Two planets slightly smaller than Saturn have been discovered orbiting a distant star, a first for NASA's Kepler space telescope, whose mission is to look for signs of planets passing in front of stars, the space agency said Thursday.
This is "the first discovery of multiple planets orbiting the same star" by looking for such transits, said William Borucki, the science principal investigator for the Kepler Mission. He spoke in a teleconference from the NASA Ames Research Center in California.
The sun-like star, designated Kepler-9, is about 2,000 light years away in the constellation Lyra, he said.
The two planets, named Kepler-9b and 9c, show a clear gravitational interaction, according to NASA. But while scientists hope Kepler will find Earth-like planets, these two do not qualify. In addition to being much larger than Earth, they are much too close to the star they are orbiting.
"The habitable zone is actually quite far out from these stars," Borucki said. These planets "are very, very hot."
Scientists also have identified what appears to be a third, smaller celestial body orbiting the star. It's about 1.5 times the size of Earth, but it has not yet been confirmed as a planet, according to mission scientists. It also is very close to the star, with an orbit of about 1.6 days, NASA said.
The Kepler space telescope launched from Cape Canaveral in March 2009 with the mission of staring at our region of the Milky Way galaxy to search for Earth-size planets that would be in a star's habitable zone.
It is looking at more than 100,000 stars, watching for tiny repeated dips or fluctuations in their brightness. That momentary dimming, scientists say, could indicate a planet has come between the star and the telescope.
Kepler, currently 18 million miles from Earth, will continue its mission for another three and a half years.
In June, NASA announced that the space observatory had identified more than 700 planet candidates in just its first 43 days of searching, including five that could have more than one transiting planet.
"This is like opening a treasure chest," said Matthew Holman of the Harvard-Smithsonian Center for Astrophysics in Cambridge, Massachusetts.
And scientists say more discoveries are on the way as Kepler and other missions peer into the depths of the Milky Way.
"We want to know, in particular, what [the planets'] atmospheres are like," Borucki said. "Kepler can't tell us that, but missions are on the planning board that may answer those questions, which will help man understand the universe and his place in it."
He added, "A couple of thousand years ago, people asked these questions, and in the Middle Ages, they asked these questions, and now, this is a very exciting period. In the next few years, we'll have the answers to these questions."
Imagine seeing better by thinking differently. That’s a vision with a future, according to Harvard University psychologist Ellen Langer.
Eyesight markedly improved when people were experimentally induced to believe that they could see especially well, Langer and her colleagues report in the April Psychological Science. Such expectations actually enhanced visual clarity, rather than simply making volunteers more alert or motivated to focus on objects, they assert.
Langer’s new findings build on long-standing evidence that visual perception depends not just on relaying information from the eyes to the brain but on experience-based assumptions about what can be seen in particular situations. Those expectations lead people to devote limited attention to familiar scenes and, as a result, to ignore unusual objects and events.
In perhaps the most eye-popping of Langer’s new findings, 20 men and women who saw a reversed eye chart — arranged so that letters became progressively larger further down the chart, with a giant “E” at the bottom — accurately reported more letters from the smallest two lines than they did when shown a traditional eye chart with the big letters on top. All volunteers had normal eyesight.
These results reflect people’s expectation, based on experience with standard eye charts, that letters are easy to see at the top and become increasingly difficult to distinguish on lower lines, the researchers suggest.
Participants who said they thought that they could improve their eyesight with practice displayed a bigger vision boost on the reversed chart than those who didn’t think improvement was possible, but only for the next-to-smallest line. Both groups did equally well at reading the smallest, topmost line.
Another set of experiments included 63 members of the Reserve Officers’ Training Corps at MIT. Eye testing determined that their vision ranged from below average to excellent.
An experimenter told a group of 22 cadets to assume the role of a fighter pilot while operating a flight simulator. During this exercise, participants tried to identify letters shown on four plane wings of approaching aircraft. Each wing contained one of the bottom four lines of an eye chart.
