The 2.8-volt battery generates a constant electrical current of 50 microamps.
This is conducted across the cervix by mucus or seminal fluid, immobilising
sperm in three to four minutes, according to researchers at the Women’s
Medical Pavilion in New York who developed the device. They believe the
current will prevent the sperm passing through the cervix and fertilising
the ovum: their in vitro studies have shown that 100 per cent of sperm are
stopped in their tracks by this level of current, and studies in baboons
seem to back up the findings.

The batteries are a modified form of a pacemaker. However, while a pacemaker
lasts for up to 10 years, the contraceptive batteries run out after a year.

Steven Kaali, medical director of the Women’s Medical Pavilion, says
human trials lasting years would be necessary before the device could be
used. However, several pharmaceuticals companies are already keen to carry
out further research and development. ‘Everyone believes in their own invention
– I think this is the best thing ever to happen to women, but the proof
will come from the R&D stages,’ said Kaali.

He believes that the device will have few side effects: there have been
no reports of problems such as burns or chemical changes in people who wear
pacemakers. An electrical current may also kill bacteria and fungi, and
he hopes that contraceptives incorporating the battery could cut down the
risk of sexually transmitted diseases.

Doctors specialising in family planning are still wary of the device,
however. Robin Foldesy, a director of Family Health International, which
does research on new contraceptives, said: ‘This is totally novel and anything
is possible. In this field we need some new and refreshing ideas, but whether
this device is a possibility, I can’t yet say.’

When a person develops Alzheimer’s disease, nerves in the central nervous
system degenerate, resulting in distinctive features in the brain known
as plaques and tangles. But research into the treatment of the disease has
been paralysed by the lack of a diagnostic test: the cells of the central
nervous system are inaccessible.

At present, changes due to Alzheimer’s can be detected only by a brain
autopsy once the person is dead. In living patients, Alzheimer’s is diagnosed
by assessing the level of dementia, and by a brain scan, procedures that
may not be accurate.

Last year, however, Barbara Talamo and her colleagues at a number of
institutes, including Tufts Medical School and the New England Medical Center,
both in Boston, Massachusetts, made the discovery that Alzheimer’s disease
has a noticeable effect on the neurons in nasal tissue. It changes their
shape, their distribution, and the relative abundance of proteins they contain.
The researchers suggested that it would be possible to remove tissue from
a patient easily, under a general or even a local anaesthetic.

Lynne Mayne and her colleagues at Sussex University’s Trafford Centre
for Medical Research are starting a community study on a much larger scale
than the research programme in the US: they expect to study several tens
of patients a year, rather than the nine of the American study. They will
take a sample of nasal tissue from any Alzheimer’s patient who is undergoing
surgery, for any reason.

The researchers are also asking patients or their relatives to allow
them to take a sample of nasal tissue within hours of a patient’s death.
Speed is important because nerve cells degenerate very quickly. GPs will
be asked to take a nasal sample from any patient with Alzheimer’s who dies.

Mayne and her colleagues intend to compare the nasal tissue with brain
tissue, and with similar samples taken from healthy people. They want to
find out whether people with Alzheimer’s can be distinguished from those
with other forms of dementia by their nasal tissue alone.

The sensory neurons high up in the nose are unique among nerve cells
because they regenerate throughout adult life. They are also the only cells
of the central nervous system that can be sampled during life.

If a test can be developed, it will be important because current methods
of diagnosing Alzheimer’s disease are not accurate enough to assess the
potential of possible drugs. Another drawback is that it is impossible to
diagnose the disease until it is well advanced, when damage may be too extensive
for treatment by potential drugs.

According to Mayne, people coming to their doctors for the first time
with symptoms usually have problems with coordination. By then, a large
number of neurons have been lost. ‘The value of a diagnostic test,’ says
Mayne, ‘is that it could pick up the disease before the neurons have been
±ô´Ç²õ³Ù.’

Mayne and Ruth Maxwell at the Trafford Centre hope to grow cells of
the central nervous system from healthy people and people with Alzheimer’s
in culture. Under controlled in vitro surroundings, they then intend to
subject the cells to a battery of environmental influences – such as aluminium
in water – which have been linked with the genesis of Alzheimer’s disease.
They hope that this will allow them to examine the way the neurons degenerate
more systematically.

Most researchers agree that nasal tissue could yield more information
about Alzheimer’s disease. But some believe that it is not the best practical
test in the pipeline. Gordon Wilcock, of the University of Bristol, a founder
of the Alzheimer’s Disease Society, says ‘I think patients will be much
happier to have their skin biopsied than their noses,’ says Wilcock. ‘I
have a feeling that the epithelial story is very interesting and may be
a useful tool for research, but it’s less likely to have major practical
¾±³¾±è±ô¾±³¦²¹³Ù¾±´Ç²Ô²õ.’

The iron lung lost popularity because of technical problems. The collar
which sealed the chamber around the patient’s neck was often uncomfortable
or badly fitting. It was difficult to check whether a baby was becoming
too cold inside the chamber, and there was no way of gaining access to the
baby without opening the chamber.

Since the 1960s, doctors have ventilated babies who cannot breathe unaided
by pushing oxygen into the lungs through tubes, a process called intubation.
This proved to be better than the iron lung, but intubation has drawbacks.
There is a risk of infection, it can damage the lungs, and it may mean less
oxygen is actually picked up by the blood because the extra pressure needed
to force air into the lungs reduces the blood flow through the lungs so
there is less effective uptake of oxygen.

