Bluetongue licks northern Europe

Bluetongue licks northern Europe

Research news and discovery ASHVIN MEHTA/ALAMY In brief– Bluetongue licks northern Europe Europe could catch a cold as Arctic waters get less salty...

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Research news and discovery


In brief– Bluetongue licks northern Europe

Europe could catch a cold as Arctic waters get less salty FISH accustomed to the salty water of the Arctic may have to think about finding a new home. As a result of global warming, the Arctic Ocean has been getting less salty over the past half century and the trend looks set to continue. The culprits are a massive increase in rainfall over the Arctic and faster melting of sea ice and glaciers. Bruce Peterson of the Marine Biological Laboratory in Woods Hole, Massachusetts, and his team gathered decades’ worth of meteorological, river, sea-ice and glacier data from the Arctic region and used it to calculate the increase in fresh water input into the ocean. They calculated that increased rainfall and river outflow between 1965 and 1995 dumped an

extra 20,000 cubic kilometres of freshwater into the ocean – equivalent to 40 years’ flow from the Mississippi river. Melting sea ice contributed a further 15,000 km3 and glaciers 2000 km3. This is consistent with the observed decrease in the salinity of the Arctic Ocean over the same period. “Our results show that there has been a global redistribution of fresh water, which is probably related to global warming,” Peterson says. Changes in patterns of atmospheric pressure over the North Atlantic, known as the North Atlantic Oscillation, appear to have speeded up the transfer of moisture from low to high latitudes. Climate models indicate that the effect will intensify, raising concerns about the flow of deep waters through the North Atlantic – driven by the sinking of dense, salty water at high latitudes. Disrupting this current could cause temperatures to plunge across northern Europe.

Can a shot of enzyme restore memory in Alzheimer’s? IT MAY eventually be possible to restore some of the lost cognitive function and learning ability of people with Alzheimer’s disease. Michael Shelanski of Columbia University in New York and his colleagues knew that an enzyme called ubiquitin C-terminal hydrolase L1 (Uch-L1) is essential for ridding brain cells of unwanted proteins, and that the beta-amyloid protein that 14 | NewScientist | 2 September 2006

forms plaques in the brains of Alzheimer’s patients somehow stops production of this enzyme. When they injected extra Uch-L1 into the brains of mice with the mouse equivalent of Alzheimer’s disease, the animals’ learning ability improved markedly. There was no change in the amount of beta-amyloid protein in their brains, however, which suggests that a defect in the

degradation of proteins other than beta-amyloid may play an important role in the disease. Most existing treatments and vaccines for Alzheimer’s aim to destroy the beta-amyloid plaques, or stop any more forming. “The main message of our work is that even in the presence of the beta-amyloid, there are ways to improve brain function,” says Shelanski.

IN THE coming weeks farmers in northern Europe will be counting sheep, but not to help them sleep. They are keeping a close eye on their flocks after the appearance of the bluetongue virus in sheep in the Netherlands. Transmitted by midges, the virus usually occurs in warm, wet areas, and has never been seen so far north. The virus causes high fever and swelling of the tongue in ruminants, and can kill up to 30 per cent of infected sheep. “It devastates sheep populations,” says Walter Tabachnick of the University of Florida in Vero Beach. Changes in Europe’s climate may mean the midges that carry the virus are more likely to survive the winter. “Global warming could theoretically change the distribution of bluetongue,” says David Stallknecht of the University of Georgia in Athens. “You can control it with vaccination, but of course that costs money.”

Bug-proof fence TRILLIONS of “friendly bacteria” inhabit our gut and help us digest our food. So it is puzzling that they so rarely invade our tissues. Now Lora Hooper and her colleagues at the University of Texas Southwestern in Dallas have shown that this may be thanks to an anti-microbial protein produced by cells lining the gut. When mice lacking the normal complement of beneficial bacteria were fed bacteria taken from the intestines of normal mice, their epithelial cells began churning out massive amounts of the protein, called RegIII gamma (Science, vol 313, p 1126). Humans make a similar protein called HIP/PAP. Hooper says the proteins form a barrier like an electric fence, zapping bacteria if they try to cross.