Another 20 cadets performed the visual task while pretending to fly a plane in a simulator that they were told was broken. Ten other cadets read a motivational essay before the exercise. A final group of 11 cadets didn’t use a simulator but practiced eye exercises that researchers described as capable of improving eyesight before taking an eye test.
Vision improved substantially for nine of 22 simulator pilots compared with none of those who pretended to fly, two of 11 eye exercisers and one person in the motivational group. Simulator pilots did so well relative to the others because they more thoroughly adopted a mind-set of being real fighter pilots with presumably superior vision, the researchers posit. An initial survey of ROTC members found that they attributed particularly good vision to fighter pilots.
Simulator pilots with below-average vision displayed the biggest jumps in visual performance, perhaps because they had more room for improvement, the researchers suggest.
These results suggest that if eye exercise programs designed to improve vision work for some people, it’s not because of any physical effect on the eyes or brain. Such regimens “may be effective because they prime the belief that exercise improves vision,” Langer and her colleagues write.
Mind-set may boost visual performance without sharpening vision itself, comments psychologist Daniel Simons of the University of Illinois at Urbana-Champaign. Experimental manipulations in the new study, such as reversing the arrangement of an eye chart, may have made volunteers more willing to guess when they felt a bit unsure, Simons says. Such guesses stand a good chance of being right, in his view.
A new study has come up empty-handed after pursuing a genetic explanation for why one identical twin developed multiple sclerosis while the other stayed healthy.
Researchers transcribed the complete genetic blueprints for a pair of identical twins, looking for differences that might explain why one has multiple sclerosis and the other does not. No trace of what caused the discrepancy appeared in the twins’ DNA. And scientists found no smoking gun when they compared levels of gene activity between the sick and well twin. The results appear in a report published April 29 in Nature.
“We looked under a lot of rocks and we found no differences that we could replicate,” says Stephen Kingsmore, a geneticist at the National Center for Genome Resources in Santa Fe, N.M., and leader of the new study. The finding “points to some novel environmental trigger that must be very important to the disease. We don’t know what it is.”
But the new study is small; it examines only three pairs of twins and one type of immune cell known to be involved in multiple sclerosis. A telling difference between sickness and health might be found in other types of cells, such as immune cells called B cells or in oligodendrocytes, which are cells that make the nerve cell insulation called myelin, says Esteban Ballestar of the Bellvitge Biomedical Research Institute in Barcelona, Spain. “They are closing a door here, but I think, perhaps, the door should be open,” he says.
In multiple sclerosis the immune system attacks and damages the myelin sheath that helps speed electrical communication between nerves, the equivalent of scraping the coating away from an electrical wire. The damage results in pain and symptoms such as loss of coordination and vision.
In the new study, Kingsmore and his colleagues determined the entire genetic makeup of immune cells called T cells from a pair of female twins. One of the women developed multiple sclerosis at age 30 while her twin remained healthy. The twins are now old enough that the healthy one is not likely to develop the disease.
Identical twins share the same genetic makeup, and the researchers confirmed that both women carried variants of genes already known to increase the risk of getting multiple sclerosis. Scientists had thought that maybe the sick twin had developed an additional mutation in her DNA that finally triggered the disease. But the team found no such mutations.
Another way to rev up the immune system and induce it to attack the body is to increase the activity of certain genes. Upping gene activity doesn’t necessarily involve changing the genes themselves, but can be done by altering chemical tags on the DNA. In two pairs of twins, the team examined more than 2 million DNA locations that had been tagged with a common label, known as a methyl group, that keeps gene activity in check.
In a previous study, Ballestar’s group found lower levels of methylated DNA when they compared people with lupus (SN: 1/16/2010, p.13) to their healthy identical twins. But Kingsmore and his colleagues found no similar differences that could account for just one twin developing MS.
