Solar flare reveals physics of an angry sun
Posted: Tuesday, October 28, 2003
Earth in path of solar-ejected cloud
By Kate Tobin, CNN
One of the largest known solar flares erupted from the sun on Tuesday, heralding a storm of superheated gas that could hit Earth within a day.
The outburst was classified an X17.2 flare, the third largest on record, according to Paal Brekke, a project scientist with the Solar and Heliospheric Observatory (SOHO), a sun-watching satellite mission jointly run by NASA and the European Space Agency.
In comparison, two solar storms observed last week were between X1 and X5, Brekke said.
Solar flares are associated with coronal mass ejections, or CMEs, eruptions from the sun that, if headed our way, can disrupt communications satellites and power grids.
As this particularly fast-moving CME is aimed directly toward Earth, it is possible that when it arrives midday Wednesday, the geomagnetic activity will be strong enough to stir up electrical trouble.
"The eruption was positioned perfectly. It's headed straight for us like a freight train," said John Kohl, a Harvard-Smithsonian Center for Astrophysics scientist, in a statement. "A major geomagnetic storm is bound to happen."
Brekke is not so sure and awaits more data from SOHO and another deep space solar-watching satellite positioned between the sun and Earth.
"Until we know the orientation of the magnetic field in this cloud, we will know who how severe the geomagnetic storm will be."
Interacting with Earth's magnetic field, the high-energy solar winds produced by a CME often increase night displays of the northern and southern lights.
"Not all CMEs trigger auroras. Several, for instance, have swept past Earth in recent days without causing widespread displays," said Tony Phillips of Spaceweather.com, which monitors cosmic conditions related to the sun and Earth.
"It all depends on the orientation of tangled magnetic fields within the electrified cloud of gas. This CME is no exception. It might cause auroras, or it might not. We will find out when it arrives."
Researchers classify solar flares using three categories: C for weak, M for Moderate and X for strong. The largest flare on record, one of two known X20s, occurred on April 2, 2001, but was not directed at Earth.
In March 1989, an X15 burst knocked out power for millions of people in Canada. In recent years, however, satellite and utility operators have devised safeguards that usually minimize damage from solar storms.
Space weather forecasters say this spate of strong solar flares unusual because it is not following normal patterns of solar behavior. The sun follows an 11-year cycle of activity and the last peak took place in 2000.
-- CNN.com's Richard Stenger contributed to this report.
Send page by E-Mail New Study Identifies Gene Signaling Puberty
Posted: Thursday, October 23, 2003
Source: NIH/National Institute Of Child Health And Human Development
NIH-funded researchers have identified a gene that appears to be a crucial signal for the beginning of puberty in human beings as well as in mice. Without a functioning copy of the gene, both humans and mice appear to be unable to enter puberty normally. The newly identified gene, known as GPR54, also appears necessary for normal reproductive functioning in human beings.
The study, funded in part by the National Institute of Child Health and Human Development (NICHD), appears in the October 23 issue of the New England Journal of Medicine. GPR54 is located on an autosomal chromosome (a chromosome that is not a sex chromosome). The study also was funded by the National Center for Research Resources and the National Institute of General Medical Sciences, both at NIH.
"The discovery of GPR54 is an important step in understanding the elaborate sequence of events needed for normal sexual maturation," said Duane Alexander, M.D., Director of the National Institute of Child Health and Human Development (NICHD). "Findings from this study may lead not only to more effective treatments for individuals who fail to enter puberty normally, but may provide insight into the causes of other reproductive disorders as well."
Puberty begins when a substance known as gonadotropin releasing hormone (GnRH) is secreted from a part of the brain called the hypothalamus. Individuals who fail to reach puberty because of inherited or spontaneous genetic mutations are infertile.
"The discovery of GPR54 as a gatekeeper for puberty across species is very exciting" said the study's first author, Stephanie B. Seminara, of the Reproductive Endocrine Unit, Massachusetts General Hospital, Boston and a member of the NICHD-funded, Harvard-wide Endocrine Sciences Center. "In the future, this work might lead to new therapies for the treatment of a variety of reproductive disorders."
The GPR54 gene contains the information needed to make a receptor. Receptors and the molecules that bind to them are analogous to a lock and a key mechanism. Like a key fits into a lock, certain molecules bind to their receptors, which usually sit atop a cell's surface. Once the binding takes place, the cell either will begin a new biochemical activity, or halt an ongoing activity. The researchers think that the molecule metastatin binds to the GPR54 receptor. As of yet, they do not know what precise effect the molecule may have on cells.
The researchers sought to learn which genes are involved in triggering the brain's release of GnRH at puberty. Two teams of researchers working independently of each other were involved in the discovery. One consisted of U.S. based researchers, the other, of British researchers.
The U.S. team included Scientists from Massachusetts General Hospital, Brigham and Women's Hospital, and Harvard Medical School who collaborated with a researcher at Kuwait University. The British team included researchers from the University of Cambridge and Paradigm Therapeutics Ltd. in Cambridge. The U.S. researchers isolated the gene from members of a Saudi Arabian family that suffered from idiopathic hypogonadotropic hypogonadism (IHH), a rare inherited disease in which sexual development is incomplete or does not occur because of insufficient release of GnRH from the hypothalamus. If untreated, individuals with this disorder fail to develop sexually.
