More than 100 different BRCA1 mutations have been identified. The mutations are scattered along the length of the gene, in different positions depending on the family. Affected families fall into two categories of roughly equal size: those with breast cancer alone and those with both types of cancer.

Simon Gayther of the Cancer Research Campaign’s Human Genetics group in Cambridge and his colleagues looked in 32 affected families for a relationship between the position of BRCA1 mutations and the type of cancer they caused. In this month’s issue of Nature Genetics (vol 11, p 428), they say that mutations in the final third of the gene usually cause breast cancer alone. In families afflicted by both types of tumour, the mutations occur nearer the beginning.

No one knows which protein the BRCA1 gene makes, or how the nonmutated form of this undiscovered protein prevents cancer. The researchers say that the protein must still be able to perform its function in the ovary if the alteration in its sequence of amino acids occurs near the end. For some reason, however, the protein must be unable to prevent cancer in both breast and ovary if the defect occurs near the beginning of its sequence. “We’d like more data from other labs to confirm that this observation holds true,” says Gayther.

Eivind Thorling of the Danish Cancer Institute and Kjele Fredens from the University of Aarhus set out to study the effect of small increases in gravity on bone growth. They placed rats in gondolas inside a 3-metre centrifuge and spun them slowly to simulate the effect of increased gravity. During the experiment, however, they discovered that female rats which spent a week at forces up to 2.5 times Earth’s gravity – equivalent to spinning at 40 revolutions per minute – were lighter than their Earthbound peers (see Graph).

Turning their attention to this discovery, they put young rats into the centrifuge and compared their development with rats in stationary cages. Over 17 weeks, they increased the gravity in small increments from 1g to 2.5g.

During the week after each step, the female rats’ weights dropped a little and then stabilised at the lower level. If the rate of rotation was reduced by similar increments, the animals regained the lost weight. As gravity returned to normal, the rats’ weights converged with those of the control rats. Thorling and Fredens found a simple exponential relationship between loss of weight and increase in gravity. At forces above 2.5g the rats became uncomfortable and the relationship no longer held.

The Danes say that the weight loss did not seem to be due to any distress suffered by the spinning rats. Their behaviour was similar to that of rats in the stationary cages: they even mated and had normal pups. Thorling says the rats would not have felt dizzy or nauseous because the acceleration and deceleration were too gradual, they could not see out of the centrifuge and the cages were insulated from turbulence and draughts.

Life in high gravitational fields may demand more energy than normal, but this is unlikely to explain the weight loss. Past work has shown that when female rats (but not males) exercise more, their weight does not fall. They simply eat more to compensate.

But the spinning rats did not do this. They ate less during their first week in the higher gravitational field. And although they regained their appetites, they did not put the extra weight back on until gravity was reduced.

In the latest issue of Obesity, Thorling and Fredens speculate that the bones, muscles and joints in the rats’ legs do not “feel right” in the new gravitational field, and somehow this information feeds into the limbic system of the brain where appetite is controlled. Thorling is now looking for changes in the levels of hormones that might convey this information around the body.

Does this mean new hope for frustrated dieters? Thorling says he has no plans to scale up the centrifuge for human use. But the findings may explain why people who spend much of their time sitting down gain weight. If these people put on weight simply because they exercise less, their appetites should adjust and they should eat less. “This is just a guess,” says Thorling, “but maybe if our theories are correct, that information about appetite comes from the bones, joints and muscles of the legs, then depriving them of these impulses may give them a tendency to gain weight.”

T lymphocytes, immune cells which circulate in the blood, must migrate across the walls of blood vessels in order to reach inflamed tissue. Much is known about how these cells pass through vascular walls, but the controls that operate once they get to the other side are less well understood.

When T cells encounter specific antigens, molecules which provoke an immune response, they start to produce large amounts of heparanase. This enzyme breaks down heparan sulphate, a major component of the dense complex substance known as the “extracellular matrix” that binds and stabilises tissues and blood vessels. This allows the T cells to penetrate the matrix and reach sites of inflammation.

