Climate Change Pollution Rising—Thanks to Overwhelmed Oceans and Plants

Climate Change Pollution Rising—Thanks to Overwhelmed Oceans and Plants

Carbon dioxide levels in the atmosphere continue to rise thanks to dirtier economies and a weakening in natural systems' ability to remove the greenhouse gas

	WINDS OF CHANGE:  Changed circumpolar winds are interfering with the Southern Ocean's ability to absorb carbon dioxide.

The world may finally acknowledge that global warming is a major environmental hazard. But new research shows that reducing the main greenhouse gas behind it may be even more difficult than previously believed. The reason: the world's oceans and forests, which scientists were counting on to help hold off catastrophic rises in carbon dioxide, are already so full of CO₂ that they are losing their ability to absorb this climate change culprit.

"For every ton of CO₂ emitted [into] the atmosphere, the natural sinks are removing less carbon than before," says biologist Josep "Pep" Canadell, executive director of the Global Carbon Project—an Australia–based research consortium devoted to analyzing the pollution behind global warming. "This trend will continue into the future."

Specifically, oceans and plant growth absorbed only around 540 kilograms per metric ton (1,190 pounds per short ton) of the CO₂ produced in 2006, compared with 600 kilograms per metric ton (1,322 pounds per short ton) in 2000. Coupled with an emissions growth rate of 3.3 percent—triple the growth rate of the 1990s—the atmospheric burden is now rising by nearly two parts per million of CO₂ a year, the fastest growth rate since 1850, the international team of researchers reports in Proceedings of the National Academy of Sciences USA.  

"We have yet to make real progress in turning the world toward decreasing CO₂ emissions," says the study's co-author Chris Field, director of the Carnegie Institution of Washington's Department of Global Ecology in Stanford, Calif. "A greater buildup of CO₂ means more warming."

Atmospheric concentrations of the most ubiquitous greenhouse gas reached 381 parts-per-million in 2006 after emissions of CO₂ from burning fossil fuels rose to 8.4 billion metric tons (1.85 X 10¹³ pounds) per year, according to figures from the United Nations, British Petroleum and the U.S. Geological Survey.

All told, human activity released 9.9 billion metric tons (2.18 X 10¹³ pounds) of carbon in 2006, up from just 8.4 billion metric tons (1.85 X 10¹³ pounds) in 2000. At the same time, poleward shifts of westerly winds in the Southern Ocean reduced the region's ability to suck up CO₂ as have mid-latitude droughts, which slowed the growth rate of forests and plants that capture carbon.

New maritime measurements over the past decade also show that the North Atlantic's ability to absorb CO₂ has been cut in half, according to researchers from the University of East Anglia who were not affiliated with the study by Canadell and his colleagues. "Until now, we thought that the decline in the efficiency of natural sinks was going to happen during the 21st century and more strongly during [its] second half," Canadell says. "If we didn't [include in the assumptions] that this was going to happen [so soon], have we underestimated the decline in the efficiency into the future?"

In addition, this research shows that CO₂ emissions over the past decade were higher than those considered in the most dire scenarios for future climate change, which means that even more drastic actions will be needed to stem global warming. "The longer we wait to reduce emissions," Canadell says, "the harder the cuts that will be required to stabilize atmospheric CO₂ emissions."

Taming Baby Rage: Why Are Some Kids So Angry?

Taming Baby Rage: Why Are Some Kids So Angry?

New research indicates babies are born with violent tendencies that most learn to control

	FAILURE TO UNLEARN:   A Canadian researcher suggests that all children have a tendency to be aggressive as toddlers, but, through socialization, many learn to communicate through different means.

It is not the cartoons that make your kids smack playmates or violently grab their toys but, rather, a lack of social skills, according to new research.

"It's a natural behavior and it's surprising that the idea that children and adolescents learn aggression from the media is still relevant," says Richard Tremblay, a professor of pediatrics, psychiatry and psychology at the University of Montreal, who has spent more than two decades tracking 35,000 Canadian children (from age five months through their 20s) in search of the roots of physical aggression. "Clearly youth were violent before television appeared." 

