科学与翻译

Autumn leaves turn fiery-red in an attempt to store up as much goodness as possible from leaves and soil before a tree settles down for the winter. The worse the quality of soil, the more effort a tree will put in to recovering nutrients from its leaves, and the redder they get.

That’s the conclusion that Emily Habinck from the University of North Carolina, Charlotte, came to after looking at trees in a flood plain and in an adjacent upland area. The soil in the upland area was low in nutrients, and the leaves there were bright red. In the floodplain, where the soil was packed full of goodness, the autumn leaves remained yellow.

“In a nutshell: the redder a leaf is, the more nutrients it is going to recycle,” explains Habinck, who presents her findings at the Geological Society of America’s annual meeting in Denver, Colorado, today.

It’s not easy being red

Unlikely as it may seem, colour changes in leaves are not fully understood — at least not when it comes to the redder hues.

As autumn approaches, trees begin to break down the green chlorophyll in their leaves and redistribute the nutrients contained there to their trunk and roots. This keeps them going throughout the winter, when sunlight is sparse.

The yellow colour seen in some autumn trees results from the loss of chlorophyll simply unmasking the yellow carotinoids that were there all along. But red coloration comes from a nitrogen-containing pigment called anthocyanin, which has to be made afresh as autumn takes hold.

Why trees would bother to spend energy doing this as things are winding down for the winter has been widely debated. Some researchers have suggested that these pigments act as antioxidants, which help a tree combat harsh conditions. Others say it helps to attract birds that can then disperse fruits. Or it might increase leaf temperature, helping to protect from the cold.

Sunscreen

Some people have observed that trees tend to turn redder when an autumn is particularly bright and cold. In 2001, William Hoch, now at Montana State University, Bozeman, suggested that the pigment acts as a protective sunscreen, helping to keep leaves on the trees for longer so that more nutrients can be harvested from them. Photosynthesis becomes more difficult as chlorophyll is broken down, and leaves become more susceptible to damage from the Sun. Damaged leaves will fall more quickly, and rid the tree of a nutrient supply.

Hoch did a study in which he made mutant trees that couldn’t produce anthocyanins. These dropped their leaves while they were still green when exposed to the high-stress environment of bright light and cold temperatures. The mutant trees were much less efficient at storing up nitrogen for the winter.

Habinck’s study of natural sweetgum and red maple trees in a nature preserve in Charlotte supports this notion. Trees in the upland areas, where soils don’t have much nitrogen, had much redder leaves than the trees in the flood-plain environment.

“A plant on a nutrient-poor soil is going to be more concerned about keeping the nutrients it has,” says Hoch. So it will turn red to stop its leaves dropping prematurely.

Habinck’s supervisor, Martha Eppes, now wants to look at satellite data to see whether there is a wider correlation between tree colour and soil type over large areas.

原文：http://www.nature.com/news/2007/071029/full/news.2007.202.html

The gift of gab sets humans apart from all other species. But what about Neandertals? A new genetic study offers tantalizing evidence that our closest extinct cousins may have been talkative, too.Nailing down whether Neandertals spoke to each other has been tricky. Studies show that they had big brains and engaged in some sophisticated behaviors, including burying their dead. But the evidence has been indirect because the soft structures of the throat don’t fossilize, and researchers have debated whether they could speak as well as we do. Recent work on a gene known as FOXP2 seems to undermine the speaking hypothesis. Many animals, including mice and bats, have the gene, but specific variations in the human version appear to have contributed to our language ability. Research indicates that these variations appeared in the past 120,000 years–long after our species split from Neandertals. “So the speculation was that [the FOXP2 variations] were unique to humans and not there in Neandertals,” says evolutionary geneticist Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who traced FOXP2’s ancestry. “If there was one single gene I really wanted to see in Neandertals, it was this one.”

Pääbo appears to have gotten his wish: His team extracted ancient DNA from two 43,000-year-old Neandertal bones found in a cave in northern Spain. Genetic analysis revealed that the FOXP2 sequence in both Neandertals matched that in living people. It harbored the two mutations that help set the human gene apart from those of all other animals. This doesn’t necessarily prove that Neandertals could speak, because many other, unknown genes probably influence language ability. But “with respect to FOXP2, there’s nothing to say that Neandertals could not speak just like we do,” says Pääbo. He now suggests that the gene was favored by selection much earlier, before Neandertals and modern humans had completely diverged, perhaps 300,000 or 400,000 years ago. The team reports its findings online 18 October in Current Biology.