Now it appears that the action of the enzyme is “switched” on and off depending on the pH of tissues. Dalia Gilat at the Weizmann Institute of Science in Rehovot, working with colleagues there and at Hadassah-Hebrew University Hospital in Jerusalem, found that heparanase functions as an enzyme only at low pH levels (Journal of Experimental Medicine, vol 181, p 1929). Acidic conditions are found in inflamed tissue and in growing tumours that are beginning to spread to other sites in the body. The pH in these tissues is around 6.8 because oxygen levels are low, causing carbon dioxide and lactic acid to accumulate.

At the higher pH of normal tissues (around 7.2), however, heparanase was found to function in an entirely different way. It binds to heparan sulphate without degrading it, and also binds to proteins on the surfaces of T cells. This anchors T cells in the extracellular matrix, stopping them invading normal tissue.

Most literate mothers learnt to read in primary school, and the fact that a women has had an education may simply indicate her family’s wealth or that it values its children more highly. Now a long-term study carried out in Nicaragua has eliminated these factors by showing that teaching reading to poor adult women, who would otherwise have remained illiterate, has a direct effect on their children’s health and survival.

In 1979, the Somoza family that had ruled Nicaragua for half a century was overthrown by a Marxist group called the Sandinistas. The new government established a number of popular reforms and social programmes, including the National Literacy Crusade (the Cruzada Nacional de Alfabetizacion). The literacy crusade and a follow-up literacy programme were sponsored by the Nicaraguan government, UNESCO and the US Agency for International Development. By 1985, about 300 000 illiterate adults from all over the country, many of whom had never attended primary school, had learnt how to read, write and use numbers.

Researchers from the Liverpool School of Tropical Medicine, the Central American Institute of Health in Nicaragua, the National Autonomous University of Nicaragua and the Costa Rican Institute of Health interviewed nearly three thousand women, some of whom had learnt to read as children, some during the literacy crusade and some who had never learnt at all.

The women were asked how many children they had given birth to and how many of them had died in infancy. The research teams also examined the surviving children to find out how well nourished they were.

The investigators’ findings were striking. In the late 1970s, the infant mortality rate for the children of illiterate mothers was around 110 deaths per thousand live births. At this point, those mothers who later learnt to read had a similar level of child mortality (105/1000). For women educated in primary school, the infant mortality rate was significantly lower, at 80 per thousand.

In 1985, after the literacy crusade had ended, the figures for those who remained illiterate and those educated in primary school remained more or less unchanged. For those women who learnt to read through the campaign, the infant mortality rate was 84 per thousand, an impressive 21 points lower than for those women who were still illiterate. The children of the newly literate mothers were also better nourished than those of women who could not read. The researchers describe their findings in the current issue of Population Studies.

In previous studies in more than forty countries, researchers have tried to unravel the various factors that might be at work by estimating, and then subtracting, the contribution of social status or economic circumstances.

In separate studies, the World Bank and the UN concluded independently that each year of a mother’s education significantly improved her children’s chances of survival. The Nicaraguan study is the first to demonstrate that educating women has a direct effect on their children’s health and that this has nothing to do with these other factors.

Why are the children of literate mothers better off? According to Peter Sandiford of the Liverpool School of Tropical Medicine, no one knows for certain. Child health was not on the curriculum during the women’s lessons, so he and his colleagues are looking at other factors. They are working with the same group of three thousand women, to try to find out whether reading mothers make better use of hospitals and clinics, opt for smaller families, exert more control at home, learn modern childcare techniques more quickly or whether they merely have more respect for themselves and their children.

The Nicaraguan study may have important implications for governments and aid agencies that need to know where to direct their resources. Sandiford says that there is increasing evidence that female education, at any age, is “an important health intervention in its own right”. The results of the study lend support to the World Bank’s recommendation that education budgets in developing countries should be increased, not just to help their economies, but also to improve child health.

“We’ve known for a long time that maternal education is important,” says John Cleland of the London School of Hygiene and Tropical Medicine. “But the snag has been that even if we started educating girls today, we’d have to wait a generation for the payoff. The Nicaragua study suggests that we may be able to bypass that.”

Cleland says that the Nicaraguan literacy crusade was special in many ways, and similar campaigns elsewhere might not work as well. It is notoriously difficult to teach adults skills that do not have an immediate impact on their everyday lives, and many literacy campaigns in other countries have been much less successful.