The team also measured gene activity in three sets of identical twins, including the sisters who had their genomes sequenced. The researchers did find some minor differences, but none could explain why one twin got sick and the other didn’t.
Frogs have hopped onto the list of organisms that have had their genetic codes unraveled.
A new study, published April 30 in Science, lays out the genetic blueprint of the Western clawed frog, Xenopus tropicalis. A larger cousin of X. tropicalis, called Xenopus laevis, is a popular laboratory organism for studying development. But with a genome about half the size of X. laevis’, the Western clawed frog has easier DNA to decode, says Uffe Hellsten of the Department of Energy Joint Genome Institute in Walnut Creek, Calif.
Analysis of the Western clawed frog’s genome reveals that versions of 80 percent of genes that have been linked to disease in humans turn up in frogs.
Researchers hope that the genome sequence will help scientists track down the molecular steps that lead to amphibians’ high sensitivity to hormones and other toxins and offer clues to what is causing a worldwide decline of the animals.
People with post-traumatic stress disorder seem to accumulate an array of genetic changes different from those found in healthy people, researchers report online May 3 in the Proceedings of the National Academy of Sciences.
The new findings, while showing differences between people with and without PTSD, don't shed light on whether these differences might play a role in PTSD, says study coauthor Sandro Galea, a physician and epidemiologist at Columbia University in New York City.
Only a fraction of people who witness a traumatic event develop PTSD. In an attempt to identify what makes people who develop PTSD biologically different from those who don’t, Galea and his colleagues obtained blood samples from 100 people in the Detroit area. All had been exposed to at least one potentially traumatic event, and 23 were diagnosed with PTSD. The scientists tested 14,000 genes in these blood samples for chemical changes to DNA that can affect gene activity without altering the genetic information itself.
The researchers focused on the methylation of genes, a process in which a methyl molecule is added to DNA, typically turning off a gene and inhibiting production of the protein that the gene encodes. If people with PTSD have more or less methylation in specific genes, that might somehow contribute to PTSD, Galea says.
The team found that the people with PTSD showed less methylation in several immune system genes and more methylation in genes linked to the growth of brain cells. “There is evidence that PTSD is involved in immune dysfunction, and we suggest that that’s part of a larger process,” Galea says. Although previous studies have also suggested a PTSD link to immune gene activation, the connection is unclear.
“This is interesting data, but there are a lot of things still to do,” says Manel Esteller, a molecular geneticist at the Bellvitge Institute for Biomedical Research in Spain and the University of Barcelona who was not part of the study. “What’s missing is an explanation of how the traumatic stress really causes these changes in methylation — what is the mechanistic link?”
What’s more, the sample size of 23 patients is small, and PTSD diagnosis is tricky, says Naomi Breslau, a sociologist and epidemiologist who studies PTSD at Michigan State University in East Lansing. “I don’t believe this can be taken as a breakthrough.”
Galea agrees that finding the mechanisms involved will be the key to determining whether these methylation differences matter for PTSD. If further research clarifies how these changes play out in the body, he says, “that may allow us to eventually do something about it.”
The finding may represent a new species that lived alongside Neanderthal people and anatomically “modern” humans in that region, according to the researchers.
“I at first didn’t believe” that the result could be possible, said one of the researchers involved with the finding, Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology, Leipzig, Germany. However, Pääbo said, genetic test results showed “it’s some new creature that has not been on our radar screen so far.” The findings are published in the March 25 issue of the research journal Nature.
The conclusions were based on the sequencing, or decoding, of the organism’s “mitochondrial genome,” that is, DNA from a cellular structures called the mitochondria.
Mitochonchondrial DNA is not inherited the same way as the rest of an animal’s DNA, but rather is passed down only from the mother. Because unlike other DNA it remains relatively unchanged when passed down through generations, it plays an important role in ancestry studies, in particular in determining an organism’s mother-line ancestry.
The genetic sequencing pointed to a previously unknown hominin, or extinct member of the human lineage, who lived in the Altai mountains of southern Siberia between 48,000 and 30,000 years ago, said the researchers.