By analyzing genetic material from men and women with IHH using tools from the NIH-sponsored Human Genome Project, the U.S. researchers first discovered that a certain region of chromosome 19 carried the mutant gene responsible for IHH. The researchers then identified GPR54 as the possible gene.
Working independently of the U.S. and Kuwaiti researchers, the British researchers created mice lacking GPR54. The mice without GPR54 also failed to reach puberty. The study authors found, however, that the brains of the mice contained normal levels of GnRH. The researchers do not yet know why the animals were unable to enter puberty, despite producing normal amounts of the hormone.
The findings from the two research teams complement each other, explained NICHD project officer Louis De Paolo, Ph.D, of NICHD's Reproductive Sciences Branch.
"Through some careful detective work, the U.S. researchers pinpointed the gene that causes IHH in this family," said Louis De Paolo, Ph.D., project officer in NICHD's Reproductive Sciences Branch. "Using the mouse model, the British researchers gained an important insight into the function of the gene."
The NICHD is part of the National Institutes of Health (NIH), the biomedical research arm of the federal government. NIH is an agency of the U.S. Department of Health and Human Services. The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. NICHD publications, as well as information about the Institute, are available from the NICHD Web site, http://www.nichd.nih.gov, or from the NICHD Information Resource Center, 1-800-370-2943; e-mail NICHDClearinghouse@mail.nih.gov.
Send page by E-Mail Discovery in Ethiopia sheds new light on history of man
Posted: Wednesday, October 22, 2003
by Abram Katz, www.zwire.com
Michael Rogers was scaling a slope in Ethiopia when he spotted the earliest evidence that tools were used to butcher animals 2.3 million years before the first modern humans appeared on earth.
The small angular rock that Rogers found was chipped from a stone blade.
This significant find shows that our hominid ancestors were far more capable than previously thought.
The trove of stone flakes and associated bones also suggests that Homo sapiens evolved a large brain in response to growing manual dexterity, rather than the other way around.
Rogers, assistant professor of anthropology at Southern Connecticut State University and his international colleagues were exploring the Gona region of the Ethiopian badlands in 2000 when the tools and bones were discovered.
The research was published in the September Journal of Human Evolution.
"One of the main goals is to find the maker of those tools," Rogers said.
The earliest human-like primates found so far are 2 to 3 million years old.
Modern humans did not inhabit the plains of Africa until about 200,000 years ago.
"We traditionally thought that the hominid Australopithecus didn’t use tools. This may have to change," Rogers said.
Two species of Australopithecus lived about 2.3 to 2.8 million years ago in the Gona area.
"There’s no reason Australopithecus couldn’t have used tools. Modern chimpanzees use sticks and stone … to crack nuts," Rogers said.
Whoever chopped up animals at Gona 2.6 million years ago did not pick up the first handy rock.
Stone flakes show that the Gona hominids intelligently selected stones and fashioned them into sharp edges.
"They obviously had the capability to know good stones from bad," Rogers said.
They selected chert, aphanamitic lava and trachyte, which split naturally into pieces with sharp edges.
Finding the bones mingled with the stones is especially significant, Rogers said.
Geologists had previously found bones with tool marks — but no tools, and stone tools without bones.
"This is the first site of bones and stones of this age," he said.
The site, which is only about 4 meters by 1 meter, was located on the banks of a prehistoric channel.
Strata of rock that gradually formed above the site include a 20-foot band of volcanic ash, which can be precisely dated.
Analysis put the excavation site at 2.58 million years ago.
"Bone preservation is very poor," Rogers said, so no cut marks were evident.
However, a stone flake was found embedded in one of the bones. The largest bone belonged to a 200-pound mammal of some kind.
Rogers said the initial flake was lying on the surface.
"Purposeful flaking is not hard to recognize. I saw a dozen of them," he said.
Rogers said the site contained a wide range of rocks and fragments, ruling out the possibility that the materials were washed together in a prehistoric stream.
"Finding a hominid that goes with the tools is the next step," Rogers said.
That will depend largely on luck. "We know what to look for and where to look," he said.
If the tool chippers turns out to be Australopithecus, then that will be evidence that fabrication of tools came before increased brain capacity, Rogers said.
That would answer a longstanding "chicken and egg" question about whether bigger brains led to tool making, or tool making resulted in Homo sapiens’ big brain.
"Any future find will reshape what we know," Rogers said.
Meanwhile, all of the bones, tools and stone flakes are in storage in Addis Ababa, Ethiopia.
Rogers was part of the international Gona Paleoanthropological Research Project, led by Sileshi Semaw, an Ethiopian anthropologist at Indiana University.
Send page by E-Mail Integral Discovers Hidden Black Holes
Posted: Tuesday, October 21, 2003
Source: European Space Agency
European Space Agency's Integral Discovers Hidden Black Holes
Integral, ESA's powerful gamma-ray space telescope, has discovered what seems to be a new class of astronomical objects.