Tremblay's previous results have suggested that children on average reach a peak of violent behavior (biting, scratching, screaming, hitting…) around 18 months of age. The level of aggression begins to taper between the ages of two and five as they begin to learn other, more sophisticated ways of communicating their needs and wants.

Tremblay on Wednesday is set to present preliminary study results showing a genetic signature consistent with chronic violent behavior at a meeting of The Royal Society, the U.K.'s academy of science, in London.

"We're looking at to what extent the chronically aggressive individuals show differences in terms of gene expressions compared to those on the normal trajectory," he told ScientificAmerican.com. "The individuals that are chronically aggressive have…more genes that are not expressed." The fact that a gene can be silenced or the level of protein it encodes reduced, he added, "is an indication that the problem is at a very basic level."

When children first begin to poke, prod and even slap, parents, teachers and siblings often react by indicating that those behaviors are inappropriate. But, citing studies done in animals, Tremblay notes that an unfit environment beginning in the womb may affect a child's ability to learn this lesson in the first place. And he plans to extend his genetic studies to include expectant mothers to determine if their behavior during pregnancy is linked to the down tuning of genes that may be associated with chronic aggression.

"In the long studies we've been doing, we've measured a number of characteristics during pregnancy and after birth that are good predictors'' of chronic aggression in children, Tremblay notes. Possible factors that might influence neurobiological development of the fetus, he says, include smoking, drinking, poor nutrition and excessive stress.

Tremblay speculates that genes play a significant role: for instance damaged genes may make it hard for children to acquire language, frustrating them and making them prone to violence, among other means of making themselves heard. "When you don't master language," Tremblay says, "it's hard to get people to understand what you want."

Kate Keenan, an associate professor of psychiatry at the University of Chicago, views this new genetic analysis as the logical next step in Tremblay's long-term exploration into childhood aggression. She believes Tremblay's work may help uncover genetic profiles distinct to chronically aggressive children that may allow researchers to answer questions like, "Can we differentiate [between these kids] even earlier?" [and] "How early can you intervene?" 

Climate change blamed for fading foliage

Climate change blamed for fading foliage

Every fall, Marilyn Krom tries to make a trip to Vermont to see its famously beautiful fall foliage. This year, she noticed something different about the autumn leaves.

"They're duller, not as sparkly, if you know what I mean," Krom, 62, a registered nurse from Eastford, Conn., said during a recent visit. "They're less vivid."

Other "leaf peepers" are noticing, too, and some believe climate change could be the reason.

Forested hillsides usually riotous with reds, oranges and yellows have shown their colors only grudgingly in recent years, with many trees going straight from the dull green of late summer to the rust-brown of late fall with barely a stop at a brighter hue.

"It's nothing like it used to be," said University of Vermont plant biologist Tom Vogelmann, a Vermont native.

He says autumn has become too warm to elicit New England's richest colors.

According to the National Weather Service, temperatures in Burlington have run above the 30-year averages in every September and October for the past four years, save for October 2004, when they were 0.2 degrees below average.

Warming climate affects trees in several ways.

Colors emerge on leaves in the fall, when the green chlorophyll that has dominated all spring and summer breaks down.

The process begins when shorter days signal leaves to form a layer at the base of their stems that cuts off the flow of water and nutrients. But in order to hasten the decline of chlorophyll, cold nights are needed.

In addition, warmer autumns and winters have been friendly to fungi that attack some trees, particularly the red and sugar maples that provide the most dazzling colors.

"The leaves fall off without ever becoming orange or yellow or red. They just go from green to brown," said Barry Rock, a forestry professor at the University of New Hampshire.

He says 2004 was "mediocre, 2005 was terrible, 2006 was pretty bad although it was spotty. This year, we're seeing that same spottiness."

