ScienceShot: Is Venus Slowing Down?

Venus, our closest planetary neighbor, has the slowest rotational period of any world in our solar system—and according to data recently gathered by the European Space Agency's Venus Express orbiter, it's getting slower. In the 1990s, NASA's Magellan probe measured the Venusian day, the length of time needed for the planet to complete one rotation, to be 243.0185 Earth days. But new measurements by Venus Express (artist's concept above), which has been orbiting the cloud-shrouded planet since 2006, reveal the current rotational period to be about 6.5 minutes slower, researchers report this month in Icarus. Although that difference seems minor, it places some features on Venus about 20 kilometers away from where scientists were expecting—a big deal for future missions looking to set a lander or rover down at a particular site. Reasons for the rotational slowdown aren't clear. Friction caused by fierce weather systems may be slowing the planet's rotation, just as weather and tides cause Earth's day to vary. Or, gravitational interactions between Earth and Venus when the planets pass near each other in orbit may be sapping our neighbor of its angular momentum. Finally, the researchers suggest, Magellan's 4-year mission may simply have occurred at a time when the Venusian rate of rotation was temporarily faster than normal, because the new data actually match long-term measurements made by radar from Earth.

ScienceShot: Solar Wind Stifles Mercury's Magnetic Field

Ever since NASA's Mariner 10 spacecraft zipped past Mercury in 1974, scientists have wondered why the planet's magnetic field is so much wimpier than expected. Now, a new study led by researchers at Braunschweig University of Technology in Germany suggests that the solar wind—the incessant flow of charged particles boiling off the sun's surface—suppresses the field generated by the flow of molten iron in the planet's outer core. On the sunward side of Mercury, the magnetopause—the protective shield created by the planet's magnetic field—sits just 1200 kilometers above the planet's surface. That's so close, the team's computer models indicate, that magnetic fields created by particles flowing along the magnetopause reach deep into Mercury itself, counteracting the internally-generated field. Without the external fields generated by the solar wind, Mercury's magnetic field might be about 30 times stronger than it actually is, the researchers report today in Science. NASA's MESSENGER probe (artist's concept above) has been orbiting Mercury since mid-March and will provide unprecedented measurements of the strength and direction of the planet's magnetic field, revealing more about how such fields are generated in the first place.

Opioids’ molecular magic unmasked

Proteins turned on by opium and similar substances in the body have now been caught in action. Two new snapshots show how cellular proteins lasso molecules in the opium family, revealing the 3-D structure of such pairings for the first time.

The work represents a major step toward designing more specific analgesics and other drugs that lack opioids’ nasty side effects, two teams of researchers report online March 21 in Nature.

“Both are landmark studies,” says Gavril Pasternak, a neuroscientist who designs opioids at the Sloan-Kettering Institute in New York City, and who wasn’t involved in either study. “These structures will quickly be utilized with goal of developing nonaddicting painkillers and new ways to combat drug abuse.”

Smallest planet yields big surprises

THE WOODLANDS, Texas — Mercury is even weirder than expected, NASA’s MESSENGER probe is showing.

For starters, the planet’s interior is built differently than anything else scientists have blueprints for. Unlike Earth’s, Mercury’s core — which gobbles up 85 percent of the planet’s radius — consists of three layers instead of two. At the planet’s heart lies a probable solid layer, surrounded by a swirling liquid iron layer, all encapsulated by a third, solid iron-sulfur layer.

The new MESSENGER results were presented on March 21 at the Lunar and Planetary Science Conference, as well as in two papers appearing online in Science. One paper discusses the gravity measurements leading to the new model of the planet’s interior, and the other describes surface features in the northern hemisphere.

Vesta seems more planet than asteroid

THE WOODLANDS, Texas — The enormous asteroid Vesta is more like a small, rocky planet than other space rocks wandering around the asteroid belt between Mars and Jupiter. Among other planetlike characteristics, Vesta’s interior is probably divided into layers like Earth’s — and scientists have detected traces of an ancient magnetic field.

“We have a hard time working on this body and not thinking about it as a planet,” said UCLA’s Christopher Russell, principal investigator of the Dawn spacecraft that has been buzzing around Vesta since July.

Like Earth, Vesta probably has an iron core, a mantle and crust. Scientists don’t know how thick the crust is, but Dawn measurements suggest that the core’s radius is between 107 and 113 kilometers, Carol Raymond of the Jet Propulsion Laboratory said on March 22 at the Lunar and Planetary Science Conference. Vesta is only about 530 kilometers across, meaning that the core occupies almost half its diameter. And new gravity maps from Dawn reveal anomalies in the crust, or areas where there’s “likely mantle material close to the surface,” Raymond reported.

When Nerve Meets Muscle, Biglycan Seals the Deal

ScienceDaily (Feb. 14, 2012) — In the absence of the protein biglycan, synapses at neuromuscular junctions in mice began to break up about five weeks after birth, according to a new study led by Brown University researchers. Reintroducing byglycan helped fix the loss of synaptic stability in cell culture. The research may be relevant to efforts to treat motor neuron diseases, such as amyotrophic lateral sclerosis (ALS, Lou Gherig's Disease) and spinal muscular atrophy.

A protein that has shown early promise in preventing the loss of muscle function in mouse models of Duchenne muscular dystrophy, has been found in a new study to be a key player in the process of joining nerves to muscles.