The investigating team, which included also researchers from the United States, Austria and Russia, sequenced genes from a tiny piece of pinky finger bone found in Denisova cave in the Altai Mountains. They compared the mitochondrial genome with that of modern humans and Neanderthals.
The analysis indicated that the creature shared a common female or “mitochondrial” ancestor with modern human and Neanderthals about a million years ago, the scientists said. That’s about twice as old as what is believed to be the most recent common mitochondrial ancestor of modern humans and Neanderthals. Neanderthals were a stocky, now extinct subgroup of our species, Homo sapiens, who lived in Europe and parts of Asia from around 100,000 to 30,000 years ago.
The age of the fossil and the layers of earth in which they turned up also suggest “the Denisova hominin lived close in time and space with Neanderthals as well as with modern humans,” the researchers wrote.
Although researchers said they lacked definitive enough information to declare the fossil a new species, they said it also likely represented a separate migration out of Africa from modern humans and Neanderthals, both of whom are thought to have originated in that continent. The investigators also said they have no information yet that could serve to physically describe any unusual characteristics that the newfound human ancestor might have possessed.
Researchers have identified a chemical chain of events that leads cancer cells to age, and thus stop reproducing. By exploiting this process, they propose, scientists might be able to develop new cancer therapies.
The molecular sequence of events, called a signaling pathway, is described in the March 18 issue of the research journal Nature by investigators Paolo Pandolfi of the Harvard Medical School and colleagues.
Cancer cells are normally able to reproduce themselves indefinitely without ageing; this indeed is a core aspect of the problem confronting cancer victims. The out-of-control cell division leads to the creation of an ever-growing load of tumors.
The newfound pathway drives cell aging, or “senescence,” only in cancerous conditions, according to Pandolfi’s group. A key component of the pathway is a gene called Skp2, the scientists reported. By suppressing this gene, they found that they could profoundly restrict tumor formation in mice by causing cancer cells to age. The process curbed cell division.
The researchers also found that a Skp2-blocking drug induced aging in a laboratory culture of human prostate cancer cells.
Because the newfound aging pathway seems to operate only in cancer, it raises hopes that it could prove a useful target for anti-cancer treatments, which might avoid harming healthy cells, the researchers argued. Such a treatment might also have the advantage of operating in a wide array of different cancer types.
“The challenge ahead is to test whether these preclinical studies in mice can be translated into more effective cancer therapies,” wrote Manuel Serrano is of the Spanish National Cancer Research Centre in Madrid, in a commentary accompanying the study in Nature.
The study from from Vanderbilt University in Nashville, Tenn. is published in the March 14 issue of the research journal Nature Neuroscience.
“Psychopaths are often thought of as cold-blooded criminals who take what they want without thinking about consequences,” Joshua Buckholtz, a graduate student in psychology and lead author of the new study, said. “We found that a hyper-reactive dopamine reward system may be the foundation for some of the most problematic behaviors associated with psychopathy, such as violent crime, recidivism and substance abuse.”
Dopamine is the brain chemical most closely associated with pleasure and excitement.
Previous research on psychopathy has focused on what these people lack—fear, empathy and interpersonal skills. The new research, however, examines what they have in abundance—impulsivity, heightened attraction to rewards and risk taking, said Buckholtz and his co-authors. Importantly, the latter traits are those most closely linked with the violent and criminal aspects of psychopathy, researchers said.
“There has been a long tradition of research on psychopathy that has focused on the lack of sensitivity to punishment and a lack of fear, but those traits are not particularly good predictors of violence or criminal behavior,” said Vanderbilt psychologist David Zald, co-author of the study.
“Our data is suggesting that something might be happening on the other side of things. These individuals appear to have such a strong draw to reward—to the carrot—that it overwhelms the sense of risk or concern about the stick.”