"Leaf peeping" is big business in Vermont, with some 3.4 million visitors spending nearly $364 million in the fall of 2005, according to state estimates.

State tourism officials reject the notion that nature's palette is getting blander. Erica Housekeeper, spokeswoman for the state Department of Tourism and Marketing, said she had heard nothing but positive reports from foresters and visitors alike this year.

The problem is perception, Housekeeper says: Recollections of autumns past become tinged by nostalgia.

"Sometimes, we become our own worst critics," Housekeeper said.

People who rely on autumn tourism in New England are worried.

"I don't have a sense that the colors are off, but the timing is definitely off," said Scott Cowger, owner and innkeeper at the Maple Hill Farm Bed & Breakfast Inn at Hallowell, Maine.

"Some trees are just starting to change now," Cowger said Thursday. "It used to be, religiously, it was the second week of October when they were at their peak. I would tell my guests to come the second week if you want to see the peak colors. But it's definitely the third or fourth week at this point."

People in Northampton, Mass., are still waiting on fall color. If foliage-viewing is the goal, "I wouldn't send anybody down this way yet," Autumn Inn desk clerk Mary Pelis said this past week.

"The way things are going, the foliage season is the one sure thing for us," said Amie Emmons, innkeeper at the West Mountain Inn, in Arlington, Vt. "We book out two years in advance. It's very concerning if you think the business could start to be affected."

The colors of fall are seen on trees that frame the First Congregational Church in...

 

Cave Speak: Did Neandertals Talk?

Cave Speak: Did Neandertals Talk?

Discovery of the human variant of the FOXP2 gene in Neandertals suggests they may have had language skills

	PREHISTORIC PRATTLERS:  New study finds Neandertals had human gene for speech

German researchers have discovered Neandertals apparently had the human variant of a gene that is linked to speech and language. A team of scientists, primarily from the Max Planck Institute for Evolutionary Anthropology in Leipzig, made the discovery during efforts to reconstruct a full genome of the extinct hominid.

The findings push back the estimated timing of the FOXP2 gene's selective sweep (rapid spread of a gene mutation due to the survival advantage it conferred) from 200,000 to 350,000 years ago, when the common ancestor of Neandertals and humans roamed the earth.

"From the point of this gene, there is no reason to think that Neandertals did not have language as we do," says Planck Institute geneticist Johannes Krause, a co-author of the study published in Current Biology. "However, many other as yet unknown genes are involved in language, so in the future these will have to be found and looked at in Neandertals."

 

The human version of the FOXP2 (short for fork-head box P2) differs from that of the chimp (the closest living relative of humans) in two places along the genetic code, causing differences in two amino acids in the protein coded by the gene. FOXP2 was first tied to language in 2001, when a mutation in it was shown to affect a person's ability to speak.

To determine which version of FOXP2 Neandertals carried, the research team extracted DNA from a well-preserved fossil found in the El Sidrón Cave in northern Spain. This marks the first time a particular gene was sequenced from a Neandertal's nuclear DNA. Although DNA taken from the cellular mitochondria (energy centers) is typically easier to access, fossils are often contaminated by human contact.

The team took steps to ensure they were sequencing Neandertal DNA and not modern human residues. Among them: sequencing specific parts of the Y chromosome and comparing them with those of modern human DNA. The samples were distinct, indicating that they were dealing with an authentic specimen.

When the sequencing was complete, the Neandertal FOXP2 showed the same two mutations that the human gene carries (compared with the chimp version). The group did not find any genetic evidence of interbreeding between humans and Neandertals, leading them to conclude this incarnation of the gene must have propagated and spread prior to the genetic split of the two hominid species more than 300,000 years ago.

Simon Fisher, a molecular neuroscientist at the University of Oxford in England, says the new work shows a better method for dating the evolution of certain genes, as opposed to inferring from changes throughout human evolution. He was more cautious about its link to Neandertal's speaking ability. "We do not think of FOXP2 as 'the speech gene,'" he says. "It is instead just one piece of a complicated puzzle, which likely involves many different factors. … The FOXP2 gene has been around for a very long time, found in similar form in distantly related vertebrate species, and it may be important not only for brain development and function but also in other tissues."

