Somehow, the end of the line for ancient human ancestors in Europe has long attracted more attention than the beginning, what with painstaking research as well as rampant speculation about how long Neandertals hung on in Spain and Portugal and whether they interbred with Homo sapiens. (If the latter, then modern humans have a little bit of Neandertal in them, something I find easy to believe every time I ride the subway.)

But now scientists are rewriting the beginning of that timeline, too. Teeth and a jaw bone discovered in Atapuerca, in northern Spain, they say, mean that the first direct human ancestors—of Neandertals as well as Homo sapiens (including Cro Magnon, for you Clan of the Cave Bear fans) and the rest—reached Europe 1.2 million years ago, not 800,000 years ago as had long been thought.

The first humans left their natal continent of Africa about two million years ago, walking out of the northeast corner through what is now Egypt. They turned right, anthropologists have long believed, probably because it was too cold and tough-going toward the north and west. Only later did some of the hominids leaving Africa make it to Europe—but that “later” has been vague.

With the stone tools, animal remains and human teeth and jawbone found in Spain by a team led by Eudald Carbonell of the Institut Català de Paleoecologia Humana i Evolució Social in Tarragona, Spain, “later” now means 1.2 million years old. As the team reports today in the journal Nature, these first Europeans were enthusiastic carnivores; the animal bones found along with the human ones, and dated to the same 1.2 million years, show signs of a butcher’s fine hand.

Who were these pioneers? The oldest known hominid fossils in Eurasia were found in Dmanisi, Georgia, and have been dated at 1.8 million years. Paleoanthropologists believe that Homo ergaster was the species that left Africa, and that’s who—along with, perhaps, another species—settled in Dmanisi. But Carbonell and his team conclude that the Atapuerca fossils look sufficiently different to be a distinct species, and so give them the name Homo antecessor.

She—for the fossil jawbone and teeth seem to come from a female—is now the best candidate for the last common ancestor of Neandertal and modern humans, Homo sapiens.

Antecessorapparently knew how to hunt, make stone tools with sharp edges for butchering their prey, and hammer. They probably doubled back from Asia and headed west into Europe. It is possible, though, that they represent a second wave of out-of-Africa wanderers, turning left at Egypt—rugged terrain and cold climate be damned. The new date for the first Europeans means there's a lot more fossils—400,000 years worth—to be found that anthropologists dreamed of, all of them offering the possibility of revealing how the children of a little band of primitive primates that left Africa 2 million years ago came to rule the world.

There’s nothing like another dramatic effect of global warming to make you think, gee, this whole climate change thing looks like it’s going to be more problematic than a few extra balmy days in March. And while Hurricane Katrina, vanishing glaciers, the current drought in the American southwest and the floods in Missouri last week all have their partisans as far as uh-oh moments go, there’s nothing like the collapse of an Antarctic ice shelf to demonstrate the catastrophic—as opposed to gradual—effects of climate change.

This week’s exhibit A: a hunk of an Antarctic ice shelf larger than the state of Connecticut is collapsing into the sea.

We have been this way before. In 2002, part of the Larsen B ice shelf, which had been floating on the eastern side of the Antarctic Peninsula, broke off from the continent and gave birth to an armada of thousands of icebergs in the Weddell Sea. It took all of 35 days for an area of the ice shelf measuring 3,250 square kilometers (larger than Rhode Island) to disintegrate, starting on January 31 of that year. Other ice shelves that have collapsed recently: the Prince Gustav Channel, Larsen Inlet, Larsen A, Wordie, Muller, and the Jones.

Now the Wilkins Ice Shelf, also on the Antarctic Peninsula and about 1,000 miles south of the tip of South America, is following suit, as captured in a series of satellite images.

