Posted on behalf of Helen Pearson.

Anyone interested in combing through data on over half a million ageing Brits will have their chance beginning today, when the UK Biobank throws open its databanks to researchers. The bank, unusual for its size and depth of data, should help scientists to identify the genetic and environmental causes of diabetes, obesity, cancer, depression and many other diseases.

In 2006, the UK Biobank started recruiting people aged 40–69. Researchers set up assessment centres in shopping malls, where volunteers gave blood and urine samples and spent 2–3 hours answering medical questions and undergoing measures of height, weight and body fat and tests of hearing, grip strength and lung function. The aim is collect a gigantic set of ‘baseline’ biomedical data, and then track the participants through follow-up questionnaires and through the United Kingdom’s National Health Service.

By 2022, an estimated 10,000 of the cohort will have breast cancer, 9,000 will have Alzheimer’s disease and some 28,000 will have died from heart disease. Scientists can look back at data collected at the beginning and work out what distinguishes those who develop disease from those who stay healthy. But in the planning stages, some scientists were sceptical of what all this expensive data collection (costing nearly £100 million (US$160 million) so far from the Wellcome Trust, Medical Research Council and other funders) would really achieve: a commentary in The Lancet once asked if it was “a project without a procedure”.

Six years on, the study has signed up over 500,000 participants. Around 10 million samples of blood, urine and saliva take up a –80ºC freezer the size of several double-decker buses on the outskirts of Stockport. The medical information eats up 20 terabytes. The one thing the biobank doesn’t have is any research projects — yet. Beginning today, researchers around the world can register on the biobank website and send in applications to use the data. Continue reading →

Posted on behalf of Leila Haghighat.

The woes of those affected by jet lag may soon come to an end. Two papers published today in Nature (here and here) explore how our internal clocks are regulated at the molecular level and how two compounds that alter this regulation could help us readjust to new time zones.

The body’s internal clock is governed by its circadian rhythm, the natural oscillations that occur within a 24-hour period and coincide with natural sleeping and feeding cycles. Each organ maintains its own individual clock, but the master regulator of circadian rhythms lies in the hypothalamus of the brain, more specifically in a structure called the suprachiasmatic nucleus (SCN), which is sensitive to light.

But synchronizing the circadian rhythm with the time of day involves more than just external light cues. Over a decade ago, researchers identified two receptors on the nucleus that also have a key role in the process: REV-ERB-α and REV-ERB-β. At certain times of the day, these receptors suppress the expression of certain genes to send the body into a dormant state. After the molecule that activates REV-ERBs was found in 2007, researchers set their sights on creating synthetic molecules that could mimic it. Turning on REV-ERBs by popping a pill could trick the body into dormancy, thereby adjusting the circadian rhythm.

A team of chemists and biologists led by Thomas Burris at the Scripps Research Institute in Jupiter, Florida, tested two compounds that activate REV-ERB in mice and showed that they change the expression of circadian-associated genes in both the hypothalamus and liver, making the animals less active.

The team kept the mice for 12 days in either constant darkness or alternating 12-hour cycles of light and dark. Constant darkness dampens the master regulator of the circadian rhythm and provides researchers with a look into the “purer rhythms” of individual organs, according to Burris.

The differences found between the two groups make developing a drug for human use more complicated. In the group of mice kept in the dark, those given the maximum dose of either drug could run only half as much as those not given the drug at all. The activity of mice exposed to regular lighting was delayed by only 1–3 hours.

“This suggests that light may in some way be interacting with REV-ERB to control its activity and adds a complication, since from a practical therapeutic point of view, such drugs are going to have to be active in normal lighting cycles,” says Andrew Loudon, a biologist at the University of Manchester, UK, who studies how REV-ERBs regulate immune function.

Beyond jet lag, the two compounds may also hold promise for those looking to lose weight or improve their cholesterol. “Circadian rhythms really have an important role in all types of human disease. Their circuitry controls not just our sleep but also our metabolism,” Burris notes.

Burris’s team fed mice a high-fat diet for 14 weeks and administered the drug twice a day. Mice given the drug lost more weight than controls, and had lower levels of cholesterol and fat in their blood.

Ronald Evans, senior author of the other Nature paper, says: “Together the two papers provide new insights into how clock function and circadian behaviour is established. It shows that the ‘clock’ and indeed our own body rhythm can be considered a therapeutic target.”

Photo courtesy of xlibber via Flickr under Creative Commons.

Posted on behalf of Katherine Rowland.

In many fish species, an injured individual will release a substance researchers call Schreckstoff — or scary stuff — causing the rest of the school to swim away to safety.

This flight en masse from possible danger was first documented in the 1930s, and researchers have since puzzled over both the chemical identity of the alarm compound and the evolution of a signal that offers no clear benefit to the sender.

Researchers from Singapore and Switzerland have identified that the signal released from the skin of an injured fish does not consist of a single compound, as previously believed, but rather a mixture. Examining zebrafish, they found that the components of Schreckstoff include glycosaminoglycan (GAG) chondroitin, which can trigger a fear response in the group. Their findings are published today in Current Biology. Continue reading →

Posted on behalf of Susan Young.

A newly discovered dwarf chameleon is among the smallest lizards in the world, with the diminutive males reaching a total length of less than 24 millimetres.

Brookesia micra (pictured) and three other species of tiny leaf chameleons were discovered in both rainforests and dry forests in extreme northern Madagascar by Miguel Vences of the Technical University of Braunschweig in Germany and his colleagues. Each of the four new species occupies a small, discrete range in the northern island region, and the striking differentiation amongst the miniaturized lizards evolved some 10 to 20 million years ago, the authors suggest in PLOS One.

Image credit: PLOS One