gel to disperse over the cloud formation,” says JD Dutton, President of Dyn-0-Mat, Florida, a company which makes gel-like flakes that have been used to seed clouds.

In the past 50 years, cloud seeding has been carried out in attempts to relieve drought and to encourage snowfall in ski resorts.

From droplet to drip

Rain making involves dropping material into clouds to encourage water vapour to coalesce into raindrops. In natural circumstances, water gathers around specks of dust or salt and forms ice crystals that attract other droplets, until they are heavy enough to fall.

The RAF is suspected of spraying salt, dry ice or silver iodide from aeroplanes. These compounds mimic the structure of ice, and droplets would condense around them.

But meteorologists from Reading University told New ĐÓ°ÉÔ­´´ that rain-making had very little credibility in the scientific community. Of the Lynmouth downpour, Brian Hoskins said: “I very much doubt that anyone was able to influence the cloud.”

Anthony Illingworth added: “The main problem is that because rainfall is so variable from day to day, it’s incredibly difficult to tell if you’ve done anything or not.”

In order to try and settle the matter, scientists from the British Geological Survey are now studying soil sediments from the Lynmouth area for traces of silver iodide.

The new evidence is presented in a BBC Radio 4 radio programme The Day They Made It Rain broadcast at 2000 BST on 30 August.

The information might help women estimate how long they will be fertile, according to Jan-Peter de Bruin at the Diakonessen Hospital, Utrecht, The Netherlands, who led the team. But knowing a mother’s menopause age provides only a rough guide, he cautions.

The team is now aiming to discover which genes control the onset of menopause. “There’s probably a lot of genes involved”, de Bruin told New ĐÓ°ÉÔ­´´. He hopes that a woman may one day be able to take a blood test that scans her genotype and reveals her expected age of menopause.

Roger Gosden, a reproductive endocrinologist at McGill University, Montreal, suspects that the effect is due to genes or gene polymorphisms that influence the size of the egg store laid down before birth.

Waste management

“The bigger the store, the later the menopause,” he says. He adds that it is also possible that genes influence the rate at which eggs are used up. Most eggs are wasted, rather than ovulated, he notes.

Slowing down this wastage would extend the lifetime of a woman’s ovaries, and this could be the eventual outcome of de Bruin’s research. If the menopause genes do promote egg wastage, they must do so by releasing proteins that could theoretically be blocked.

“We hope that one day we can get some drugs that delay the eggs leaving the pool,” de Bruin speculates.

Sets of sisters

In the study, post-menopausal sisters -118 twins and 243 non-twins – were asked how old they were when their menstrual cycles stopped. The results showed that the age of menopause was more similar between sisters, and that genetics are mainly responsible for it.

Previous studies have also shown that menopause age is dependent on genetics, but to a lesser extent. De Bruin suspects this resulted from non-random samples of the population.

Although the study indicates that the timing of menopause is largely out of a woman’s control, there are environmental factors that influence the timing of menopause. Smoking and short menstrual cycles bring it forward, and taking the contraceptive pill and having a lot of babies can delay it, according to de Bruin.

“Menopause just comes down to depletion of the follicle store (in the ovaries),” he explains.

Journal reference: Human Reproduction (vol 16, p 2014)

But instead of settling the debate, the move has led to suggestions that some of the eligible lines could be useless for medical research.

Stem cell researchers in the US had been tentatively lauding their government for agreeing to fund their work in some form. But in order to prevent human embryos being destroyed while harvesting the cells, the funding is only available for lines of cells created before 9 August 2001. President Bush pinned his decision on the existence of around 60 such lines.

ĐÓ°ÉÔ­´´s were sceptical that so many lines exist and are concerned that access to a restricted number of stem cell lines might limit the quality of research. “You have to replicate your results with other cell lines,” says stem cell researcher Maeve Caldwell at Cambridge University. “It’s fundamental that they all behave the same.”

Crossed lines

The 64 lines named on the NIH website come from countries around the world, including India, Australia and Sweden (see below). But even scientists from the named institutes have raised doubts that all their lines are viable.

A spokesperson for the team at Göteborg University in Sweden admitted surprise that they were listed by the NIH as having 19 lines. “Maybe they misinterpreted a bit”, he told the Washington Post. Of the 19 batches they had, he classed at most three of them as stem cell lines.

The San Diego and Mumbai-based laboratories also expressed doubt that all their lines will be usable.

Data drought

Stem cells are harvested from young embryos and then multiplied in culture. Ideally, they keep dividing indefinitely to provide cells that can develop into any type of body tissue.

Much of the federally funded research will be aimed at using them to replace diseased or damaged cells in people. But not all of the lines included on the NIH list have been shown to be able to divide indefinitely, or to be pluripotent – that is, able to develop into many different tissues.

Some of the uncertainty may be dispersed when the human embryonic stem cell registry promised by the NIH is launched. Details such as how well the cell lines divide and the molecular markers of their pluripotency will be provided – but only at the discretion of the investigators who derived the lines. “It may not be enough information for the scientific community to use”, says Caldwell.