Photo: National Snow and Ice Data Center/NASA

My favorite story about the Dalai Lama doesn’t concern his activities on behalf of Tibet, which is one unrelieved tragedy, but is about his interest in neuroscience. A few years ago the Dalai Lama was visiting an American medical school and watched a brain operation. Afterwards, he chatted with the surgeon, telling him how his scientist friends had patiently explained to him that all of our thoughts, feelings, memories, dreams and other mental activities are the products of electrical and chemical activity in the brain. But he had always wondered something, the Dalai Lama told the surgeon. If electricity and chemistry can produce thoughts and all the rest, can thoughts act back on the physical stuff of the brain to change its chemical, electrical and other physical properties?

The surgeon dismissed the question with a polite but indulgent no. (The Dalai Lama's English translator, Thupten Jinpa, told me this story in 2005.) The brain produces and shapes mental activity, the brain surgeon said; mental activity does not alter the brain.

That wasn’t a stupid answer 10 years ago, before scientists had fully grasped the potential of the adult brain to change in structure and function—an ability called neuroplasticity. But now researchers have documented a long list of examples of how the brain, once thought to be basically unchangeable after the ripe old age of 3, can indeed change.

The first things that were found to change the brain were sensory inputs. If you spend a lot of years playing violin, say, then the regions of the motor and somatosensory cortexes that correspond to the fingering digits (the fingers on the left hand, if you're right-handed) expand.

But now neuroscientists have documented how “mere” thoughts can also sculpt the brain. Just thinking about playing a piano piece, over and over, can expand the region of motor cortex that controls those fingers; just thinking about depressive thoughts in new ways can dial down activity in one part of the brain that underlies depression and increase it in another, leading to clinical improvement.

The scientist who has worked most closely with the Dalai Lama is Richard Davidson of the University of Wisconsin, Madison. Davidson first met the Dalai Lama in 1992, and since about 2000 has been investigating a question dear to the heart of the leader of Tibetan Buddhism: can mental training such as meditations change the brain in an enduring way? That “enduring” is key: of course the brain “changes”—in the sense that some areas become more active—when you meditate, just as it changes when you think of pink elephants, watch Obama or try to remember your first kiss. Everything we think has a corresponding brain activity. But once the thought stops, so does the activity. Usually. What Davidson wanted to know was whether meditation left a long-lasting imprint on the brain, some change of function or structure.

Since 2004, Davidson and his colleagues have reported that meditation can alter the brain’s attention capabilities and that it can increase production of brainwaves called gamma, which are associated with consciousness. Now they have found another long-lasting brain change produced by Buddhist meditation: practicing compassion meditation (more on this below) alters regions of the brain that make us empathetic, Davidson and his colleagues are reporting this evening in PLoS ONE.

In compassion meditation, as the French-born Buddhist monk Matthieu Ricard explained it to me when we were both visiting the Dalai Lama in Dharamsala for a meeting of neuroscientists and Buddhist scholars, you focus on the wish that all sentient beings be free of suffering. You generate an intense feeling of love for all beings, not fixating on individuals but encompassing all of humanity. It takes practice, since the natural tendency is to focus on one or a few specific suffering people.

Davidson conducted his new study as he has his others on meditation, enlisting expert meditators (the Dalai Lama has asked Buddhist scholars to volunteer their brains to Davidson’s research). Antoine Lutz has the meditators (monks who have 10,000 hours or more of meditation under their belts—er, saffron robes) lie in a functional magnetic resonance imaging (fMRI) tube. The fMRI detects which regions of the brain are active during meditation and which are quiet. It also detects which are active during periods between meditations. The scientists compare these readings to those on non-meditators, who undergo a quickie course in compassion meditation. In this case, Davidson and Lutz enlisted 16 monks plus 16 age-matched controls, members of the UW-Madison community.

Each of the 32 subjects lay in the fMRI and turned compassion meditation on and off, on Lutz’s command. Throughout, Lutz piped in happy sounds (a baby laughing and cooing), distressed ones (a woman who sounded as if she were in pain) and neutral ones (restaurant noise). Two regions lit up with activity:

Finally, something to look forward to as the world warms due to greenhouse gases: bigger waves along the United States’ east coast. It probably won’t be enough to make surf shops on Maui or in Santa Barbara worry about new competition for boarders, but the increased wave heights promise to give eastern surfers something more challenging than they’re used to.

