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Emily Brooke, a design student at the University of Brighton, may just be the best friend that a biker has ever had. Anyone who has tried to ride a bike on crowded city streets knows how much of a challenge it can be to get in and out of traffic unscathed will be grateful for her new invention. Known only as BLAZE the handlebar mounted system. The system projects a laser image onto the road in front of the bike, alerting near by drivers that there is a cycle in the lane in situations where the driver may not have otherwise been aware of the presence of a bike rider. Hopefully, this early warning system will prevent drivers from changing into lanes with a bike in them.

"Eighty per cent of cycle accidents occur when bicycles travel straight ahead and a vehicle maneuvers into them," Ms. Brooke, told reporters. "The most common contributory factor is 'failed to look properly' on the part of a vehicle driver. The evidence shows the bike simply is not seen on city streets."

The system, which Ms. Brook developed in consultation with Brighton & Hove City Council, the Brighton & Hove Bus Company and driving psychologists projects the sharrow symbol in a green light bright enough to be seen in full daylight. For those of you not familiar with it the sharrow symbol is the sign for a shared lane. The system can be mounted to pedal bikes, scooters and motorcycles.

This design has already won its inventor a paid course at Babson College in Massachusetts, where she can continue to develop BLAZE. No word yet on when BLAZE will be on sale.

National Institutes of Health researchers have identified a new pathway that sets the clock for programmed aging in normal cells. The study provides insights about the interaction between a toxic protein called progerin and telomeres, which cap the ends of chromosomes like aglets, the plastic tips that bind the ends of shoelaces.

The study by researchers from the National Human Genome Research Institute (NHGRI) appears in the June 13, 2011 early online edition of the Journal of Clinical Investigation.

Telomeres wear away during cell division. When they degrade sufficiently, the cell stops dividing and dies. The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin.

Progerin is a mutated version of a normal cellular protein called lamin A, which is encoded by the normal LMNA gene. Lamin A helps to maintain the normal structure of a cell's nucleus, the cellular repository of genetic information.

In 2003, NHGRI researchers discovered that a mutation in LMNA causes the rare premature aging condition, progeria, formally known as known as Hutchinson-Gilford progeria syndrome. Progeria is an extremely rare disease in which children experience symptoms normally associated with advanced age, including hair loss, diminished subcutaneous fat, premature atherosclerosis and skeletal abnormalities. These children typically die from cardiovascular complications in their teens.

"Connecting this rare disease phenomenon and normal aging is bearing fruit in an important way," said NIH Director Francis S. Collins, M.D., Ph.D., a senior author of the current paper. "This study highlights that valuable biological insights are gained by studying rare genetic disorders such as progeria. Our sense from the start was that progeria had a lot to teach us about the normal aging process and clues about more general biochemical and molecular mechanisms."

Collins led the earlier discovery of the gene mutation responsible for progeria and subsequent advances at NIH in understanding the biochemical and molecular underpinnings of the disease.

In a 2007 study, NIH researchers showed that normal cells of healthy people can produce a small amount of progerin, the toxic protein, even when they do not carry the mutation. The more cell divisions the cell underwent, the shorter the telomeres and the greater the production of progerin. But a mystery remained: What was triggering the production of the toxic progerin protein?

The current study shows that the mutation that causes progeria strongly activates the splicing of lamin A to produce the toxic progerin protein, leading to all of the features of premature aging suffered by children with this disease. But modifications in the splicing of LMNA are also at play in the presence of the normal gene.

The research suggests that the shortening of telomeres during normal cell division in individuals with normal LMNA genes somehow alters the way a normal cell processes genetic information when turning it into a protein, a process called RNA splicing. To build proteins, RNA is transcribed from genetic instructions embedded in DNA. RNA does not carry all of the linear information embedded in the ribbon of DNA; rather, the cell splices together segments of genetic information called exons that contain the code for building proteins, and removes the intervening letters of unused genetic information called introns. This mechanism appears to be altered by telomere shortening, and affects protein production for multiple proteins that are important for cytoskeleton integrity. Most importantly, this alteration in RNA splicing affects the processing of the LMNA messenger RNA, leading to an accumulation of the toxic progerin protein.