The researchers used a brain imaging technique called positron emission tomography, or PET, to measure dopamine release, in concert with a probe of the brain’s reward system using functional magnetic imaging, or fMRI. “The really striking thing is with these two very different techniques we saw a very similar pattern—both were heightened in individuals with psychopathic traits,” Zald said.
Volunteers for the study took a personality test to gauge their level of psychopathic traits. These traits lie on a spectrum: violent criminals fall at its extreme end, but a normally functioning person can also have psychopathic traits to some degree. These traits include manipulativeness, egocentricity, aggression and risk taking.
The researchers gave the volunteers a dose of amphetamine, or speed, and then scanned their brains using PET to view dopamine release in response to the stimulant. Substance abuse has been shown in the past to be associated with alterations in dopamine responses. Psychopathy is strongly associated with substance abuse.
“Our hypothesis was that psychopathic traits are also linked to dysfunction in dopamine reward circuitry,” Buckholtz said. “Consistent with what we thought, we found people with high levels of psychopathic traits had almost four times the amount of dopamine released in response to amphetamine.”
The research subjects were later told they would receive some money for completing a simple task. Their brains were scanned with fMRI while they were performing the task. The researchers found in those participants with more psychopathic traits the dopamine reward area of the brain, the nucleus accumbens, was much more active while they were anticipating the reward.
“It may be that because of these exaggerated dopamine responses, once they focus on the chance to get a reward, psychopaths are unable to alter their attention until they get what they’re after,” Buckholtz said. Added Zald, “It’s not just that they don’t appreciate the potential threat, but that the anticipation or motivation for reward overwhelms those concerns.”
Artist'srendering of what HD 131488's inner planetary system might look like as two large rocky bodies collide. Inset illustrates the location of HD 131488's dust belts (top) and comparable regions to our own Solar System (bottom). HD 131488's hot inner dust belt has similar separations from its host star as the terrestrial planet zone around our Sun while the star's cool dust belt has similar separations from its host star as the Kuiper Belt region in our Solar System. Also shown for our Solar System are the orbits of Jupiter, Saturn, Uranus, and Neptune.<
A far-off solar system seems to be forming from a strange dust whose makeup is unlike that of our and other solar systems, astronomers say.
The researchers at the University of California Los Angeles found evidence for the formation of young, rocky planets from dust circling a star some 500 light-years away. A light-year is the distance light travels in a year
“Until now, warm dust found around other stars has been very similar in composition to asteroidal or cometary material in our Solar System,” said the university’s Carl Melis, who led the research while a graduate student.
But this case is different, he said.
“Typically, dust debris around other stars, or our own Sun, is of the olivine, pyroxene, or silica variety, minerals commonly found on Earth,” he noted. But this material “is not one of these dust types. We have yet to identify what species it is.”
Melis reported the findings last Wednesday at the annual American Astronomical Society meeting in Washington, D.C.
The star, known as HD 131488, appears to be surrounded by warm dust in a region called the terrestrial planet zone, where temperatures are similar to those on Earth, Melis said. He added that the dust seems to harbor rocky, embryonic planets that have recently collided.
“What makes HD 131488 truly unique is the unidentified dust species released from the colliding bodies as well as the presence of cold dust far away from the star,” said astronomer Benjamin Zuckerman of the university, a co-author of the research. “These two characteristics make HD 131488 unlike any other star with evidence for massive quantities of dust in its terrestrial planet zone.”
The researchers analyzed the warm inner dust through infrared imaging and spectroscopy using an instrument called T-ReCS on the Gemini South telescope in Chile. Spectroscopy is the analysis of the composition of objects using the spectrum of light they give off.
Melis and his team argue that the most plausible explanation for the unusual abundance of warm dust is a recent collision of two rocky planetary mass bodies.
While the mysterious warm dust lies at a distance from HD 131488 that is comparable to the Earth-Sun separation, the team also found cooler dust about 45 times further out. This outer dusty region is analogous to the Kuiper Belt in our own Solar System where many minor planets orbit the Sun just beyond the orbit of Neptune.