Although the rise in sea level due to global warming gets all the attention, the effect of warming on wave heights promises, or threatens, to be just as dramatic.Analyzing data from one ocean buoy in the Gulf of Mexico about 200 miles south of Louisiana and three along the central eastern shore from off South Carolina to off New Jersey—operated by the National Data Buoy Center—going back to the 1970s, scientists have found that wave heights during the summer have risen steadily over the last three decades.

Big waves were both higher and more common starting in the mid-1990s than they were earlier, Paul Komar of Oregon State University and Jonathan Allan of the Oregon Department of Geology and Mineral Industries report in the Journal of Coastal Research. The largest ones now measure about 30 feet, compared to about 21 feet in decades past.

The reason: the greater intensity of tropical storms that charge up the Atlantic coast. A warmer atmosphere packing more moisture and forming cyclonic storms above warmer seas adds up to stronger hurricanes (see p. 239 and 304 of the most recent report of Working Group 1 of the Intergovernmental Panel on Climate Change). Stronger hurricanes, even those that do not make landfall, stir up the seas enough to generate greater waves. Surf’s up!

More ominously, of course, bigger waves mean more beach erosion, storm surges and similar destruction. So while boarders may rejoice in the new surf conditions along the eastern seaboard, people on dry land will likely see it very differently.

The Hubble Space Telescope didn’t quite spy little green men waving back at its camera, but it has taken the next step in the search for life beyond our solar system. As astronomers are reporting this afternoon in the journal Nature, the telescope detected an organic molecule in the atmosphere of a planet orbiting another star—the first such detection ever for any of the 277 known “extrasolar” (outside our own solar system) planets.

The molecule is methane. Although best known on Earth as the gas that rises from rotting garbage, it has a much greater allure on other planets. On Neptune and Uranus, the abundant methane in the atmosphere makes the planets look blue-green. But the discovery of methane on the planet named HD 189733b, which orbits a star 63 light years away in the constellation Vulpecula (the fox), goes beyond aesthetics. Under the right conditions of temperature, presence of water and other molecules, methane can be a star player in what is called prebiotic chemistry, the reactions that produce amino acids, nucleic acids and eventually the first living cells. (In 1953 chemist Stanley Miller zapped a mixture of methane, ammonia, hydrogen and water with electricity and got amino acids, the building blocks of proteins.

“This is a crucial stepping stone to eventually characterizing prebiotic molecules on planets where life could exist,” Mark Swain of NASA's Jet Propulsion Laboratory in Pasadena, Calif., who led the team that made the discovery, said in a statement.

The discovery comes from observations made last May with Hubble’s Near Infrared Camera and Multi-Object Spectrometer, which identifies molecules by their telltale spectra. As long as it was aiming at HD 189733b, the spectrometer also confirmed that the planet’s atmosphere contains water molecules, as the Spitzer Space Telescope found last year. With both water and organic molecules, HD 189733b would seem to have the basic ingredients for cooking up something biological.

There is only one problem. Floating out in Vulpecula (the constellation is visible from the north pole to 55 degrees south latitude, with the best visibility is in September), HD 189733b is what’s called a “hot Jupiter.” That means it is massive and so hot—because it is so close to its parent star it whips around in a mere two days—as to be beyond tropical: its atmosphere bursts the mercury at 1,700 degrees Fahrenheit, hot enough to melt silver. That makes HD 189733b too hot for life as we know it: any biological molecules fortunate enough to form would be torn apart by heat before they could do anything interesting.

So consider the discovery a proof of concept. Actually, two concepts. One, it shows that the Hubble can detect interesting molecules on distant planets using spectroscopy. Two, it shows that prebiotic molecules can form on these planets, improving the odds that they also form on planets that orbit in the “habitable zones” around stars, where temperatures are right for water to remain liquid rather than ice or vapor. Consider the measurements an important step toward determining which worlds have the conditions of temperature, pressure and chemistry for life to exist.