Cells age as part of the normal cell cycle process called senescence, which progressively advances through a limited number of divisions in the cell lifetime. "Telomere shortening during cellular senescence plays a causative role in activating progerin production and leads to extensive change in alternative splicing in multiple other genes," said lead author Kan Cao, Ph.D., an assistant professor of cell biology and molecular genetics at the University of Maryland, College Park.

Telomerase is an enzyme that can extend the structure of telomeres so that cells continue to maintain the ability to divide. The study supplied support for the telomere-progerin link, showing that cells that have a perpetual supply of telomerase, known as immortalized cells, produce very little progerin RNA. Most cells of this kind are cancer cells, which do not reach a normal cell cycle end point, and instead replicate out of control.

The researchers also conducted laboratory tests on normal cells from healthy individuals using biochemical markers to indicate the occurrence of progerin-generating RNA splicing in cells. The cell donors ranged in age from 10 to 92 years. Regardless of age, cells that passed through many cell cycles had progressively higher progerin production. Normal cells that produce higher concentrations of progerin also displayed shortened and dysfunctional telomeres, the tell-tale indication of many cell divisions.

In addition to their focus on progerin, the researchers conducted the first systematic analysis across the genome of alternative splicing during cellular aging, considering which other protein products are affected by jumbled instructions as RNA molecules assemble proteins through splicing. Using laboratory techniques that analyze the order of chemical units of RNA, called nucleotides, the researchers found that splicing is altered by short telomeres, affecting lamin A and a number of other genes, including those that encode proteins that play a role in the structure of the cell.

The researchers suggest that the combination of telomere fraying and loss with progerin production together induces cell aging. This finding lends insights into how progerin may participate in the normal aging process.

Efficiency is a problem with today's solar panels; they only collect about 20 percent of available light. Now, a University of Missouri engineer has developed a flexible solar sheet that captures more than 90 percent of available light, and he plans to make prototypes available to consumers within the next five years.

Patrick Pinhero, an associate professor in the MU Chemical Engineering Department, says energy generated using traditional photovoltaic (PV) methods of solar collection is inefficient and neglects much of the available solar electromagnetic (sunlight) spectrum. The device his team has developed – essentially a thin, moldable sheet of small antennas called nantenna – can harvest the heat from industrial processes and convert it into usable electricity. Their ambition is to extend this concept to a direct solar facing nantenna device capable of collecting solar irradiation in the near infrared and optical regions of the solar spectrum.

Working with his former team at the Idaho National Laboratory and Garrett Moddel, an electrical engineering professor at the University of Colorado, Pinhero and his team have now developed a way to extract electricity from the collected heat and sunlight using special high-speed electrical circuitry. This team also partners with Dennis Slafer of MicroContinuum, Inc., of Cambridge, Mass., to immediately port laboratory bench-scale technologies into manufacturable devices that can be inexpensively mass-produced.

"Our overall goal is to collect and utilize as much solar energy as is theoretically possible and bring it to the commercial market in an inexpensive package that is accessible to everyone," Pinhero said. "If successful, this product will put us orders of magnitudes ahead of the current solar energy technologies we have available to us today."

As part of a rollout plan, the team is securing funding from the U.S. Department of Energy and private investors. The second phase features an energy-harvesting device for existing industrial infrastructure, including heat-process factories and solar farms.

Within five years, the research team believes they will have a product that complements conventional PV solar panels. Because it's a flexible film, Pinhero believes it could be incorporated into roof shingle products, or be custom-made to power vehicles.

Once the funding is secure, Pinhero envisions several commercial product spin-offs, including infrared (IR) detection. These include improved contraband-identifying products for airports and the military, optical computing, and infrared line-of-sight telecommunications.

Sharing about 95 percent of their genes with humans, mice are recognized around the world as the leading experimental model for studying human biology and disease. But, says Jackson Laboratory Professor Gary Churchill, Ph.D., researchers can learn even more “now that we really know what a laboratory mouse is, genetically speaking.”

Thanks to an in-depth analysis by a team led by Fernando Pardo-Manuel de Villena, PhD, in the University of North Carolina, Chapel Hill Department of Genetics and Gary Churchill, PhD, at The Jackson Laboratory in Bar Harbor, Maine, researchers will be able to use an online resource dubbed the Mouse Phylogeny Viewer to select from among 162 strains of laboratory mice for which the entire genome has been characterized.

Phylogeny is the connections among all groups of organisms as understood by genetic relationships. The results of the analysis that make this tool possible were published online today in the journal Nature Genetics.