Several experts say that vocal Neandertals fit what we know of these hominids, especially the fact that they had large brains and lived in groups. “I think many of us are prepared to grant Neandertals language capacity, even if … it may not have reached our modern levels,” says Chris Stringer of the Natural History Museum in London. Still, evolutionary geneticist Jeff Wall of the University of California, San Francisco, cautions that it’s possible that the Neandertal samples were contaminated with modern human DNA. Pääbo says that for this paper, the team added extra controls to try to make sure that they were analyzing Neandertal rather than modern human DNA.

Even if there were no contamination, Wall says, it’s not clear exactly when Neandertals acquired the humanlike FOXP2 gene and its potential effect on speech. Instead of belonging to a common ancestor of both species, Wall says it’s possible that the study’s Neandertals, who lived in Europe just as modern humans were beginning to enter the continent, picked up the FOXP2 variant by mixing with the newcomers. Pääbo calls that scenario “a formal possibility but one we think unlikely.”

原文网址：http://sciencenow.sciencemag.org/cgi/content/full/2007/1018/3

By exploiting millions of hours of computing time donated by the users of 150,000 home computers, scientists have predicted the structure of a protein using just its sequence of amino acids. The project marks a significant advance in a field that’s been flush with hope yet short on tangible results, experts say.

Determining the shape of a protein is normally a matter of firing X-ray beams at its crystalline form and measuring their diffraction, and protein chemists have long been sceptical of attempts to replace this practice with modelling or theory. “Modelling right now has a terrible name in the field,” says Michael Levitt, a computational biologist at Stanford University. But in a Nature paper published online on 14 October, David Baker, a biochemist at the University of Washington in Seattle, and his colleagues report results that may do much to dispel that scepticism (B. Qian et al. Nature doi:10.1038/nature06249; 2007).

A protein’s shape — and therefore its activity — is determined by the precise way its constituent string of amino acids folds up. “If you think of the whole thing as like an utterly flexible snake, there are hundreds of degrees of freedom at every site,” says Eleanor Dodson, a structural biologist at the University of York, UK. The final shape depends on the molecular interactions each amino acid has with its neighbours, with surrounding water molecules and with other amino acids that are a long distance away in terms of sequence, but which become close as a result of folding. It’s a horrendous problem to model.

Rather than trying to solve the problem from first principles, Baker’s technique combines information from the sum of what is already known about protein structures with the vast computing power available through the Berkeley Open Infrastructure for Network Computing. This software, developed at the University of California, Berkeley, allows people to contribute spare computing power on their desktops to scientific projects (most famously, the search for extraterrestrial intelligence, in the form of SETI@home); 150,000 volunteers used it to download a copy of the Baker lab’s Rosetta@home program.

Rosetta breaks a protein’s sequence into short stretches that can be matched to identical stretches from proteins with known structures. These shapes offer many ways to sew the protein under study back together, and the program chooses those that minimize the free energy of the structure (a measure of its stability). By running the program over and over again on thousands of computers, the researchers lurched towards an ever more accurate protein model.

When fed the sequence of T0283, a 112-amino-acid protein from a bacterium, the network spat out several million structures after a million hours of computing time. Those millions were whittled down to five by further repeated computer analysis, and one of the structures was spot on, correlating with the structure as determined from its crystal.

Although the structure’s precision was not on a par with high-resolution crystal models, it was good enough for researchers to think that the technique could simplify the process of obtaining X-ray structures in the future. To turn X-ray patterns into structures, researchers must produce patterns from crystals that have either been spiked with heavy-metal ‘markers’ or come with some indication of what the final structure will look like, for example from the shape of a related protein. Rosetta’s structure for T0283 was good enough to function in this way. The program should now be able to provide such reference points for proteins for which there are already X-ray data, but which lack useful relatives and whose structures thus languish unsolved. “You will be able to solve a whole bunch of these structures rather quickly,” says Adrian Roitberg, a protein modeller at the University of Florida in Gainesville.