This observation is one of the first steps in the search for life on another planet, astrophysicist Marc Kuchner of NASA Goddard Space Flight Center said. “We need to study the chemistry in a planet's atmosphere in order to determine whether the planet could harbor life.

Ice. Bling bling. Rocks. Diamonds. However you know them, it’s always risky replacing mystique and magic with science. But while regular diamonds haven’t lost their allure even among those who know they’re basically just a compressed hunk of coal, colored diamonds—like the famous Hope—have an advantage in the mystery department: despite centuries of study, scientists aren’t sure what gives some—they come in pink, blue, red, orange, green, yellow, purple and five other basic hues—their color.

Alan Bronstein wouldn’t mind changing that. To that end, the New York City-based diamond collector and dealer has amassed two world-class collections of colored diamonds: the 296 naturally-colored-diamonds of the Aurora Collection (total carats: 267.45), now on display at the Natural History Museum in London, and the 240 of the Butterfly of Peace (166.94 carats), which was at the Smithsonian Institution from 2004 to 2005.

I’ve known Alan for almost a decade, and although I don’t know any other diamond merchants I suspect he is one of the few who gets more joy from seeing his gems written up in scientific papers with such titles as “Fluorescence Spectra of Colored Diamonds Using a Rapid, Mobile Spectrometer” than he does seeing one on a bride’s ring finger.

While the Butterfly was at the Smithsonian, Bronstein’s gave scientists there permission to subject it to an ultraviolet laser that caused the stones to fluoresce. His stones were in good company. As researchers led by James Butler of the Naval Research Laboratory reported in January in the journal Geology, they studied the blue diamonds in Bronstein’s Butterfly—plus the Hope diamond and the Blue Heart, the world's two largest known natural blue diamonds. The 45.52-carat Hope is the record-holder among deep-blue diamonds; owned once upon a time by one English and three French kings, it’s now in the Smithsonian’s National Gem Collection.

Unbeknownst to most admirers, when the Hope is exposed to ultraviolet (UV) radiation, it phosphoresces red. When the NRL’s Butler and colleagues shined UV on three synthetic, one treated, and 67 natural blue diamonds including the Hope, the Blue Heart and blues from the Aurora Butterfly and the Aurora Collection, they wound up with a way to distinguish natural blues from synthetic and treated ones. Basically, the color of the phosphorescence serves as a “fingerprint,” the scientists say, with specific wavelengths of the phosphorescence—500 (greenish blue) and 660 (orange red) nanometers--for natural blues, but no 660 for synthetics.

Colored diamonds have not given up their secrets by far, however. Scientists have figured out that blue diamonds get their color from boron and asoupçon of nitrogen, while greens get their hue from radiation and pinks from crystal deformation. But the defect or doping agent (that is, the natural element that is present in trace amounts) that produces brown diamonds is unknown, the NRL’s Butler and colleagues note in the Winter issue of Gems & Gemology, a publication of the Gemological Institute of America. And although hydrogen has been identified in purple (the rarest colored diamond) and gray-blue diamonds, they acknowledge, “the specific configuration causing the color has not yet been identified.” Nor do scientists know what gives orange diamonds their color. Mystery intact.

Biomedical researchers who challenge the conventional wisdom on health and disease are quick to claim that the establishment is trying to shut them down, and that if only they were given a chance to apply their theories and animal studies to people, patients would be cured.

Denise Faustman can make a good case for the first point. More on that below. Now we’ll see about the second: whether her iconoclastic approach to juvenile diabetes will lead to a true cure for this cruel disease. After years of setbacks, a clinical trial of a therapy that cures diabetes in mice is finally getting underway in people.

It has been seven years since Faustman, a scientist at Massachusetts General Hospital and Harvard Medical School, reported that a novel approach she developed had cured mice of type-1 diabetes. She proposed the next logical step, trying the same therapy in patients with type-1 diabetes. But the Juvenile Diabetes Research Foundation declined to fund a clinical trial (which can cost millions), and no drug company wanted to turn her idea into a commercial therapy.