“The viewer provides scientists with a visual tool where they can actually go and look at the genome of the mouse strains they are using or considering, compare the differences and similarities between strains and select the ones most likely to provide the basis for experimental results that can be more effectively extrapolated to the diverse human population,” explains Pardo-Manuel de Villena.

“As scientists use this resource to find ways to prevent and treat the genetic changes that cause cancer, heart disease, and a host of other ailments, the diversity of our lab experiments should be much easier to translate to humans,” he noted.

In 2004 Churchill and Pardo-Manuel de Villena launched the Collaborative Cross, a project to interbreed eight different strains--five of the classic inbred strains and three wild-derived strains. In 2009 Churchill’s lab started the Diversity Outbred mouse population with breeding stock selected from the Collaborative Cross project.

The research team estimates that the standard laboratory mouse strains carry about 12 million single nucleotide polymorphisms (SNPs), single-letter variations in the A, C, G or T bases of DNA.

The Collaborative Cross mice deliver a whopping 45 million SNPs, as much as four times the genetic variation in the human population. “All these variants give us a lot more handles into understanding the genome,” Churchill says.

“This work creates a remarkable foundation for understanding the genetics of the laboratory mouse, a critical model for studying human health,” said James Anderson, Ph.D., who oversees bioinformatics grants at the National Institutes of Health.

“Knowledge of the ancestry of the many strains of this invaluable model vertebrate will not only inform future experimentation but will allow a retrospective analysis of the huge amounts of data already collected,” he concluded.

Their analysis exponentially increases the data available to geneticists who work with mice, allowing them to statistically impute the whole mouse genome sequence with very high accuracy for hundreds of laboratory mouse strains. This will lead to much greater precision in the interpretation of existing biomedical data and optimal selection of strains in future experiments.

Researchers have discovered that the ultraviolet (UV) light that causes the temporary but painful condition of snow blindness in humans is life-saving for reindeer in the arctic.

A BBSRC-funded team at UCL has published a May 12 paper in the Journal of Experimental Biology that shows that this remarkable visual ability is part of the reindeer's unique adaptation to the extreme arctic environment where they live. It allows them to take in live-saving information in conditions where normal mammalian vision would make them vulnerable to starvation, predators and territorial conflict. It also raises the question of how reindeer protect their eyes from being damaged by UV, which is thought to be harmful to human vision.

Lead researcher Professor Glen Jeffery said "We discovered that reindeer can not only see ultraviolet light but they can also make sense of the image to find food and stay safe. Humans and almost all other mammals could never do this as our lenses just don't let UV through into the eye.

"In conditions where there is a lot of UV – when surrounded by snow, for example – it can be damaging to our eyes. In the process of blocking UV light from reaching the retina, our cornea and lens absorb its damaging energy and can be temporarily burned. The front of the eye becomes cloudy and so we call this snow blindness. Although this is normally reversible and plays a vital role to protect our sensitive retinas from potential damage, it is very painful."

Human beings are able to see light with wavelengths ranging from around 700nm, which corresponds to the colour red, right through all the colours of the rainbow in sequence to 400nm, which corresponds to violet. Professor Jeffery and his team tested the reindeer's vision to see what wavelengths they could see and found that they can handle wavelengths down to around 350-320nm, which is termed ultraviolet, or UV, because it exceeds the extreme of the so-called visible spectrum of colours.

The winter conditions in the arctic are very severe; the ground is covered in snow and the sun is very low on the horizon. At times the sun barely rises in the middle of the day, making it dark for most of the time. Under these conditions light is scattered such that the majority of light that reaches objects is blue or UV. In addition to this, snow can reflect up to 90% of the UV light that falls on it.

Professor Jeffery continued "When we used cameras that could pick up UV, we noticed that there are some very important things that absorb UV light and therefore appear black, contrasting strongly with the snow. This includes urine - a sign of predators or competitors; lichens - a major food source in winter; and fur, making predators such as wolves very easy to see despite being camouflaged to other animals that can't see UV."

This research raises some interesting questions about the effect of UV on eye health. It had always been assumed that human eyes don't let UV in because of the potential that it will cause damage, just as it does to our skin. In our eyes, UV could damage our sensitive photoreceptors that cannot be replaced. This would lead to irreversible damage to our vision. Arctic reindeer are able to let UV into their eyes and use the information effectively in their environment without suffering any consequences.