These are binary systems, probably including a black hole or a neutron star, embedded in a thick cocoon of cold gas. They have remained invisible so far to all other telescopes. Integral was launched one year ago to study the most energetic phenomena in the universe.
Integral detected the first of these objects, called IGRJ16318-4848, on 29 January 2003. Although astronomers did not know its distance, they were sure it was in our Galaxy. Also, after some analysis, researchers concluded that the new object could be a binary system comprising a compact object, such as a neutron star or a black hole, and a very massive companion star.
When gas from the companion star is accelerated and swallowed by the more compact object, energy is released at all wavelengths, from the gamma rays through to visible and infrared light. About 300 binary systems like those are known to exist in our galactic neighbourhood and IGRJ16318-4848 could simply have been one more. But something did not fit: why this particular object had not been discovered so far?
Astronomers, who have been observing the object regularly, guess that it had remained invisible because there must be a very thick shell of obscuring material surrounding it. If that was the case, only the most energetic radiation from the object could get through the shell; less-energetic radiation would be blocked. That could explain why space telescopes that are sensitive only to low-energy radiation had overlooked the object, while Integral, specialised in detecting very energetic emissions, did see it.
To test their theory, astronomers turned to ESA's XMM-Newton space observatory, which observes the sky in the X-ray wavelengths. As well as being sensitive to high-energy radiation, XMM-Newton is also able to check for the presence of obscuring material. Indeed, XMM-Newton detected this object last February, as well as the existence of a dense 'cocoon' of cold gas with a diameter of similar size to that of the Earth's orbit around the Sun.
This obscuring material forming the cocoon is probably 'stellar wind', namely gas ejected by the supermassive companion star. Astronomers think that this gas may be accreted by the compact black hole, forming a dense shell around it. This obscuring cloud traps most of the energy produced inside it.
The main author of these results, Roland Walter of the Integral Science Data Centre, Switzerland, explained: "Only photons with the highest energies [above 10 keV] could escape from that cocoon. IGR J16318-4848 has therefore not been detected by surveys performed at lower energies, nor by previous gamma-ray missions that were much less sensitive than Integral."
The question now is to find out how many of these objects lurk in the Galaxy. XMM-Newton and Integral together are the perfect tools to do the job. They have already discovered two more new sources embedded in obscuring material. Future observations are planned.
Christoph Winkler, ESA Project Scientist for Integral, said: "These early examples of using two complementary ESA high-energy missions, Integral and XMM-Newton, shows the potential for future discoveries in high-energy astrophysics."
The original news release can be found here.
This story has been adapted from a news release issued by European Space Agency.
Send page by E-Mail Only 15 Minutes Of Life For Lone Neutrons
Posted: Wednesday, October 15, 2003
Source: National Institute Of Standards And Technology
Only 15 Minutes Of Life, No Fame, For Lone Neutrons
Once freed from its home inside the nucleus of an atom, a neutron lives on average 886.8 seconds (about 14.8 minutes), plus or minus 3.4 seconds, according to recent measurements performed at the National Institute of Standards and Technology.
This result, published in the Oct. 10 issue of Physical Review Letters, is the most precise ever achieved using beams of neutrons and is the culmination of almost 10 years of work. The new neutron lifetime value is consistent with physicists' current theories about the particles and forces of nature. It also will help scientists better understand the creation of matter immediately after the birth of the universe, an important factor in determining what the universe is made of today.
Scientists have been measuring the lifetime of the neutron since the early 1950s. While slightly less precise than a measurement made in 2000 by a different research group using a different method, the in-beam technique provides a strong, independent check on the neutron lifetime and reduces the overall uncertainty in the recommended value.
As neutrons die, they disintegrate into other particles, including protons. The NIST-led group simultaneously counted both the number of neutrons and the number of protons formed as the neutrons fell apart. A beam of slow moving neutrons was passed through a vacuum system. As the neutrons decayed, protons---which have a positive charge---formed and were captured in a powerful electromagnetic trap. Periodically the trap was opened and the protons were counted as they crashed into a semiconductor detector, producing an electrical signal.
The research team included participants from NIST, Tulane University, Indiana University, University of Tennessee/Oak Ridge National Laboratory, and the European Commission's Joint Research Centre (Institute for Reference Materials and Measurements) in Belgium.
The research was funded by NIST, the U.S. Department of Energy and the National Science Foundation.
Send page by E-Mail Genes That Distinguish Human, Nonhuman Primate Brains
Posted: Tuesday, October 14, 2003
Source: Emory University Health Sciences Center
Researchers Discover Genes That Distinguish Human, Nonhuman Primate Brains
ATLANTA -- A research team from the Salk Institute, the Yerkes National Primate Research Center of Emory University and the University of California – Los Angeles (UCLA), has identified genes in the cerebral cortex that differ in levels of activity between humans and nonhuman primates, including chimpanzees and rhesus monkeys. These findings, which appear in the online journal of the Proceedings of the National Academy of Sciences, may provide essential clues to the unusual cognitive abilities of humans. They also may help researchers understand why humans have a longer lifespan than other primate species and yet are so vulnerable to age-related, neurodegenerative diseases.