Not that Faustman had any illusions about what the diabetes establishment thought of her. Still, even she was surprised, after she cured yet more diabetic mice in a 2003 study, by a letter two Harvard colleagues sent to the New York Times. In it, they slammed her claims and apologized to people with diabetes “on behalf of Dr. Faustman” for “having their expectations cruelly raised.” JDRF circulated the (unpublished) letter.

Declining Faustman’s requests for funding, JDRF did fund three competitors (including a team led by one of the scientists who wrote the scathing letter to the Times) who wanted to test her theory—or, as supporters suspected, bury it once and for all.

It didn’t work out that way. In March 2006, all three teams reported in the journal Science that they had confirmed the key aspect of Faustman’s work: that it was possible to bring the cells that produce insulin back from the dead, curing the diabetes in about one-third of the mice.

Some quick background. In juvenile (type-1) diabetes, the pancreas does not produce insulin, usually because cells of the immune system mistakenly attack and destroy the organ’s insulin-making “beta cells.” Insulin breaks down a hormone that turns the sugar (glucose) that you get in food and drink into a form cells can use for energy. Without insulin, sugar builds up in the blood, which is why diabetics require at least three daily insulin shots (or an insulin pump) and finger-*** blood glucose monitoring to avoid hypoglycaemia (low blood sugar) or hyperglycaemia (high blood sugar). Because keeping glucose in balance is so difficult, diabetes can lead to kidney failure, blindness, cardiovascular disease including stroke and heart attacks, and nerve damage that can lead to limb amputation. Type-1 diabetes is different from the more common type-2, also known as adult-onset diabetes, in which you make insulin just fine but your cells lose sensitivity to it. Faustman's work does not address type-2.

To bring beta cells back from the dead, Faustman—and then the three teams of rivals—did two things. She gave diabetic mice a compound called BCG. Bacillus Calmette-Guerin has been used for 80 years as a vaccine against tuberculosis, but it also destroys cells of the immune system called killer T-cells. Destroying killer-T cells is supposed to stop the immune system from chomping up beta cells. In mice, it did.

The real shock, however, was that with the killer T-cells eliminated, beta cells apparently regenerated enough to pump out sufficient insulin to cure the mice’s diabetes. No one had any idea before this that a diabetes-ravaged pancreas might still harbor enough beta cells, or be able to resurrect them, to reverse diabetes, at least in lab animals.

Now for people. With the usual sources unwilling to fund a clinical trial of what worked in mice, the Iacocca Foundation stepped in with $11.5 million. (Former Chrysler executive Lee Iacocca established the foundation in 1984 after his wife, Mary, died of type 1 diabetes.) In the clinical trial now enrolling volunteers at Mass General under the direction of David Nathan (and answering questions at DiabetesTrial@partners.org), volunteers will get BCG injections. They will be monitored for adverse reactions—phase-1 trials are designed primarily to assess the safety of a new treatment—as well as for signs that BCG is getting rid of the killer-T cells that destroy insulin-making beta cells.

“This is the very first step in what is likely to be a long process in achieving a cure,” Nathan said in a statement. “We first need to determine whether the abnormal autoimmune cells that underlie type 1 diabetes can be knocked out with BCG vaccination, as occurred in the mouse studies.”

Now the diabetes establishment, not to mention patients desperate for a cure, will learn whether Faustman has been tilting at windmills and “cruelly” raising patients’ hopes—or whether she has truly discovered a cure for diabetes.

Memo to everyone who doesn’t care about climate change—you know who you are—because you figure 1) more heat waves? I have A.C.; 2) rising sea levels? I don’t live in Bangladesh, and I have enough money to keep rebuilding the sea walls around my weekend place; 3) more droughts and floods, causing food shortages? I won’t have any problem buying whatever I need. Scientists have identified consequences of climate change that you won’t be able to buy your way out of: the worst airplane delays you can imagine.