Professor Jeffery added "The question remains as to why the reindeer's eyes don't seem to be damaged by UV. Perhaps it's not as bad for eyes as we first thought? Or maybe they have a unique way of protecting themselves, which we could learn from and perhaps develop new strategies to prevent or treat the damage the UV can cause to humans."

Professor Douglas Kell, Chief Executive, BBSRC said "We can learn a lot from studying the fundamental biology of animals and other organisms that live in extreme environments. Understanding their cell and molecular biology, neuroscience, and other aspects of how they work can uncover the biological mechanism that meant they can cope with severe conditions. This knowledge can have an impact on animal welfare and has the potential to be taken forward to new developments that underpin human health and wellbeing."

"Until experts in Germany and Spain are able to positively identify the source of the pathogen, general warnings about vegetables remain valid," Consumer Affairs Minister Ilse Aigner told the Bild am Sonntag newspaper.

"The relevant authorities are doing all they can to clear this up, nationally and internationally."

The European Commission said on Friday that organic cucumbers from southern Spain have been confirmed as a source of the outbreak of enterohaemorrhagic E. coli (EHEC) poisoning.

Germany's national disease institute, the Robert Koch Institute (RKI), has said two deaths were from haemolytic uraemic syndrome (HUS), a disease caused by EHEC that can lead to bloody diarrhoea and serious liver damage.

But there are eight other suspected HUS deaths, and the RKI has said that close to 300 people have contracted the disease in recent weeks. Normally about 60 people in Germany a year contract HUS.

Spanish authorities said Saturday they had introduced restrictions on two distributors. Andalusia's regional council said suspect batches had been withdrawn pending tests, results of which were due on Monday.

But the European Commission said a batch of cucumbers originating either in The Netherlands or in Denmark, and traded in Germany, was also under investigation.

The deaths included four fatalities announced on Saturday in the northern state of Schleswig-Holstein and in Hamburg, including three women in their 80s and a fourth in her 30s. Nine of those who have died so far are women.

The epicentre of the outbreak has been in northern Germany, with more than 1,000 people suspected of being infected, reports said. Several are said to be fighting for their lives.

Hospitals in the city of Hamburg, where more than 400 people are believed to have been infected with EHEC, were said to be overwhelmed and sending patients to clinics elsewhere.

In nearby Luebeck, a spokesman for the university hospital, where some 20 suspected HUS cases were being treated and where one patient has died, told AFP that staff were "close to exhaustion."

Sweden has reported 25 E. coli cases, of whom 10 developed HUS, according to the European Commission. Denmark reported seven E. coli cases (including three HUS) while Britain counted three cases (two HUS).

More cases have been reported in France, the Netherlands, Switzerland and Austria, where authorities ordered organic cucumbers, tomatoes and aubergines delivered from Germany but grown in Spain withdrawn in 33 shops.

Denmark's veterinary and food products agency said Friday it had found contaminated cucumbers from Spain in the stocks of two wholesalers in the west of the country and ordered them withdrawn.

The Czech Republic has imported a batch of tainted organic cucumbers from Spain, the CTK news agency said Saturday, citing the country's agriculture and food inspection authority SZPI.

The Stockholm-based European Centre for Disease Prevention and Control (ECDC) said Friday that all of these cases involved people who had recently been in northern Germany.

The RKI said last week that a study conducted with the Federal Institute for Risk Assessment (BfR) had shown that those affected had eaten significantly above-average amounts of tomatoes, lettuce and cucumbers.

(c) 2011 AFP

When it comes to visiting asteroids, NASA doesn't pick run-of-the-mill space rocks. The target of NASA's latest asteroid mission is not only thought to be rich in the building blocks of life, it also has a chance — although a remote one — of threatening Earth in the year 2182.

The asteroid 1999 RQ36 is the target of a new unmanned spacecraft, which NASA plans to launch in 2016 to collect a sample from the space rock and return it to Earth by 2023.

The mission's leaders spent a long time surveying possible destinations for the mission, and finally settled on 1999 RQ36. NASA calls the mission OSIRIS-Rex, which is short for Origins-Spectral Interpretation-Resource Identification-Security-Regolith Explorer.