Because the DNA sequences of humans are so similar to those of chimpanzees, scientists have long speculated that differences in the activity levels of particular genes, otherwise known as gene expression, and, as a result, the amounts of particular proteins cells produce, are what distinguish humans from chimpanzees. The recent sequencing of the human genome has led to the development of "gene chips" that enable researches to examine the expression levels of thousands of genes at a time as well as compare expression levels in different species.
Using gene chips to compare samples of the cerebral cortex of humans, chimpanzees and rhesus monkeys, the research team at the Salk, the Yerkes Center and UCLA identified 91 genes that are expressed in different amounts in humans compared to the other primate species. Upon further study, the team observed 83 of these genes showed higher levels of activity in humans, and as a result, regulated neural activity.
"When we looked at other tissues, such as heart and liver, we found nearly equal numbers of genes showing higher or lower levels of expression in humans as compared to chimpanzees and rhesus," said Todd Preuss, PhD, associate research professor of neuroscience at the Yerkes Research Center. "The changes in gene activity in the cortex suggest increases in the rate of brain activity, providing a basis for the evolution of the enhanced cognitive abilities in humans."
In addition to finding changes in activity-related genes, the researchers found the human brain shows increased expression of genes that protect against activity-related damage. This finding may help explain why humans have the potential to live decades longer than other primates, but also why humans are especially vulnerable to age-related, neurodegenerative diseases, such as Alzheimer's disease.
"It is probable that the combination of long lifespan and high neural activity makes humans particularly vulnerable to neurodegenerative disease," said Mario Caceres, PhD, a postdoctoral fellow now at Emory University and lead investigator on the study. "Activity-related damage accumulates with age and has the potential to cause catastrophic breakdown late in life. By understanding how humans protect their brains from activity-related damage, we hope to better understand why those mechanisms fail."
The Yerkes National Primate Research Center of Emory University is one of eight National Primate Research Centers funded by the National Institutes of Health. The Yerkes Research Center is a multidisciplinary research institute recognized as a leader in biomedical and behavioral studies with nonhuman primates. Yerkes scientists are on the forefront of developing vaccines for AIDS and malaria, and treatments for cocaine addiction and Parkinson's disease. Other research programs include cognitive development and decline, childhood visual defects, organ transplantation, the behavioral effects of hormone replacement therapy and social behaviors of primates. Leading researchers located worldwide seek to collaborate with Yerkes scientists.
We acknowledge support of the National Institute of Mental Health and the James S. McDonnell Foundation.
Send page by E-Mail Nerve Disorder In Mice And Men Linked
Posted: Tuesday, October 14, 2003
Source: University Of Michigan Health System
Nerve Disorder In Mice And Men Linked To Mutated Gene
ANN ARBOR, MI – In a small town on Grand Cayman Island in the Caribbean, people are living with a serious neurological disorder, called Cayman ataxia, found nowhere else in the world.
People born with this rare, inherited condition have poor muscle coordination, some degree of mental retardation, uncontrollable head and eye movements and difficulty speaking or walking.
Now, in a discovery that reinforces the importance of the mouse to human genetics, scientists at the University of Michigan Medical School have discovered two mutations in a gene called ATCAY, which appear to be responsible for Cayman ataxia in humans and for similar neurological disorders in mice.
Cayman ataxia is one of about 100 rare inherited neurological disorders with symptoms that include ataxia, according to Margit Burmeister, Ph.D., a senior associate research scientist at the U-M Mental Health Research Institute and an associate professor of psychiatry and of human genetics in the University of Michigan Medical School. While the severity of symptoms can vary, people with ataxia have limited or no control over posture or coordination of their arms and legs.
"Because these disorders are so rare, it is difficult to collect DNA samples from enough affected individuals in different families with the same disorder to pinpoint the mutations that cause them," Burmeiser says. "Unless we can identify the mutated gene, it's hard to develop a diagnostic test or a therapy to help people with the disease."
A paper describing the research study will be published online October 12 by Nature Genetics, and will appear in the November issue of the journal. It is the result of a collaboration between scientists at the University of Michigan, the University of Miami, the University of Iowa and the National Human Genome Center at Howard University.
Before the U-M study, scientists knew that Cayman ataxia was caused by a recessive mutant gene originating in one of the early residents of Grand Cayman Island and passed on through the generations by his or her descendants. In 1994, scientists at the University of Iowa narrowed the search to one region on human chromosome 19, which included 50 to 100 genes, but couldn't locate the specific gene responsible for the disorder.
Meanwhile, Burmeister was working with a strain of mutant mice, called "jittery", with similar neurological symptoms, but so severe that affected mice die a few weeks after birth. She wondered if the gene that caused the disorder in mice could be the same gene responsible for Cayman ataxia in humans. So she compared overlapping DNA sequences between the region on mouse chromosome 10 defined by the "jittery" mice and the region on human chromosome 19 implicated in Cayman ataxia.
