Features

Half the elephants from West and Central African savannahs have vanished in the past 40 years, scientists report in PLoS One.

A team, including Iain Douglas-Hamilton of Oxford University’s Department of Zoology, estimate that around 7,750 elephants remain in the Sudano-Sahelian zone, which covers 20% of the continent, a 50% decline in four decades.

Of the 23 elephant populations studied half are now thought to number fewer than 200 animals and so are unlikely to survive. The survey covered protected areas so populations in unprotected regions are likely to have fared even worse.

A reduction in rainfall and increasing competition with humans for land and water resources used for livestock and agriculture are, the researchers believe, the main factors behind the decline. Warfare and the illegal trade in ivory have also helped to drive some elephant populations to the brink of extinction.

The loss of these elephant populations would affect many other species which rely on the habitat created by these giant herbivores as they browse, clear the brush and disperse seeds.

To protect the remaining animals the researchers propose that eight new protective corridors be established as soon as possible to connect the main elephant populations.

They also recommend working with private sector wildlife initiatives and channelling more wildlife revenues to local communities as a way of securing the future for elephants on Africa’s northern savannahs.

The mechanisms used by the brain to distinguish contrasting sounds may be similar to those used to visually pick out a face in the crowd.

Scientists at Oxford University’s Department of Physiology, Anatomy and Genetics are studying the ways in which sound is represented in the brain and their latest research, published in the journal Neuron, looks at how the brain’s nerve cells respond to sounds heard under different conditions.

The study, carried out by Neil Rabinowitz, Ben Willmore, Jan Schnupp and Andrew King, shows that neurons in the auditory cortex of the ferret's brain adjust their activity to compensate for the contrast between a sound and its background. Examples in human terms could be situations where the underlying environment is silent or very quiet - such as the countryside at night - or very loud, as in a busy pub or high street.

This is known as contrast gain control, a mechanism that our visual systems are thought to use to help focus attention on a particular object. Professor King says: ‘There could be a similar mechanism in the auditory system for picking out sounds of interest against a background of other sounds of different frequencies.’

The research is contributing to the efforts of Professor King’s group to unravel the way the brain processes sound. ‘Auditory scenes around us are changing all the time. We are interested in how our experience of this influences the way information is processed in the brain, and whether that helps to maintain a reliable perception of where and what a sound is under different listening conditions.’

These findings could have significance for our understanding of how the brain compensates for partial loss of hearing and, in time, have implications for the development of cochlear implants and hearing aids.

‘For cochlear implants and hearing aids to work the brain must be able to re-learn how to interpret sounds that have been restored,’ Professor King explains.

Professor King and his team have already shown that the brain can compensate for partial hearing loss. In research published last year, human subjects wore an earplug in one ear and were asked to identify which of several speakers was producing a sound.

‘Our ability to place sound relies on the comparison of signals between our two ears and when tested, when the earplug was first worn, subjects were very poor at locating the sound. But with practice several times a day for a week they re-learnt how to localise the sounds and once again became very accurate. In other words although the inputs received by the brain had changed, by practising the task, the study showed that we can recover from partial hearing loss.’

Professor King and colleagues are working closely with clinicians and with the hearing charities Deafness Research UK and Action on Hearing Loss (RNID), which aim to help those suffering hearing loss.

‘We hope our work will lead to improvements in the design of devices aimed at restoring hearing. Being aware of the plasticity or adaptability of the brain is important in understanding our ability to respond to hearing loss.’

Back in World War II there was a clever idea to use icebergs as floating aircraft carriers, but now we know birds of prey got there first.

A recent study that tracked the seasonal movements of 48 gyrfalcons with radio transmitters showed that some birds spent most of the winter over the ocean, probably using sea ice and icebergs as floating bases to hunt from.

A report of the research is published in the journal Ibis.

Kurt Burnham, who led the research whilst at Oxford University’s Edward Grey Institute and now runs the High Arctic Institute, told Matt Walker at BBC Nature:
‘I was very surprised by this finding… These birds are not moving between land masses, but actually using the ice floes or pack ice as winter habitat for extended periods of time.'