"We went through a whole series of selection criteria," OSIRIS-Rex's deputy principal investigator Dante Lauretta, a planetary scientist at the University of Arizona, told SPACE.com. "There are over 500,000 asteroids known. [1999 RQ36] looks really optimum."

A potentially dangerous asteroid

In addition to digging up clues about our solar system's history, the OSIRIS-Rex mission may be able to help Earth fend off potentially deadly space rocks. That's because asteroid 1999 RQ36 — which is about 1,900 feet (580 meters) wide — is public enemy No. 1 for space rock scientists.

"1999 RQ36 has the highest probability of impacting the Earth of any known Potentially Hazardous Asteroid," according to a mission proposal submitted to NASA by the OSIRIS-Rex in 2009.

A recent calculation found that the asteroid has a 1-in-1,800 chance of hitting Earth in the year 2170, and a 1-in-1,000 chanceof slamming into us in 2182.

While those are slim odds, they put 1999 RQ36 at the top of the danger list.

"I wouldn't go buy asteroid insurance," Lauretta said. "We're OK for 150 years or so. We're not saving the Earth from immediate danger."

Still, he said studying the asteroid and its orbit up close could help us better predict the risk, and outline a strategy to protect ourselves if necessary.

One reason the likelihood of Earth impact can't be better predicted is because scientists don't fully understand the Yarkovsky effect, which causes asteroids to accelerate slightly when they absorb sunlight and then re-emit it as heat.

"[1999 RQ36's] orbit is currently well known because of optical and radar data but the long-term motion is less well understood because of the poorly defined Yarkovsky effect," said Donald Yeomans, manager of NASA's Near-Earth Object Program Office, who is not directly involved with the OSIRIS-Rex mission. "This mission should allow a much better understanding of these effects once the asteroid's size, mass, rotation characteristics and thermal properties are studied."

Target: Asteroid 1999 RQ36

One of the most attractive features of asteroid 1999 RQ36 for scientists is its size: It is as large as five football fields, which means it won't be spinning too fast when OSIRIS-Rex approaches. The asteroid should also have a large supply of lose dirt, or regolith, on its surface for easy sampling.

1999 RQ36 is thought to be carbonaceous, or rich in carbon and organic material, and likely to contain some of the building blocks of life, such as the amino acids used to build the proteins vital to life on Earth.

"We cannot tell from telescopes exactly what kind of material, but we believe it's the sort of stuff that came in through the Earth's atmosphere after liquid oceans first formed, perhaps by 4.45 billion years ago, and provided those building blocks," said OSIRIS-Rex principal investigator Mike Drake of the University of Arizona, during a news conference yesterday (May 25).

In fact, the asteroid is a primitive B-class carbonaceous asteroid, a class that has never been studied up close by a spacecraft before, and should provide an unprecedented opportunity to learn about the history of the solar system and the origin of life on Earth.

The material inside 1999 RQ36 is thought to date to the very formation of our solar system around 4.56 billion years ago. While the space rock now orbits relatively near Earth — making it a convenient target for visiting — scientists think it is a fragment of an even larger asteroid that collided with another rock in the main asteroid belt between Mars and Jupiter, a few million years ago.

Building on asteroid successes

The OSIRIS-Rex mission is not NASA's first mission to an asteroid, but it will be the first U.S. probe to retrieve samples and return them to Earth. Only Japan's Hayabusa spacecraft, which returned samples of the asteroid Itokawa to Earth in June 2010 after a seven-year journey, has performed a similar feat.

NASA has sent probes to visit asteroids before. The agency's NEAR spacecraft rendezvoused with the asteroid Eros and ultimately touched down on that space rock at the end of its mission in February 2001.

NASA's Dawn probe, meanwhile, is nearing the asteroid Vesta — the second-largest space rock in the asteroid belt. Dawn will orbit Vesta for many months, then head off to visit Ceres, the largest asteroid in the solar system.

But the NEAR and Dawn missions are only visiting asteroids. OSIRIS-Rex will bring pieces back home. And that has scientists brimming with anticipation.

"Asteroid 1999 RQ36 is a perfect target for sample return and I can't wait to see the exciting results from both the in situ science activities and the sample return analysis," Yeomans said.

John Collins Rudolf has posted a thorough overview of the latest murder on the eroding perimeter of the Amazon rain forest in Brazil. There’s been enormous progress in efforts to bring governance to forest frontiers in Brazil since the late 1980s, when I spent months in the western Amazon reporting on the life and assassination of Chico Mendes for “The Burning Season,” my first book. But pistols and shotguns still sometimes blaze.