There is still room for improvement, though, says Rhiju Das, a postdoc working on the Rosetta@home project and a co-author on Baker’s paper. Each home computer works in isolation, he explains. If the program could be rewritten to run on the many parallel processors in a supercomputer, Rosetta might become considerably more powerful.

One pay-off of better structure prediction would be the prospect of custom-made proteins, says Baker, who uses Rosetta to hunt for sequences that correspond to desired structures. His lab and that of University of Washington biochemist Bill Schief are currently working on redesigning the gp120 protein of HIV to make a vaccine that could stimulate the immune system in a different way from the natural virus. The reshaped protein should elicit antibodies that attack the virus more effectively than antibodies created after infection.

The days when protein modellers thought they could make crystallization obsolete are long gone, Baker adds. But melding the two techniques could offer biologists insight into many more proteins — and faster. “If you really care about the structure of your protein, you should get some experimental data and combine it with modelling,” he says.

原文网址 http://www.nature.com/news/2007/071016/full/449765a.html

Next time you whisper sweet nothings to the object of your affections as they peacefully doze off, don’t be surprised if they can’t remember a word of it the next morning. Neuroscientists have shown that the brain’s pathways for deciphering speech, and forming memories of it, switch off as anaesthetized patients begin to nod off. They suspect the same holds true for normal, non-drug-induced sleep.

Researchers led by Matt Davis of the Medical Research Council Cognition and Brain Sciences Unit in Cambridge, UK, studied 12 volunteers under the influence of varying amounts of an anaesthetic called propofol, which induced varying levels of drowsiness. They played them recordings of speech or other sounds, and monitored their brains using a technique called functional magnetic resonance imaging.

The volunteers’ brains were more active in response to speech than to generic noise, suggesting that they still recognised spoken words. But the part of the brain involved with the more subtle job of untangling words that can have alternative meanings depending on context or spelling (such as ‘bark’, or ‘pear/pair’) showed no activity in the drowsiest volunteers. Neither did the part involved with forming memories of speech.

This suggests that the brain simply shuts down higher-level aspects of speech recognition as sleep starts to set in, making it hard to remember or understand what was said in the moments before sleep. The results appear in the journal Proceedings of the National Academy of Sciences.

The results also show that speech comprehension can suffer even when only lightly sedated, or when slightly sleepy, says anaesthetist David Menon of the University of Cambridge, who also worked on the study. This, he adds, would explain why “when you’re falling asleep when your wife is telling you something, sometimes you don’t remember it”.

Asleep or awake

Menon and his colleagues hope that this type of work might one day help them to discover more about the degree of awareness experienced by patients in operating theatres.

Data on how many people are aware of, or have memories of, their operations, are sketchy. But the overall figure is estimated at as much as 0.2% of patients. That incidence may be even higher in certain procedures in which anaesthetists err on the side of caution and administer less anaesthetic, such as caesarian sections, heart surgeries and operations on elderly people.

So researchers are keen for improved methods for gauging the level of awareness among people under anaesthetic. “We don’t want to overdose but we want to provide a measure of how much is ‘enough’ anaesthetic,” Menon says.

Mind readers

Menon admits that it is difficult to know, simply by scanning the brain, exactly what the patient is experiencing. But he hopes that more studies of lightly sedated healthy volunteers will yield accurate descriptions of their cognitive experience to go with their brain readings. “This has to be seen as a first step, where we try and calibrate brain responses,” Menon says.

He notes that because memory seems to be impaired before other functions relating to awareness, patients may be aware of their operations but have no explicit memories of them afterwards. This could potentially lead to post-traumatic stress disorder or a worse recovery without the patient knowing why or being able to tell doctors what had happened. “They might be aware of ongoing events but we’d never know about it,” Menon says.

Another area in which such work could be useful is in measuring the cognitive experience of people in vegetative or minimally conscious states. Although these conditions feature little or no outward signs of consciousness, previous research has shown that patients can potentially achieve remarkable feats, such as mentally walking around a house or even imagining themselves playing tennis.

原文：http://www.nature.com/news/2007/071008/full/news.2007.151.html