I’ve long thought that Americans don’t really care all that much about climate change because they figure its worst impacts will hit other people. In particular,the poor (Hurricane Katrina, anyone?). But a report by the National Research Council released today on how climate change will affect transportation points out that this is one environmental mess that you won’t be able to buy your way out of.

The biggest impact of climate change on transportation will be flooding of roads, railways and airport runways in coastal areas because of rising sea levels and storm surges (which will be more intense as a warmer atmosphere holds more moisture). Bridges and roads built to withstand the proverbial “100-year storm” will face such monsters more frequently, meaning there will likely be more catastrophes like bridges being washed away, as happened to the U.S. 90 Bridge after Katrina. Planning any scenic coastal drives? An estimated 60,000 miles of coastal highways are subject to storm flooding even today, and that will rise as storm intensity and sea levels do. Even better: many of these are the same highways that are supposed to serve as hurricane evacuation routes!

Remember the Midwest floods of 1993, which inundated towns, and transportation routes along 500 miles of the Mississippi and Missouri river systems? Get used to it. Major east–west traffic was halted for about six weeks from St. Louis west to Kansas City and north to Chicago, the report recounts, affecting one-quarter of all U.S. freight to or from the flooded region. But where the climate is projected to dry out, such as in watersheds supplying the St. Lawrence Seaway, the Great Lakes and the Upper Midwest river system, lower water levels will leave ships high and dry, like during the drought of 1988, when barges were stranded all along the Mississippi.

Do you like being stranded at work? Climate change will bring more 24-hour rainstorms such as the one that slammed Chicago and its suburbs in July 1996, causing huge travel delays on metro highways and railroads and damaging streets and bridges. “Commuters were unable to reach Chicago for up to 3 days,” the NRC report notes, “and more than 300 freight trains were delayed or rerouted.”

Now, about those airport delays. Heat extremes and heat waves will keep getting more intense, longer and more frequent. By 2032, the chance of five summer days in Dallas being at or above 110 ^o F. will be 5 percent, for instance, up from 2 percent today, and will be 25 percent in 50 years. Good news: airports won’t have as many days when they need to de-ice planes. Bad news: because hotter air is less dense than cooler air, extreme heat reduces aircraft lift, as I explained in a recent column. Concludes the NRC, “If runways are not sufficiently long for large aircraft to build up enough speed to generate lift, aircraft weight must be reduced or some flights cancelled altogether. Thus, increases in extreme heat are likely to result in payload restrictions, flight cancellations, and service disruptions at affected airports.”

Brain-imaging studies have proliferated so mindlessly (no pun intended) that neuroscientists should have to wear a badge pleading, “stop me before I scan again.” I mean, does it really add to the sum total of human knowledge to learn that the brain’s emotion regions become active when people listen to candidates for president? Or that the reward circuitry in the brains of drug addicts become active when they see drug paraphernalia?

Sometimes, though, a brain-imaging study does tell us something we didn’t know. I’d wager that most people do not know how much of their brain power cuts out when they listen to a conversation that demands even a modicum of cognitive power. If polite requests have not made your significant other, kids or other passengers shut up when you're behind the wheel, maybe this will.

Researchers at Carnegie Mellon University had 29 volunteers use a trackball or mouse to drive along a (virtual) winding road at 43 miles per hour in a simulator while having their brain scanned. As they report in a study scheduled for publication in the journal Brain Research, listening and concentrating on spoken questions reduced by 37 percent the amount of activity in a brain circuit that you tap for driving. Result: drivers weaved out of their lane in the simulator, just like drunks.

In one condition the volunteers drove along undisturbed, while in the other they heard sentences and had to decide if they were true or false by pressing a button with their left hand. (Among the statements: "botany is a biological science and it deals with the life, structure, and growth of plants,” and “a phobia refers to a person’s extreme attraction to some object, situation, or person.”)