The protein biglycan needs to be present to stabilize synapses at the neuromuscular junction after they have formed, according to research led by Brown University that appears in the Feb. 14, 2012, issue of the Journal of Neruoscience.

"What neuromuscular junctions do second-by-second is essential for our brain to control movement and they are also important for the long-term health of both muscle and motor neurons," said Justin Fallon, profesor of neuroscience at Brown University and the paper's senior author. "A treatment that sustains or supports the synapse could promote the health of motor neurons and muscle."

In previous work, Fallon, a member of the Brown Institute for Brain Science, has shown that in mice with the same genetic mutation as Duchenne patients, biglycan promotes the activity of another natural protein, utrophin, that can significantly reduce the muscle degradation that patients suffer. Utrophin essentially takes over for dystrophin, which is the protein Duchenne patients cannot produce. In 2010 Brown licensed Fallon's biglycan intellectual property to the Providence startup company Tivorsan Pharmaceuticals, which is working toward human trials of biglycan. (Last month, Tivorsan received a $1-million grant from the Muscular Dystrophy Association.)

Now Fallon's research group has found another important role for biglycan. In the new multi-institutional study, lead author Alison Amenta and a team of other scientists found that biglycan binds and helps activate and target a receptor enzyme called MuSK, which works like a foreman or master regulator over other proteins that build and stabilize the neuromuscular junction.

Mice engineered to lack biglycan developed normal junctions at first, but by five weeks after birth their synapses became much more likely to break into fragmented shadows of their former selves. In experiments the scientists saw that up to 80 percent of synapses in biglycan-lacking mice were unstable.

Biglycan-lacking mice also showed other structural defects including misaligned neurotransmitter receptors and extra folds near synapses.

"We think it is most likely that these folds are remnants of previous synaptic sites," that have since withered, the authors wrote in the paper.

Amenta, Fallon, and their team also found that in mice lacking biglycan, levels of MuSK at neuromuscular junction synapses were reduced by a factor of more than 10. In another experiment, they found that recombinant biglycan could rescue the stability of synaptic structures in model cell culture system.

Relevance to motor neuron diseases

The findings help set the stage for testing biglycan as a potential therapy in animal models of motor neuron disease, Fallon said.

"As an extracellular protein that can be delivered systemically that acts to stabilize the neuromuscular junction, we propose that biglycan could be a protein therapeutic for motor neuron diseases such as spinal muscular atrophy and amyotrophic lateral sclerosis, or ALS," Fallon said.

In addition to Fallon and Amenta, other Brown authors include Hillary Creely, Mary Lynn Mercado, Hiroki Hagiwara, Beth McKechnie and Beatrice Lechner. Other authors are Susana Rossi, Emilio Marrero and Richard Rotundo of the University of Miami; Qiang Wang and Lin Mei of the Medical College of Georgia; Rick Owens and David McQuillan of Lifecell Corp.; the late Werner Hoch of the University of Houston; and Marian Young of the National Institute of Dental and Craniofacial Research.

Several grants from the National Institutes of Health and support from the Muscular Dystrophy Association funded the research.

Are Humans to Blame for Africa's Lost Rainforests?

About 3000 years ago, Central Africa was a landscape in transition. Lush evergreen forests were gradually giving way to savannas and grasslands as regional climate change pushed the formerly humid weather patterns toward drier, slightly warmer conditions. But climate was not the only factor at play. According to a new study, an influx of humans into the region at this time may have helped drive some of the original rainforests into oblivion.

The paper's results, published online today in Science, came as a surprise to the researchers. "To be honest, at the beginning we were not at all aware of this human issue," says lead author Germain Bayon, a geochemist at the French Research Institute for Exploration of the Sea in Plouzané.

Eating your greens is good for you, but if you're a bluetongue lizard, it might just save your life. New research finds that the toxic mother-of-milli

Dip a toe into the wrong lake in the Amazon, and it may get bitten off. Here, gangs of piranhas swarm almost anything that moves. Anything, that is, except the arapaima. This humungous fish swims unchewed, even in piranha-infested lakes and rivers. A new study reveals how: The arapaima's unique scales are tough enough to deflect a piranha's razor-sharp bite.

Study co-author Marc Meyers, a mechanical engineer at the University of California, San Diego, is no stranger to the Amazon's deadly waters. He's spent several months sport fishing in Brazil and once reeled in an arapaima (Arapaima gigas). It was a whopper. These fish—often known as "living fossils" because they still harbor lungs and need to breathe air—frequently stretch to 2.5 meters and weigh 200 kilograms.

ScienceShot: Toxic Greens Protect Smurf-Tongued Lizards

Eating your greens is good for you, but if you're a bluetongue lizard, it might just save your life. New research finds that the toxic mother-of-millions plant (Bryophyllum spp.) protects some bluetongues (Tiliqua scincoides) from cane toad (Rhinella marina) toxins. Both the plant and the toad were introduced to different parts of Australia around 1935, both produce a similar toxin (bufadienolide) that can stop the heart, and both are consumed by bluetongues. When injected with non-lethal doses of bufadienolide, bluetongues from areas without mother-of-millions (inset) swam 50% slower than before they were injected, while those that live in areas with the plant only swam 20% slower, researchers report in a forthcoming issue of American Naturalist. That suggests that bluetongue lineages from mother-of-millions areas have built up a resistance to bufadienolide over time. The team hopes bufadienolide resistance will lessen the impact of another potential invader with similar toxins, the black-spined toad (Duttaphrynus melanostictus), on this native lizard.