Krause says the Planck team will continue to cobble together the Neandertal genome and chart the evolution of other genes by comparing Homo sapiens with Neandertal DNA. Some other candidates include ASPM, which is tied to microcephaly (a condition when the head is disproportionately smaller than the body), and MC1R, implicated in skin pigmentation.

Lessons Learned—Or Overlearned: It Makes All the Difference in How the Brain Copes

Lessons Learned—Or Overlearned: It Makes All the Difference in How the Brain Copes

Study may offer a new therapeutic target for counteracting post-traumatic stress disorder and depression by switching coping methods

	BUM OUT OR BOUNCE BACK?:  New study shows that the level of a protein in the brain's reward circuitry indicates whether a person will withdraw or recover quickly from a traumatic event.

The neural activity and physical behavior of mice recovering from several stressful encounters may illustrate alternative ways that mammals respond to traumatic events.

Researchers at the University of Texas (U.T.) Southwestern Medical Center at Dallas noticed that mice used two primary methods to cope with defeat after being repeatedly pummeled by larger, more aggressive foes: Some of the weaker members withdrew, avoiding all types of social interaction for more than a month, whereas others rolled with the punches, so to speak, quickly bouncing back to their normal behavior.

The observation of different coping mechanisms led the team to probe the animals' brains, where they discovered that the level of a certain protein in its reward circuitry determines whether the mice will be traumatized for several weeks or only temporarily down. Researchers found that levels of neurotrophic factor (BDNF) nearly doubled in the brains of vulnerable mice, a finding that could point to a therapeutic target in humans for combating post-traumatic stress disorder and depression.

In an earlier study, the research team, led by U.T. Southwestern psychiatry professor Eric Nestler, found that levels of BDNF—which is implicated in learning because of its role in creating stronger connections between neurons—increase in the nucleus accumbens in response to chronic stress. (The nucleus accumbens is a region in the rear of the forebrain that plays a role in determining whether a stimulus is rewarding or negative.) This rise in BDNF concentration, the scientists say, results from increased activity of neurons in the ventral tegmental area, a midbrain structure that sends signals to the nucleus accumbens via the chemical messenger dopamine.

"Vulnerability is caused by an increase in the frequency of dopamine impulses; a side-effect of that is an increase in the levels of BDNF," says study co-author Vaishnav Krishnan, a graduate student in Nestler's lab. "Resilient mice overcome this change by counteradapting their gene expression [the suite of genes that act on the nucleus accumbens that are either turned on or off] to clamp down the levels of activity in the ventral tegmental area."

Because the mice involved in the study were genetically similar, researchers ruled out a genetic link to the different responses. "These two end points," Krishnan explains, "are really the manifestations of two different types of coping styles."

According to the researchers, as they plunged into despair, mice that experienced the increase in BDNF levels showed symptoms similar to those of human depression: they interacted less with other mice, lost weight and were not interested in sugar or sexual activity, both of which they naturally find rewarding.

"The increase in BDNF may have an adaptive role normally, allowing an animal to learn that a situation is bad and [to] avoid it in the future," Nestler says. "Under conditions of extreme social stress, susceptible animals may be 'overlearning' this principle and generalizing it to other situations."

The U.T. Southwestern team, in an effort to get a clearer parallel between the animal and human condition, conducted autopsies on the brains of depressed and normal individuals. The group suffering from depression had BDNF levels that were as much as 40 percent higher than their counterparts.

"If we can understand how to promote resilience to [chronic] stress," Krishnan says, "we can find new ways of treating depression…. Off the top of my head, a drug that would decrease the amount of BDNF that's released in response to [dopamine] activity would be a good antidepressant." He cautions, however, that such therapy would have to be localized, so that it did not interfere with the protein's role in learning in other brain regions.