Stem cell line owners reported to NIH (number of lines)

BresaGen, Athens, Georgia (4)

CyThera, San Diego, California (9)

Karolinska Institute, Stockholm, Sweden (5)

Monash University, Melbourne, Australia (6)

National Center for Biological Sciences, Bangalore, India (3)

Reliance Life Sciences, Mumbai, India (7)

Technion-Israel Institute of Technology, Haifa, Israel (4)

University of California, San Francisco, California (2)

Göteborg University, Göteborg, Sweden (19)

Wisconsin Alumni Research Foundation, Madison, Wisconsin (5)

Catnip is one of several plants used in folk medicine to ward off insects, but most people turn to DEET when they want serious deterrence. Now researchers at Iowa State University, Ames, have shown that a relatively weak solution of catnip extract repels mosquitoes as effectively as a DEET solution ten times more concentrated.

To test the effect, they put groups of 20 mosquitoes in a glass tube which had filter paper in one end treated with either a catnip extract or DEET. Ten minutes later, just over half the insects remained at the end containing DEET-treated paper. In contrast, an average of only 25 per cent remained closer to paper treated with the most potent catnip compound, a monoterpene called nepetalactone.

“Essential oils of plants have huge potential for insect control”, according to entomologist Joel Coats, who was part of the Iowa team. “And they are very safe for mammalian use.”

The team has previously shown that nepetalactone repels flies and cockroaches. They are applying to patent the compound as a repellant, and hope to register it as a biopesticide with the US Environmental Protection Agency (EPA).

Highly volatile

“We haven’t yet tested whether it will work against mosquitoes when on human skin,” says Coats. “But our results are directly relevant to repellency on things like clothing and tents.”

However, the duration of the effect is crucial, according to Jose Ribeiro, a medical entomologist of the US National Institute of Health, Bethesda. “To have a smell things have to vaporise, but if they vaporise too fast the effect is lost”, he explains.

DEET is known to have a long-lasting effect and Coats admits that nepetalactone is more volatile than DEET. “That is something that can be worked on in a slow-release formula”, he says.

“Anything that is as good or better than DEET is welcome, because DEET has some side effects”, says Ribeiro. DEET is classified as “moderately toxic” by the EPA and can harm birds, fish and aquatic invertebrates. However, the EPA believes it does not present a health concern to the general US population.

In the tests, elderly female patients wearing skin patches that released oestradiol scored higher in tests of attention and recent verbal and visual memory than women wearing placebo patches. Before the trial, scores had been the same between groups. Depending on the test, the performance of the hormone-treated women was up to 35 percent higher.

“Any improvement in the disease is very welcome to these patients and their families”, says Sanjay Asthana, who led the study at the Veterans Affairs Puget Sound Health Care System, Tacoma.

“We used oestradiol, the most potent form of oestrogen”, Asthana told New ĐÓ°ÉÔ­´´. They also used double the standard dose.

Nerve growth

Oestrogen has failed to improve memory at all in other studies of Alzheimer’s patients, and Asthana suspects that the high level of the potent form that his patients received was crucial to the positive results.

Richard Harvey, Director of Research at the UK Alzheimer’s Society, is optimistic about the use of oestrogen. But he reserved final judgement due to the small size of the study, which followed 20 women for eight weeks.

“The current drugs for the disease have a definite place to play, but are definitely limited”, he says. “Anything that gives us a further effect would be a definite advance.”

Asthana speculates that the effect may be due to stimulation of nerve growth in the brain. He is planning a larger scale study using oestradiol.

Journal reference: Neurology (vol 57, p 605)

In an effort to fight the notorious food-poisoning bacterium Salmonella, Audrey McElroy of Virginia Tech University, Blacksburg, fed chickens with capsaicin, the chemical that gives chilli its bite.

The birds were then dosed with Salmonella enteritidis. The hot food reduced the number of birds with the germs in their internal organs by almost half compared to a normally-fed group.

Fortunately for those averse to spicy food, a taste panel found that the chilli flavour did not end up in the meat.

Taste deterrent

Research reported in July 2001 suggests that the chilli’s fiery taste deters creatures who are poor at dispersing the plant’s seeds. Fortunately for the poultry industry, this does not include birds. “Birds appear not to have the receptors to the hot pungent part of the peppers”, says McElroy. “It appears not to affect them in any way.”

The chickens did get inflamed intestines, however, and this is the main clue to how the spice might be working.

“Is it causing just a mild influx of immune cells that allows the bird to fight off the infection, or does it change the binding sites so the Salmonella passes through the birds?”, wonders McElroy.

Antibiotic alternative

There is evidence that feeding antibiotics to poultry leads to the emergence of antibiotic resistant bacteria. The practice is still the norm in Britain and the US, but McElroy believes that her findings could be more important in the future because of the push to get rid of antibiotics in poultry.

But Richard Young of the UK Soil Association, which promotes organic farming, urges caution. He says killing off one set of bugs could make way for another.

“One would want to be convinced that in using a product like this to reduce Salmonella they’re not simply leaving the way open for other food poisoning bacteria,” he told New ĐÓ°ÉÔ­´´.