Perhaps, the literacy crusade succeeded because it took place in a revolutionary context, says Cleland. “There was a mood of change and optimism in Nicaragua in the early 1980s. The crusade was part of a larger effort to bring a better life to the people.” The classes also had a strong political content. Replicating those conditions in other countries, in a nonpolitical way, will be a challenge for development workers (see Graph).

In future, doctors may use the test to help them decide whether women who have just had a tumour removed need further treatment with radiation or drugs.

Doctors treating cancer patients face the problem of judging how big a tumour is, how fast it is growing and whether it is responding to treatment. One way to do this is to measure certain chemicals in the blood. Tumours often produce unusual proteins and other molecules which vary in concentration as the tumour grows or regresses. For several years doctors have known that a protein called prostate-specific antigen is found in unusually large quantities in the blood of men with prostate cancer. Blood levels of PSA reflect the size of a prostate tumour, rising as it grows and falling as it responds to treatment.

But in a report due to appear in the May issue of Cancer Research, researchers at Toronto Hospital led by Eleftherios Diamandis, and researchers at the Jefferson Cancer Center in Philadelphia, say that PSA is not prostate-specific after all: it is also made by breast tumours. They have also found that patients with breast tumours containing high levels of PSA have a much better prognosis that those with low levels. This is because breast tumours make large amounts of PSA until the cancer cells begin to spread to other parts of the body. PSA levels then begin to fall.

According to Diamandis, this means that a doctor will be able to remove a tumour, test it for PSA and then decide what course of treatment to take next. If PSA levels in the tumour are high, the woman may need no further treatment. But if levels are low, the tumour may have spread so radiation or chemotherapy may be necessary.

The discovery of PSA in breast tumours has made researchers think again about the protein’s function. In the prostate gland, PSA functions as a protease enzyme, digesting other proteins. Before semen is ejaculated it consists of a thick gel. But during ejaculation the prostate releases PSA and other proteases which break down the proteins that form the gel, liquefying the semen so the sperm can move around.

But what is PSA doing in breast tumours? Diamandis and his team are uncertain, but they believe it may help control cell division. There are several ways in which a protease such as PSA might promote cell growth. Cells carry proteins on their surfaces that tell them to stop dividing when they become overcrowded, and PSA has been shown to digest these molecules. Another possibility is that PSA controls the activity of soluble molecules called growth factors which carry instructions telling cells whether or not to divide. For example, PSA is known to digest a protein that inactivates insulin-like growth factor 1, which stimulates the growth of breast cancer cells.

If either of these theories is correct, PSA may be directly involved in triggering the uncontrolled cell division that causes a breast tumour to grow. This means it may eventually be possible to treat the cancer by developing drugs which block PSA.

Two of the dead animals were juveniles, one was a sub-adult male and the fourth was an adult female. According to Annette Lanjouw of the International Gorilla Conservation Programme in Nairobi, Kenya, the poachers were probably after the female’s infant. “The female was lactating so that is the only plausible explanation,” she says.

Mountain gorillas rove through the forest in family groups and become aggressive if any member of the group is threatened. Poachers hunting an infant gorilla would probably have to kill several adults before they could capture the infant.

Only 600 mountain gorillas remain in the dense montane forests at the junction of Uganda, Zaire and Rwanda. Lanjouw believes the poachers probably intended to sell the infant to a wealthy buyer, but says it is not clear who such a buyer would be. There are no mountain gorillas in captivity today, at least none that anyone will admit to. Attempts to breed the gorillas in captivity have failed, and with such a small population left, wildlife biologists feel it is too risky to try again.

This is the first case of gorilla poaching in Bwindi for more than ten years. At one time such incidents were common, and there was a brisk trade in gorilla parts such as hands, heads and fur. But changes in public sentiment have made these artefacts unsaleable and governments have cracked down on poachers.

Lanjouw says that the poachers would have needed the cooperation and knowledge of people living in the villages around the park, and efforts to trace the poachers are focusing on those villages. Zairian and Rwandan border guards are also on the lookout for the missing infant.

The Ugandan government is trying to encourage people living near the park to protect the gorillas. Tourists from overseas pay the Uganda National Parks hundreds of thousands of dollars a year to see the gorillas. Under a new scheme, some of this money will fund local development projects such as hospitals and schools.