Doctors at the Brompton Hospital have now developed a deluxe version
of the iron lung which could give the old idea a new lease of life. The
baby is laid in the perspex box with only its head poking out. A soft latex
neck seal makes the chamber airtight, but is not so tight that it chokes
the baby.

An electric fan sucks air from the chamber through a valve which keeps
the pressure in the box at a baseline level slightly lower than atmospheric
pressure. A second valve opens intermittently and draws out more air, reducing
the pressure still further. When this happens, air rushes into the baby’s
mouth and nose, which are at atmospheric pressure, and expands the lungs.
When the second valve shuts, the pressure in the box rises again, the lungs
contract and push the air out.

There is an adjustable time setting to dictate the breathing pace, and
a safety valve to ensure the pressure stays within safe limits. Armholes
with foam gaskets which seal around the arms give access to the baby. A
heater stops it becoming too cold.

The chambers are only now being systematically assessed in comparison
with conventional breathing supports in a trial at two British hospitals.
Twenty-two babies have been treated in the trial so far. The doctors who
developed the technique are convinced that it is a safer and better option.
Intubation means the baby has to be cared for in intensive care, but babies
using the chamber may be looked after in an ordinary ward, or even be taken
home.

Since its development, the technique’s inventors have used it on 140
children ranging in age from premature babies born at 25 weeks to 2-year-old
children.

Martin Samuels, a lecturer in paediatrics at the Brompton Hospital,
said: ‘We feel it’s appropriate to use in any situation, but because our
experience is still limited, we’ve used it where children are deteriorating
in spite of traditional treatment. We found that it has made a difference
where other methods have not.’

Although the success of the chambers will not be proven until the results
of the comparative trial are known, there have already been requests from
centres overseas which are interested in buying systems.

Neurologists at the University of Tennessee intend to transplant normal
human muscle cells into a small muscle in one foot of each of the children.
The team hopes that the cell transplants will ‘take’ and start producing
dystrophin, the substance that is missing from the bodies of sufferers because
they lack the gene to make it.

Doctors do not yet understand how dystrophin works in maintaining a
muscle and allowing it to regenerate: muscle strength can be maintained
for years in children who have no dystrophin but, without it, muscle deterioration
is eventually inevitable.

The children in the Tennessee experiment, who are aged between six and
10 years old, will be matched with suitable donors – usually siblings –
who will have a sample of muscle tissue removed to obtain the cells, called
myoblasts. Those cells will be cultured for three to four weeks in a laboratory,
then injected into the foot muscles of the children. The children will receive
immunosuppressive drugs to prevent them from rejecting the transplants.
The team will then monitor the survival and development of the donor cells
and the function of the treated muscle compared with the same muscle in
the other foot.

Peter Law, the team leader at the University of Tennessee, stresses
that even if the experimental implants do result in anincrease in dystrophin
production, the technique is in no sense a treatment for the children, because
the injected muscle is so small and insignificant. But if they can demonstrate
that the technique improves the muscles’ function, doctors are hopeful that
sufferers could receive transplants of dystrophin-producing myoblasts into
muscles all over the body. This should postpone the muscle wasting which
leads to immobility.

Many sufferers from muscular dystrophy die as a result of failure of
the respiratory muscles. Doctors hope that transplantsinto some of these
muscles could extendpatients’ lives by some five to 10 years untilthe disease
affects their hearts.

‘We have to tell the children and parents that this is not a treatment
yet,’ said Law. ‘But we hope that five years from now we will be able to
produce good use of all of the skeletal muscles in order to allow them to
function almost, if not totally, normally.’

Researchers in Britain are less euphoric about the possibilities of
success, however. Law has received approval for the experiments from his
university’s ethical committee. But in Britain, there could be some difficulty
in obtaining approval for giving an immunosuppressive drug to children,
leaving them more prone to infection, without being able to offer them any
individual benefit from the experiment.

So far, Law and other researchers have restricted their use of the technique
to mice. Terry Partridge of the Charing Cross and Westminster Medical School
believes that the technique is too unrefined and difficult to be attempted
in humans yet. Law has tested the theory for over a decade on mice that
have a disease which, while genetically different from human muscular dystrophy,
presents the same symptoms of muscle wasting.

Earlier this year, Partridge’s team announced their success in transplanting
myoblasts into a different kind of mouse with a genetic flaw identical to
the human condition. However, unlike humans, these mice do not show any
muscle weakness. Although they lack the gene to make dystrophin, and their
muscles degenerate, the tissues are also capable of regenerating to a greater
degree than in human sufferers. This suggests that mice are not the ideal
model for the human trials.

Another stumbling block is the matter of scale, he says: the human muscle,
a couple of centimetres long, is 20 times the size of the mouse muscles.
‘A mouse is 3000 times smaller than man, and you can’t transfer a technique
across that sort of size difference,’ said Partridge.

The transplanted cells would also have further to migrate from the injection
site in muscles the size of a human’s than in those of mice. In the studies
in mice, Partridge’s team was able to show that the transplanted cells do
synthesise new dystrophin in the right part of the muscle.

The Muscular Dystrophy Group, which funds research in Britain, is cautious
about the tests. Sarah Yeates, research manager for the group, said: ‘We
obviously want to see the outcome of the human experiments in the US, but
we’re very worried that the general public often seems to misinterpret the
nature of the experiments and believe that it is a cure. These are, literally,
experiments, and we have no idea what the results will be.’