“The hot dust almost certainly came from a recent catastrophic collision between two large rocky bodies in HD 131488’s inner planetary system,” Melis said. But the cooler dust “is probably left over from planet formation that took place farther away from HD 131488.”
HD 131488 lies in the direction of the constellation Centaurus and is three times heavier and 33 times more luminous than our own Sun. The star is part of a major, southern-hemisphere star forming region known as the Upper-Centaurus-Lupus association whose members are believed to be about 10 million years old. By contrast, the Sun and Earth are about 4.6 billion years old..
In adult female mice, switching off one gene seems to start turning the ovaries into testicles and triggers the production of male hormones at normal male levels, scientists say.
The curious findings have led two researchers to remark in a published paper that, biologically speaking, females may be engaged in a lifelong “battle to suppress their inner male.”
Both papers appear in the Dec. 11 issue of the research journal Cell.
The new results echo a previous study that found that female ovarian tissues in mice start to convert to male-like tissues in the absence of signals from estrogen, a female sex hormone. That study appeared in the Dec. 17, 1999 issue of the journal Science.
In the newer research, N. Henriette Uhlenhaut of the European Molecular Biology Laboratory in Heidelberg, Germany, and colleagues were studying genes that during development are responsible for converting glands called gonads into either ovaries or testicles, depending on the sex.
Ovaries produce eggs, the female sex cells, while testicles produce sperm.
Uhlenhaut and colleagues genetically engineered mice in which the activity of a called Fox2L could be chemically suppressed in the ovaries.
Fox2L, in turn, is a regulator gene that influences the level of activity of an array of other genes. Among other things, it keeps in check genes that tend to promote testicle development, according to Uhlenhaut’s group.
Switching off Fox2L had the immediate effect of increasing the level of activity of some of these “testis-specific” genes, the scientists reported. Critical among these, they identified one called Sox9.
Concomitant with the boost in Sox9 activity was a “reprogramming” of certain ovarian cell lineages into what appeared to be testis cell lineages, Uhlenhaut and colleagues found. Meanwhile, the modified ovaries began producing normal male-like levels of the hormone testosterone.
“Our results show that maintenance of the ovarian phenotype [form] is an active process throughout life,” the scientists wrote.
It’s unclear whether the findings would translate to humans, but because mice share over 90 percent of their genes with humans, it very often happens that mouse processes have parallels in humans.
It would seem “testicular development is actively repressed throughout the life of females,” added Andrew Sinclair and Craig Smith of the Murdoch Children’s Research Institute in Melbourne, Australia, in a paper published in the same issue of Cell. Sinclair and Smith the researchers who in their article metaphorically suggested an “inner male” may lurk within all females also noted the findings go against “conventional wisdom” that the ovary and testis are “terminally differentiated,” or irreversibly developed to their mature state.
Scientists have found that prions infectious molecules that cause fatal brain diseases can evolve in a Darwinian fashion, though they lack any DNA or similar material.
The study from Scripps Research Institute in Jupiter, Fla. found that prions can develop many mutations. Mutations that help the prions to withstand threats then tend to persist in a “population” of prions, while other prions are destroyed. This eventually leads the prions to develop adaptations such as drug resistance.
The process in other words would seem to be analogous to the way that living things evolve, according to Darwinist principles. Viruses, too which are often considered non-living can evolve. But unlike prions, viruses have in common with life forms that they contain DNA or closely related molecule, RNA.
The prion study was published in the Dec. 31 issue of the research journal Science Express, an advance, online edition of the journal Science.
Prions consist of proteins, large molecule composed of many smaller molecular subunits of so-called amino acids. Protein molecules have different characteristics depending on the precise arrangement of their subunits. This includes different ways the protein’s parts can be folded about with respect to each other.