"Comparing overlapping DNA sequences between human and mouse narrowed the interval down to a much smaller region that contained just seven genes," Burmeister says. "In one of these genes, we discovered two mutations – a recessive mutation that caused lethal ataxia in "jittery" mice and another mutation that caused milder symptoms in a different strain of mice called "hesitant".
Burmeister then analyzed anonymous DNA samples, provided by University of Iowa scientists, from Cayman Island residents with ataxia and from relatives who did not have the disorder. When they sequenced human DNA, U-M scientists found the same two mutations in the same gene, which they named ATCAY, for Ataxia, Cayman type. Both mutations were present in every patient with Cayman ataxia in the study. Neither mutation was found in 1,000 control chromosomes from people of European, Jamaican or African ancestry.
"One of the mutations in the ATCAY gene changes an amino acid and the other is a splice mutation expressing a non-functional, truncated form of caytaxin, the protein expressed by the gene," Burmeister explains.
When U-M scientists analyzed gene expression in tissue from mice in the study, they found caytaxin protein was present throughout the brain and in neurons, but nowhere else in the mouse's body.
"We don't know what this protein does, but it doesn't appear to affect the physical development or structure of the brain or nervous system in mice, which appeared completely normal," Burmeister says. "Unlike other ataxias, there were no neurodegenerative changes."
According to Burmeister, the DNA sequence encoding caytaxin protein is somewhat similar to that of a Vitamin-E transporting protein, which is involved in another rare form of ataxia. People with this form of ataxia respond well to treatment with large doses of Vitamin E. But Vitamin E does not seem to bind to caytaxin, so the same treatment would not help people with Cayman ataxia.
Currently, Burmeister is working with structural biologists to determine what molecules will fit into the binding pocket of the caytaxin protein.
"If we can determine caytaxin's function, that will tell us why these people have ataxia, which would be a major step toward finding ways to prevent or treat the disorder," Burmeister says.
She also plans additional research to see whether mutations in ATCAY could be responsible for other types of inherited ataxia.
The University of Michigan has filed two provisional patent applications on the ataxia-associated gene and its protein. The research was funded by the National Institutes of Health, the March of Dimes Birth Defect Foundation, and the government of the Cayman Islands.
Jamee Bomar, a U-M research assistant, was first author on the paper. Other co-authors from U-M included Roger Albin, M.D., U-M professor of neurology; Paresh Patel, M.D., Ph.D., U-M assistant professor of psychiatry; undergraduates Eric Slattery and Radhika Puttagunta; Larry Taylor, Ph.D, research associate; and Eunju Seong, a graudate student in neuroscience. Co-authors Arne Nystuen and Val C. Sheffield are from the University of Iowa Medical School. Co-authors Rick Kittles and Weidong Chen are from the National Human Genome Center at Howard University. Co-author Paul J. Benke, from the University of Miami Medical School, did the original clinical research on individuals with Cayman ataxia.
Nature Genetics (2003), November 2003.
Send page by E-Mail African Drought and Ocean Temperatures
Posted: Tuesday, October 14, 2003
Source: The Earth Institute At Columbia University
New Study Ties African Drought To Ocean Temperatures
A strong link has been confirmed between sea surface temperatures and precipitation in Africa's semi-arid Sahel, according to a new study published in Science on October 9. The study was co-authored by Alessandra Giannini, a climate expert with the International Research Institute for Climate Prediction (IRI), a unit of the Earth Institute at Columbia University.
Previously, it was not known how much land use changes may have led to the region's recent history of prolonged drought, or whether variability in ocean temperatures was the primary driver of the region's climate. The new study finds that "pervasive evidence" indicates that sea surface temperatures, particularly in the Indian Ocean, are the most powerful indicators of precipitation in the Sahel.
Tropical Pacific surface temperature variation, such as that occurring with the El Nińo and Southern Oscillation phenomena, have an effect on the variation of year-to-year rainfall, while the Indian and possibly Atlantic Oceans, affect longer term trends. The new study tracked sea surface temperatures and precipitation rates from 1930-2000, the first time that ocean and climate trends have been studies on a decadal time scale.
If it is true that oceanic warming is the primary driver of precipitation in the Sahel, then by implication climatologists should be able to measure ocean temperatures and predict the likelihood of future precipitation in the Sahel.
As the paper's authors write: "The recent drying trend in the semi-arid Sahel is attributed to warmer-than-average low latitude waters around Africa which, by favoring the establishment of deep convection over the ocean, weaken the continental convergence associated with the monsoon, and engender widespread drought from Senegal to Ethiopia."
"What interests me particularly is the potential for seasonal predictions of precipitation in the Sahel, and all the implications and uses for such predictions," says Giannini. One of the International Research Institute for Climate Prediction (IRI)'s unique strengths is in research connecting climate with health, agriculture, and other human factors affected by rainfall. For instance, at the IRI connections are being investigated between malaria (a wet season disease), meningitis (a dry season disease) and precipitation in Western Africa.
"Land surface factors do feed back into the climate system of the Sahel, but they are a consequence, not the cause, of variability in precipitation," Giannini explains.