When the drivers were thinking about the sentences, activity fell by 37 percent in their brain’s parietal lobe, which integrates sights, sounds and other sensory information to form a sense of where you are in space and allows you to navigate. Activity also fell in the occipital lobe, which processes visual information. (The drivers got 92 percent of the true/false questions right, suggesting they were listening hard and focusing on them.) The scientists conclude, “the addition of a sentence listening task decreases the brain activation associated with performing a driving task, despite the fact that the two tasks draw on largely non-overlapping cortical areas.”

The consequences of that drop in brain activity showed in the simulator. Driving with one lobe tied behind their backs, as it were, the distracted volunteers hit a simulated guardrail and failed to keep to the middle of the lane significantly more than when they were driving without someone yakking at them.

“Engaging in a demanding conversation could jeopardize judgment and reaction time if an atypical or unusual driving situation arose,” says CMU neuroscientist Marcel Just, director of the Center for Cognitive Brain Imaging and leader of the study. He has a hunch that cell phones may be especially distracting—more so than listening to the radio or to a conversation with a passenger—because you can more easily tune out the radio when you have to concentrate on the road, and a passenger will usually shut up when she sees that you have to focus on the traffic. But cell phones have a certain rude insistence.

Our cell-phone laws are bedeviled by one little problem: epidemiological studies show that the rate of accidents among people who use hands-free phones is equal to that of people using hand-held phones. That makes laws requiring the former hard to justify, if well-intentioned. I’ll let Just and his colleagues say it: Findings such as those in this study "suggest that the deterioration in driving performance resulting from cellular phone usage results from competition for mental resources at a central cognitive level rather than at a motor output level, and that legislative measures which simply restrict drivers to the use of hand-free phones fail in their intent to limit an important distraction to driving."

Let’s say you’re playing a game with three other people, with each player having 20 poker chips. Each of you decides how many chips to keep for yourself and how many to pool. You get 0.4 chip for each chip tossed into the common fund, even if you yourself kicked in zero.

So if two players donate five chips each to the pool, for a total of 10, then you and the other free-loader have 24 chips each—your original 20 + (0.4 times 10 chips, or 4)—while the generous pair have 19: 20 minus the 4 they contributed plus (0.4 times the 10 in the pool, or 4). It looks like free-loading is the smart strategy. Except for one thing: if everyone kicked in all 20 of their chips, so the pool had 80, then everyone would do better, getting 0.4 times 80 = 32 chips.

When scientists have run this “public goods” game, they have found that, especially after a few rounds, volunteers tend to kick in quite a lot of chips. That’s particularly so if contributors can punish free-loaders. From this, scientists spun tales of a universal human impulse to punish defectors, to cooperate, and the like.

Not so fast. To their credit, scientists in England and Switzerland have now run the experiment in 16 different cities, from Bonn and Zurich to Muscat (Oman), Minsk (Belarus), Seoul and Riyadh. Suddenly, human "universals" didn’t look so universal.

Over 10 rounds of the game, 1,120 middle-class college students in Boston and Copenhagen contributed about 18 chips; those in Athens, Riyadh and Istanbul, only six. The most-cooperative participants, who kicked in 90 percent of their chips, contributed 3.1 times as much as the least-cooperative, who had an average contribution of 29 percent of their chips. Readers are invited to insert their own explanation here; extra points for resisting ethnic slurs.

Then the scientists added another layer to the game. Not only were freeloaders punished. Now they could meekly accept their punishment, or retaliate—by docking their punishers for, well, enforcing the social ideal of cooperating for the common good. The frequency of “revenge punishments,” which the scientists call “antisocial punishment of prosocial cooperators,” was all over the map and “widespread in many participant pools,” they write in tomorrow’s issue of the journal Science—but, crucially, not in societies where most of earlier work on altruistic punishment has been done and which served as the basis for conclusions about universal human nature. That undermines the claim that lack of revenge punishments--that is, accepting your punishment gracefully--is part of human nature.

