That's it! By the time you're reading this, I'll be in a plane / bus to Mexico; must get up at 5 in the morning, 19 hours of travel total, will arrive at destination at midnight, courses start the next morning. Should be fun! Let's hope everything will be ok; my first flight and all, with a transit via Washington, nothing less! Don't worry too much if updates are a little slow in the next few days; I have stuff posted for the day and tomorrow, and by then I should be able to post from Mexico. See you there!

• Rock pool sponge may fight cancer
• Key gene 'may reverse hair loss'
• 'Intelligent design' goes on trial
• Penguins stay snug and secure in minefields

A lab-made version of a human protein alleviates symptoms of both acute and chronic arthritis in mice and could be the basis for a new arthritis drug for people, report scientists from the National Institute of Allergy and Infectious Disease (NIAID), part of the National Institutes of Health (NIH). The protein prevents the assembly of a cell surface receptor, thus blocking transmission of chemical signals that lead to arthritis symptoms.

If you snooze, you lose those uncomely grayish-brown crescents below your eyes. If you don't snooze, you lose a lot more. The body can't fight off infection, the muscles can't regenerate as quickly, the mind can't learn new words, and the eyes can't focus on the road. You also gain things: a bad mood and increased risk for diabetes, high blood pressure, and heart problems. Indeed, the effects of sleep deprivation can be so serious that some sleep scientists liken lifetime sleep debt to a heavy backpack: every sleep hour missed adds an extra pound to your pack until it weighs you down.

Geneticists have debated for decades the relative importance of nature versus nurture in determining how an animal looks and behaves, and now UCSD scientists report that the coupling of noise and time delay could also be an important factor in determining the variability in gene expression that may affect phenotype.

Though the study of aging in the nematode model organism C. elegans has provided much insight into this complex process, it is not yet clear whether genes involved in aging in the worm have a similar role in mammals. In a recent study, Dr. Hekimi and colleagues of McGill University (Canada) report that inactivation of the gene mclk1, the murine ortholog of the C. elegans gene clk-1, results in increased cellular fitness and prolonged lifespan in mice.

The first close-up look at a pro-inflammatory signaling molecule involved in immune response in mammals suggests that researchers "should rethink what they are doing" in creating drugs based on a fruit-fly model, scientists say.