It’s almost unheard of for a land-based predatory bird to behave in this way, the only other example is the Snowy Owl, which is known to spend up to three months living on sea ice. An abundance of prey such as gulls, black guillemots, and sea ducks are believed to tempt the gyrfalcons into adopting this unusual lifestyle.

‘In the big picture this shows how adaptable and mobile gyrfalcons have to be in order to survive and reproduce in the harsh arctic environment they live in,’ Kurt comments.

The Edward Grey Institute is part of Oxford University's Department of Zoology.

The MHC on the short arm of chromosome 6 is the most gene-dense region of our DNA with around 230 genes all crammed into this stretch of our genome.

The MHC, or major histocompatibility complex, is known to play a pivotal role in our immune system, and around a third of the genes encoded there are known to have immune functions (the functions of all the genes are not known as yet, so it could be more).

So it’s not surprising that DNA variations in this region have been linked to many autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, and coeliac disease. But the MHC has also been linked to diseases not related to the immune system, including breast cancer, asthma, infectious diseases and the adverse effects of certain drugs. It’s the genetic region with the largest number of diseases associations, period.

But finding a genetic link to a condition is one thing. Determining the specific DNA changes that cause the increased risk of disease is another.

‘It’s a long-standing problem,’ according to Dr Julian Knight of the Wellcome Trust Centre for Human Genetics [WTCHG] at Oxford University, and it’s a problem that is particularly testing in the MHC.

The reason is that large lengths of DNA in the MHC, including whole lines of genes, tend to get inherited together. So people end up grouped with whole sets of DNA variations in common.

Because this co-inheritance of variations, or ‘linkage disequilibrium’, is particularly strong in the MHC, it is very difficult to unpick what lies behind any one DNA change linked with a disease. It could be something to do with that particular gene that is having an effect, or it could be another of the many genes closely coupled to it.

Then there is the problem of defining at what level the change in DNA might be acting. The body has many layers of control to make sure genes are only active in the right places and in the right amounts.

The central process is the same of course – a DNA sequence is read out into RNA code, from which proteins are produced – but at each stage there are checks and balances to make sure each gene and its products are working at the right level to keep the biological processes they encode ticking over.

Perhaps a DNA change might alter the structure of a protein encoded by a gene, but it may also alter the activity of that gene or another it controls. It could turn a gene on or off like a switch, turn its activity up or down like a volume dial, or change the final form of the protein that is produced.

Claire Vandiedonck, Julian Knight and colleagues set out to probe some of these possibilities by investigating how sets of co-inherited DNA variants in the MHC might lead to changes in ‘gene expression’.

Controlling gene expression – the amount of RNA produced from a gene – is a way of turning up and down the gene’s activity.

The researchers mapped gene expression across the MHC for three common sets of coinherited DNA variants people can have that are known to be associated with disease. Their results were recently published in the journal Genome Research.

To do this they had to design and construct their own custom DNA chip to be able to deal with the sequence variety in the MHC region. ‘We just couldn’t take an off-the-shelf microarray to get these results,’ Julian explains.

They found that the set of variants you have in the MHC does lead to differences in gene expression, and this was a common effect. 96 out of 230 genes in the MHC showed differences in expression.

‘There were a lot more differences in gene expression that we might have guessed,’ says Julian. ‘There was also a great deal of expression from areas of DNA in between genes; a third of the RNAs produced come from outside of known genes.'

It’s likely that these are non-protein-coding RNAs. That is, these bits of DNA sequence are read off to produce RNA. But no protein is then made from the RNA sequence.

It’s been gradually recognised over the past decade and more that noncoding RNAs play an important role in regulating gene activity – it’s another layer of control to the action of our genes. This study may offer an indication of just how important these RNAs are in regulating genes in the MHC.

The researchers also found a lot more ‘alternative splicing’ in the MHC than happens in other regions of our genome.

Alternative splicing describes a process where the same initial piece of RNA produced from a single gene is cut up and stuck back together in different ways to give different proteins. The result is shorter and longer proteins, potentially carrying out different roles in the cell.