Students in Boston and Copenhagen accepted their slap-down, rarely seeking revenge on their punishers, perhaps because they knew that free-loading was reprehensible. Those in Athens and Muscat had the highest level of revenge punishments, retaliating against the enforcers about six times as often as did students in Seoul, Bonn Nottingham and several other cities. Samarra, Minsk, Istanbul and Riyadh were in the middle.

Punishment did not always increase cooperation in subsequent rounds, as had been reported in studies of the public-goods game that used only American college students; sometimes, people responded to being punished by getting huffy and refusing to kick in chips to the pool.

Sometimes you just have to toss aside high-minded considerations like how research Sheds Light on the Human Condition, or Illuminates the Secrets of Life, and simply say, gee, isn’t nature amazing?

The metamorphosis of squishy little caterpillar to magnificent butterfly is so radical that you’d think little could remain of the creature’s previous life. But in a neat paper, scientists are reporting this evening that if a Manduca sexta caterpillar (also known as a tobacco hornworm) learns that a particular odor is followed by an electrical shock—classical Pavlovian conditioning—then the Manduca moth knows to be wary of that odor, too.

The caterpillars learned to avoid the odor—they inched their way down the arm of a Y-shaped contraption that did not have the odor, avoiding the arm that did. Once the caterpillar had morphed into a moth, the moth made the same choice, flying away from the aroma associated with a jolt.

The memory survives the radical transformation of crawling caterpillar to flying moth, the scientists—led by Martha Weiss of Georgetown University—conclude in their paper in the journal PLoS One. It’s the first time anyone has shown that memory can survive metamorphosis in moths or butterflies, an idea that “challenges a broadly-held view of metamorphosis—that the larva essentially turns to soup and its components are entirely rebuilt as a butterfly,” says Weiss. Indeed, the caterpillar’s brain and nervous system are extensively reorganized as it morphs through five caterpillar stages and into a moth, but apparently not enough to destroy the synapses that encode the memory.

And I can’t remember to pick up a carton of milk on my way home.

Nature is “red in tooth and claw,” the poet Alfred, Lord Tennyson, wrote in In Memoriam, A.H.H., and an awful lot of sheep ranchers and cattle are sick and tired of it—so sick and tired that they have pushed the federal government to remove the northern Rocky Mountain gray wolf from the list of endangered species, which the U.S. Fish and Wildlife Service did last month.

But there could be a great deal more death as a result—and not only because wolves will once again be fair game for hunters.

The decision to remove the northern gray wolf from has been challenged in court by 11 environment groups. But if it stands, states will take over authority for wolves in the northern Rockies—Wyoming and part of Montana and Idaho—on March 28, which de facto means that wolves will be hunted again.

The wolves’ crime? Being wolves, which many lifelong westerners view as a capital offense in and of itself. The species was wiped out in the lower 48 states, including Yellowstone National Park, in the 19^th and 20^th centuries, surviving only in northern Minnesota and Michigan’s Isle Royale, before being restored to Yellowstone beginning in 1996.

For the study, Berger’s team radio-collared more than 100 fawns in Grand Teton National Park. They compared survival rates in areas with and without wolves. Result: 10 percent of fawns survived in wolf-free/coyote-full zones, while 34 percent survived in areas where wolves were abundant and coyotes scarce.

Federal law allows hunting of wolves that attack livestock, so it’s not as if the animals are getting off scot-free. Last year, 102 wolves were killed. Government trappers killed 63, while citizens killed seven that were chasing or attacking livestock; another four were killed after confirmed livestock losses. The rest were apparently hunted illegally. Wolves killed 75 cattle in 2007, up from 32 in 2006; 27 sheep, up from four; as well as two llamas, 12 goats and three dogs, the Daily Inter Lake reported last week.) If the gray wolf is delisted, Wyoming and Idaho have said, they will launch a hunt to reduce the wolf population by 50 percent and 80 percent, respectively. There are an estimated 300 wolves in Wyoming and 700 in Idaho.