The International Research Institute for Climate Prediction is part of the Earth Institute at Columbia University, the world's leading academic center for the integrated study of Earth, its environment, and society. The Earth Institute builds upon excellence in the core disciplines –earth sciences, biological sciences, engineering sciences, social sciences and health sciences –and stresses cross-disciplinary approaches to complex problems. Through its research training and global partnerships, it mobilizes science and technology to advance sustainable development, while placing special emphasis on the needs of the world's poor. For more information please see http://www.earth.columbia.edu.
Send page by E-Mail The Pain of Rejection is Real
Posted: Friday, October 10, 2003
Ian Sample, science correspondent
October 10, 2003 The Guardian
How scientists proved that the pain of rejection is all too real
The pain of rejection is more than mere metaphor. A team of scientists have found that to the brain, a social snub is just like stubbing a toe.
Brain scans carried out on volunteers showed that when they suffered a social snub, the brain's "pain centre" went into overdrive. The finding suggests that any emotional stress, such as the demise of a relationship or the loss of a loved one, might be far more closely linked to real pain than previously thought.
Scientists have known for some time that when a person is physically hurt, a part of the brain called the anterior cingulate flickers into action.
"It's like an alarm system. It lets you know when you're feeling pain," said Matthew Lieberman, a psychologist at the University of California in Los Angeles.
Dr Lieberman and his colleagues Naomi Eisenberger and Kipling Williams decided to see if the same part of the brain was triggered by emotional stress.
They got volunteers to lie down in a brain scanner while they played a simple computer game. The game involved hitting buttons on a handset to catch a virtual ball and then throw it to one of two other players on a screen.
Volunteers were told that the game was unimportant and that it was only being used to check that connections to the other players lying in scanners elsewhere worked. But the researchers were not telling the truth. The other two players were not real at all, but were being controlled by a computer program.
When the game started, all three players passed the ball around so that each got a fair share of the action. But after playing for a while, the computer-controlled players suddenly started throwing the ball only between themselves.
"We had people coming out of the scanners saying 'Did you see what they did to me!'," said Dr Lieberman.
The volunteers who felt most put out by the snub showed the biggest changes in brain activity. Their brain's "pain centre" had become far more active.
"The response to this social exclusion was remarkably similar to what you see in response to physical pain," said Dr Lieberman.
According to Dr Lieberman, his results should change how we think about emotional pain. "We tend to think physical harm is in a different category to emotional harm, but this shows we should be aware that emotional pain can cause the same kind of distress to someone as physical pain."
Professor Anthony Dickenson, of University College London, who specialises in the origins of pain, said: "This whole area is incredibly important because it's proving to the medical profession once and for all that emotional distress is a genuine thing, that people who are distressed and upset are not malingerers.
"It shows that the psychological aspects of pain are genuine and real and dealing with it is not a case of telling people to pull themselves together."
Dr Richard Wise, of Oxford University, who has used magnetic resonance imaging to study the effect of pain on the brain, said: "Studies like this have a broader value in that they can help us build up an idea of the networks in the brain that are involved in experiencing different feelings."
Send page by E-Mail Evolutionary origins of laughter
Posted: Tuesday, October 7, 2003
2 October 2003 13:00 GMT
by Laura Spinney, news.bmn.com
Bonobos laugh just like babies, say German researchers who believe their findings indicate that the rules for how emotion is encoded behaviorally were laid down in the common ancestor we share with our closest ape relatives.
Eight years ago, Birgit Förderreuther meticulously recorded the laughter of an infant bonobo from Wuppertal Zoo, Germany from birth to one year, in response to tickling. But before she was able to analyse the recordings, she fell ill and had to abandon the project.
Now her colleague Elke Zimmermann of the Institute of Zoology at the Tieraerztliche Hochschule in Hanover has picked up where she left off and compared sophisticated spectrographic analyses of the bonobo sounds - that is, computer-generated graphs showing variation in energy and frequency over time - with sounds made by human infants, also in response to tickling.
Zimmermann finds that, like babies, bonobos combine the visual gesture of a "relaxed open-mouth display" with vocalizations, and that these vocalizations follow broadly the same spectrographic pattern as that of infants - though bonobos laugh at higher frequencies.
She believes that her findings confirm the hypothesis that laughter originated in primates before humans, and that it represents a universal signal of wellbeing in a playful situation. In that way, it helps to regulate social interactions.
A pre-human evolutionary origin for laughter could also explain why it is still present in deaf and blind infants, and why it fulfils the same role - and sounds the same - in people from different cultures.
Robert Provine, a psychologist at the University of Maryland, Baltimore County who has studied the laughter of common chimps, thinks this field of research has a bearing on other big questions, such as the evolution of speech.
In chimps, he says, laughter is a breathy, panting sound involving both inhalation and exhalation, while the human laugh is a single, "chopped" exhalation. "That indicates why we can talk and chimpanzees can't," he said. "People have shown that chimps have symbolic capacity in that they can sign. Although chimpanzees can recognise many spoken words, they can't produce the sounds."
Provine believes that the difference was driven by the evolution of bipedality in humans. "Walking upright provides independence between breathing and running, which does not exist in other animals. All quadrupedal animals have a one-to-one relationship between breathing and running." And that, he says, is why chimps laugh as if they had been running and were out of breath.