‘The greater alternative splicing in the MHC will mean a greater diversity in the proteins produced from the DNA sequence,’ explains Julian. ‘It increases the diversity of a region that already has the greatest number of possible gene variants.’

But most importantly, pinpointing where gene expression differs could identify a set of candidates for which genes are causing increased risk of some autoimmune diseases. That’s what this study takes a step towards. These candidate genes can then be looked at in more detail.

‘We now have a route map of gene expression in the MHC that can help us understand what lies behind gene associations with various common diseases,’ Julian adds. ‘These findings have underlined the fact that we need to understand gene regulation as well as DNA sequence.’

He predicts that there will be many more of these studies in the future, as geneticists move on to unpick what lies behind genes known to be connected to many common diseases.

It seems that finding connections between DNA sequence and common conditions is one thing, but understanding how they are connected will involve investigating the many different levels of gene control and regulation there are in the body.

We’ll need to expand our knowledge of how our sequence of DNA letters is read out in organised phrases, sentences and whole paragraphs to really get the language of genetics and what it means for us. Expect stories about our genetics to get more complex before they get clearer.

It was on 1 January 1995 that a wave over 25 metres high was recorded at the Draupner platform in the North Sea off the coast of Norway.

Ever since researchers have been attempting to understand the mechanisms which produced the ‘Draupner wave’ and are responsible for other abnormally large or ‘freak’ waves.

In Proceedings of the Royal Society A this week Thomas Adcock and Paul Taylor of Oxford University’s Department of Engineering Science report that their new analysis may have the answers.

I asked Thomas about giant waves, predictions and The Poseidon Adventure…

OxSciBlog: How have people explained freak waves in the past?
Thomas Adcock: Freak waves will occur when the crests of many small waves come together to form a large wave. The random nature of waves means that this will occasionally happen – we are interested in any mechanism which will enhance this focusing.

Waves may be steered, either by currents (for instance, off South Africa) or by the sea-bed (such as near Hawaii), to produce abnormal waves. If all the waves are all moving in the same direction, then complex non-linear interactions can produce wave focusing. However, real ocean waves never all move in quite the same direction and it is a point of contention as to whether this really causes freak waves at sea.

OSB: Why is the Draupner wave interesting to study?
TA: The Draupner wave is one of few (possibly the only) instance of a high quality measurement of a freak wave in deep water. None of the mechanisms we discussed seem responsible for producing this wave.

One interesting feature is that under a large wave we expect to see a small but long and low depression (up to 1m deep) under a large wave group. Dan Walker, when a DPhil student in Oxford, found that the opposite was true for the Draupner wave. This confirms that there was something unusual about this wave.

OSB: What clues does it give to how freak waves form?
TA: The occurrence of the long low rise rather than a depression for the Draupner wave leads us to suggest the giant wave is the sum of two wave groups that were travelling at roughly right angles through each other. Mariners know that crossing sea-states are very unpleasant for the crew and potentially dangerous for ships – the wave which hit the Queen Mary in World War II, and which inspired the film The Poseidon Adventure, occurred in a crossing sea.

The idea for this paper was inspired by watching this video showing an unusual wave hitting a ship from the side. We began to think what would the consequences be if this was how the Draupner wave formed – and we realised this would explain the features which had been puzzling people about the wave.

OSB: How might your findings help to predict/mitigate their impact?
TA: Engineers and scientists are quite good at forecasting the general sea-state; Radio 4 long wave listeners will be familiar with the shipping forecast. If we can identify in which sea-states freak waves are likely then we can use this in design. For instance, if we forecast a storm in which freak waves are likely then we could route a ship around the storm.

OSB: What further research is needed in this area?
TA: Whilst scientists understand the basic features of most sea-states fairly well, we do not really understand at a local level the physics when a sea-state changes rapidly – for example if the wind suddenly starts blowing in a different direction. What we really need is far more high quality measurements of individual large waves – without this we cannot know whether our theories are right.

Dr Thomas Adcock and Professor Paul Taylor are based at Oxford University's Department of Engineering Science.