Many of the prion “mutations” boil down to different folding arrangements, said Charles Weissmann, head of Scripps Florida’s Department of Infectology, who led the study. These various foldings play an analogous evolutionary role in prions to different DNA sequences, or codes, in the evolution of living things.
“On the face of it, you have exactly the same process of mutation and adaptive change in prions as you see in viruses,” he explained.
Infectious prions short for proteinaceous infectious particles are associated with some 20 different diseases in humans and animals, including mad cow disease and a rare human form, Creutzfeldt-Jakob disease. All are untreatable and eventually fatal. Prions, which are composed solely of protein, are classified by distinct strains, originally characterized by their incubation time and the disease they cause.
Prions exist in a normal, healthy form, produced naturally in mammalian cells, called cellular prion protein or PrPC. The disease process begins when prions take on an abnormal, misfolded form. A normal prion that comes into contact with a misfolded one may as a result become misfolded itself. This zombie-like process may eventually lead to the creation of huge assemblies of these misfolded proteins. They stick together and cause massive damage.
“It was generally thought that once cellular prion protein was converted into the abnormal form, there was no further change,” Weissmann said. “But there have been hints that something was happening. When you transmit prions from sheep to mice, they become more virulent over time. Now we know that the abnormal prions replicate, and create variants, perhaps at a low level initially. But once they are transferred to a new host, natural selection will eventually choose the more virulent and aggressive variants.”
Weissmann and his colleagues transferred prion populations from infected brain cells to culture cells. When transplanted, cell-adapted prions developed and out-competed their brain-adapted counterparts, confirming prions’ ability to adapt to new surroundings, according to the scientists. When returned to brain, brain-adapted prions again took over the population.
Weissmann said the findings have implications for the development of treatments. Instead of developing drugs to target abnormal proteins, it could be more efficient to try to limit the supply of normally produced prions – in essence, reducing the amount of fuel for the fire, he proposed. Weissmann and his colleagues found some 15 years ago that genetically engineered mice devoid of the normal prion protein develop and function quite normally and are resistant to prion disease.
“Finding a way to inhibit the production of normal prion protein is a project currently being pursued in collaboration with Scripps Florida Professor Corinne Lasmezas in our department,” he said.
In a study that could help clarify the complex relationships between the brain, environment and behavior, researchers have found that four-month-old infants’ temperament predicts some aspects of their brain structure 18 years later.
Scientists at Massachusetts General Hospital in Charlestown, Mass., studied 76 eighteen-year-olds that, at four months of age, had been categorized in previous research as “high-reactive” or “low-reactive.” High-reactive generally means shy and inhibited, while low-reactive means outgoing and uninhibited.
The investigators used a form of brain scanning known as structural magnetic resonance imaging, which employs magnetic field and radio waves to produce clear and detailed pictures of the brain.
Adults with a low-reactive infant temperament showed greater thickness in a brain structure called the left orbitofrontal cortex, the scientists found. This region has been implicated in processing of emotions and of self-monitoring.
On the other hand, the adults previously categorized as high-reactive, showed greater thickness in the right ventromedial prefrontal cortex, the researchers reported. This brain area has been linked to impulse control, with greater size linked to more self-control, and with the analysis of social situations.
“To our knowledge, this is the first demonstration that temperamental differences measured at four months of age have implications for the architecture of human cerebral cortex lasting into adulthood,” the researchers wrote in the study, published in the January issue of the journal Archives of General Psychiatry. The cerebral cortex is a layer of brain cells covering the surface of the brain and linked to advanced thinking functions.
High-reactive infants are characterized at age four months by vigorous activity and crying in response to unfamiliar stimuli, according to the authors, Carl Schwartz, director of the hospital’s Developmental Neuroimaging and Psychopathol&sh Research Laboratory, and colleagues. Low-reactive infants by contrast stay more still and cry less in respose to the same situations.
High-reactive infants tend to become behaviorally inhibited in the second year of life, while low-reactive infants tend the opposite way, the authors added.