But when bonobos stand, they straighten up more than chimps, and their posture more closely resembles that of humans - which could explain why their laughter is also more similar.
The findings was presented at a meeting of the German Primate Society in Leipzig, Germany at the beginning of October.
Send page by E-Mail Half-Billion-Year-Old Ancestral Mountains In The Himalaya
Posted: Tuesday, October 7, 2003
Source: University Of Arizona
Scientists Find Half-Billion-Year-Old Ancestral Mountains In The Himalaya
The world's highest and most spectacular mountains, the Himalaya of Nepal, India, and Bhutan, are built on the foundations of a much older mountain system, University of Arizona geoscientists have discovered.
They have dated rocks that show Earth's mightiest range is predated by ancestral mountains that existed in the same area between 450 million and 500 million years ago, long before India began plowing northward into Asia 55 million years ago.
Their findings not only revise ideas on the region's tectonic history, they offer new insight on connections between uplift of the Himalaya during the past 55 million years and simultaneous global shifts in seawater chemistry and climate.
"We conclude that the modern Himalaya Mountains are built on the foundations of an ancient mountain range that may have been of similar dimensions," said UA geosciences Professor George Gehrels, who used state-of-the-art radioisotope techniques to date rock formations in the Himalayan thrust belt.
Gehrels, UA geosciences Professor Peter G. DeCelles, UA doctoral candidate Aaron Martin, UA master's degree graduate Tank Ojha, UA undergraduate geosciences major Guy Pinhassi, and geology Professor Bishal Upreti of Tribhuvan University in Kathmandu, Nepal, have collaborated in field expeditions in rugged areas of Nepal for the past several years. They report on their research in the September issue of GSA Today, a scientific journal of the Geological Society of America, online at http://www.geosociety.org Tank Ojha (left), a UA master's degree student who now runs a geo-trekking company in Kathmandu, and Tribhuvan University geology Professor Bishal Upreti here debate the origin of boulder-borne schist from the high Himalaya.
"Our model is based on observations that, between 450 and 500 million years ago, rocks in the Himalaya were pushed down to great depth and metamorphosed," Gehrels said.
The buried rocks became so hot under great pressure that they melted, producing large granite bodies. The metamorphic schists and granite bodies contained garnets and zircon crystals that Gehrels dated to around 500 million years using uranium-lead radioisotope techniques.
These deep-level rocks were brought back up to the surface by processes of faulting, uplift, and erosion soon after burial, their observations suggest. The processes of uplift and faulting formed mountains, which eroded and produced huge volumes of sediment.
The scientists studied conglomerates and sandstones found in these "ancestral Himalaya" sediments in many different areas of the present-day range. Their main area of research, in the Annapurna range of Nepal, is a 5-day walk from the end of the nearest road.
They hired porters to carry camp gear and field equipment. Because most samples weighed around 5 kilograms (11 pounds) and were collected many miles from the nearest road, the researchers processed their samples in the field, crushing granite samples by hand and extracting garnets and zircon crystals by the panning-for-gold method.
The Himalaya is the best place on the planet for studying what happens when Earth's continents collide, Gehrels noted.
Earth's surface is covered by a series of tectonic plates. Heat from deep within the Earth drives convection currents that move the plates in different directions. India rides on a plate that steadily advances north a couple of centimeters a year, about as fast as your fingernails grow. During the past 55 million years, this action has uplifted Earth's tallest mountains, capped by 29,000-foot-plus Mount Everest.
"The birth of the Himalaya is indeed this great story of rocks being shoved down and being brought to the surface, while huge amounts of erosion take place. But we now think that much of the burial, uplift, and erosion happened between 450 million and 500 million years ago," Gehrels said. "The ancestral Himalaya Mountains appear to also have formed in a regime of continental collision, with the Indian continent being shoved beneath another landmass."
However, WHICH landmass is not yet known, he said.
"According to our model, this collisional event began with a small range forming at around 508 million years ago. The faulting, burial of rocks, formation of granite bodies, and uplift then propagated toward India through time, with the mountain range growing in width and perhaps elevation," Gehrels said.
By about 450 million years ago, as the forces of mountain building waned, erosion leveled the topography down to the deep-level metamorphic rocks, generating enormous amounts of sediment. Subsequently, the ancestral Himalaya Mountains disappeared and the region eventually subsided below sea level as the landmass was rifted away from India's northern margin, Gehrels said.
"The region remained buried below marine sediments until India collided with southern Asia around 55 million years ago and the modern Himalaya Mountains began to form," he added. More research is needed to determine the relative proportions of faulting, burial, metamorphism, generation of granites, uplift and erosion that occurred during these two phases of mountain-building, he said.
The revised geologic history also challenges Earth scientists to rethink ideas on global climate change and the global shift in seawater chemistry of about 55 million years ago.
Global climate began to cool around 55 million years ago, and scientists theorize that this may have been driven by weathering reactions in the Himalaya that remove carbon dioxide from the atmosphere, decreasing the greenhouse effect and cooling Earth.