Here’s a video of a recent TEDx appearance of the new victim, José Cláudio Ribeiro da Silva, a forest activist and tree nut harvester who was gunned down on Tuesday along with his wife as they rode a motorcycle in Brazil’s still turbulent Para State (for English subtitles, press play, then engage the “cc” closed-captioning button):

Read on for the nut of Rudolf’s report and a link to the rest:

News of the slayings, emerging on the same day that Brazil’s parliament was to vote on a controversial revision of the country’s forest protection laws, rocketed through Brazil’s political classes. Within hours, senior government officials were briefed on the crime and President Dilma Rousseff had ordered an investigation by the federal police.

Yet whether that investigation results in punishment for the killers — or those who likely hired them — is deeply uncertain. More than 1,000 rural activists, small farmers, religious workers and others fighting the region’s rampant deforestation have been slain in the past 20 years, but only a handful of killers have ever been successfully prosecuted, according to a statement by the Pastoral Land Commission, a Catholic organization that tracks rural violence. [Read the rest.]

Recalling painful memories while under the influence of the drug metyrapone reduces the brain’s ability to re-record the negative emotions associated with them, according to a study published in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism. The study by a team of University of Montreal researchers at the Centre for Studies on Human Stress of Louis-H. Lafontaine Hospital challenges the theory that memories cannot be modified once they are stored in the brain.

“Metyrapone is a drug that significantly decreases the levels of cortisol, a stress hormone that is involved in memory recall,” explained lead author Marie-France Marin. Manipulating cortisol close to the time of forming new memories can decrease the negative emotions that may be associated with them. “The results show that when we decrease stress hormone levels at the time of recall of a negative event, we can impair the memory for this negative event with a long-lasting effect,” said Dr. Sonia Lupien, who directed the research.

Thirty-three men participated in the study, which involved learning a story composed of neutral and negative events. Three days later, they were divided into three groups – participants in the first group received a single dose of metyrapone, the second received double, while the third were given placebo. They were then asked to remember the story. Their memory performance was then evaluated again four days later, once the drug had cleared out.. “We found that the men in the group who received two doses of metyrapone were impaired when retrieving the negative events of the story, while they showed no impairment recalling the neutral parts of the story,” Marin explained. “We were surprised that the decreased memory of negative information was still present once cortisol levels had returned to normal.”

The research offers hope to people suffering from syndromes such as post-traumatic stress disorder. “Our findings may help people deal with traumatic events by offering them the opportunity to ‘write-over’ the emotional part of their memories during therapy,” Marin said. One major hurdle, however, is the fact that metyrapone is no longer commercially produced. Nevertheless, the findings are very promising in terms of future clinical treatments. “Other drugs also decrease cortisol levels, and further studies with these compounds will enable us to gain a better understanding of the brain mechanisms involved in the modulation of negative memories.”

This is the result of a study conducted by Xiaobin Wang of the Chinese Academy of Agricultural Sciences (CAAS) and the Wageningen UR agrotechnologist Willem Hoogmoed, as reported in this month's Journal of the Science of Food and Agriculture.

In the wealthy eastern part of China, farmers spread more than 180 kilogrammes of nitrogen on each hectare of their land. Excessive amounts of nitrogen cannot be absorbed by the crops; instead, they pollute the groundwater and the air. In the poorer western part of China, nitrogen use is below 100 and even 50 kilogrammes per hectare per year. If the eastern provinces were to limit their fertilizer use to 180 kilogrammes per year, the remainder - 1.2 million tons of nitrogen - could go to the poorer agriculture areas. That would result in additional grain production of 52 million tons, Wang calculates.

That would make quite a difference in the global grain market. For comparison, China currently produces about 500 million tons of grain annually, and the European Union produces about 130 million tons. The inefficient use of nitrogen is one of the major limiting factors in food supply in China, writes Wang.

The Chinese Academy of Agricultural Sciences is adviser to the agriculture ministry in Beijing. Its conclusions have already been shared among policy makers, says Hoogmoed. But the re-distribution of fertilizers has not yet been put into practice. The distance between China's capital city and its countryside is big, and every province has its own policy and fertiliser factories.

Provided by Wageningen University