At about the same time, Earth's oceans changed chemically, a possible result of vast quantities of Himalayan sediments carried by great rivers into the sea.
"Maybe the Himalayas have played such an important role in shaping modern climate and seawater chemistry because rocks exposed in the mountain belt were buried, metamorphosed, and uplifted during an earlier phase of mountain building," Gehrels said. "This multistage history may be key to understanding the genetic linkages between mountain building, climate change, and seawater chemistry."
Photos on UA website: http://uanews.org
The original news release can be found here.
Send page by E-Mail The Molecule That Makes Life Possible
Posted: Friday, October 3, 2003
Source: University Of Pennsylvania Medical Center
When Heme Attacks: After Trauma, The Molecule That Makes Life Possible Rampages
Philadelphia, PA -– Heme, the iron-bearing, oxygen-carrying core of hemoglobin, makes it possible for blood to carry oxygen, but researchers from the University of Pennsylvania School of Medicine have determined how free-floating heme can also make traumatic events worse by damaging tissue. The Penn researchers present their findings in the October 2nd issue of the journal Nature. Fortunately, the researchers also identified a chemical that can be targeted by drug developers to impede the deleterious effects of free-floating heme.
Following a traumatic event – such as an accident, a stroke, a heart attack or even surgery – heme floods the spaces between and inside cells and exacerbates the damage. It does so by shutting down an important cell membrane channel, an action that kills neurons and constricts blood vessels. While investigating this process, the researchers also determined that a chemical called NS1619 restores the function of the cell membrane channel. NS1619 and its derivatives could be the source for a new drug – one that prevents the secondary events that worsen trauma damage.
"Following a heart attack, a stroke, or any really severe physical injury, heme is literally shaken loose from hemoglobin," said Xiang Dong Tang, MD, PhD, Staff Scientist in Penn's Department of Physiology. "Normally, cells can compensate and recycle loose heme. But when larger concentrations are released, heme can gum up the works, specifically the Maxi-K ion channel, a cell membrane protein important for blood vessel relaxation and neuron excitability."
Maxi-K is a channel that moves potassium ions out of cells. In the Nature paper, Tang and his colleagues prove that the Maxi-K protein possesses sites that bind heme. If these sites were removed or altered, heme could not effect Maxi-K proteins.
"Maxi-K is found in the lining of blood vessels. When it is turned off, the vessel constricts, increasing blood pressure, which is decidedly not beneficial following a heart attack, " said Toshinori Hoshi, PhD, Associate Professor in Penn's Department of Physiology and co-author of the Nature article. "In neurons, disrupting Maxi-K leads to excessive calcium accumulation. Eventually, this ionic buildup triggers cell suicide and, therefore, the loss of the neuron."
The chemical heme is essential for most forms of life. It exists in hemoglobin for oxygen transport, in cytochromes for cellular energy production, and in guanylate cyclase for blood pressure regulation. The molecule itself is tiny, a flat snowflake of a carbon framework surrounding a single atom of iron, but it is crucial for the cellular process of respiration and the action of nirtroglycerine.
"Generally, the heme molecule is attached to larger molecules, such as hemoglobin, but it is easily set loose. Indeed, there is an entire cellular industry behind recycling and reusing 'lost' heme," said Tang. "But that system can get overwhelmed in times of serious trauma and bleeding."
Studying the heme recycling system might prove useful in developing treatments for preventing the secondary damage set off by heme. Certain cells, such as neurons, do have ways of transporting heme. If the 'heme transport' is identified and the specific blocker is found, it could help prevent symptoms resulting from trauma and bleeding.
Meanwhile, according to Tang and his colleagues, there is already a known agent that can relieve Maxi-K from heme inhibition. NS1619 is known as the "Maxi-K opener," and, as the researchers have shown, readily reverses the heme-mediated inhibition.
"I can envision the use of a drug similar to NS1619 as an emergency treatment," said Tang. "In the emergency room, after an accident or heart attack, it could be used to keep the damage from continuing on a cellular level – before it could result in bad effects for the entire body."
Scientists also contributing to this research include Rong Xu from Penn, Mark F. Reynolds, from St. Joseph's University, Marcia L. Garcia, from Merck Research Laboratories, and Stefan H. Heinemann, from Friedrich Schiller University. Funding for this research came from the National Institutes of Health.
This story has been adapted from a news release issued by University Of Pennsylvania Medical Center.
Send page by E-Mail New View On How The Brain Functions
Posted: Thursday, October 2, 2003
Salk Researcher Provides New View On How The Brain Functions
La Jolla, Calif.- Scientists are developing a new paradigm for how the brain functions. They propose that the brain is not a huge fixed network, as had been previously thought, but a dynamic, changing network that adapts continuously to meet the demands of communication and computational needs.
In the Sept. 26 issue of Science, Salk Institute professor Terrence Sejnowski and University of Cambridge professor Simon Laughlin argue that the human brain has evolved to operate as an enormously efficient "hybrid device," capable of making far more sophisticated computations than the most powerful computers, and the long-distance communication systems in brains have been optimized by evolution for energy efficiency.
"In the past, we were only able to look at brain function by looking at single neurons or local networks of neurons. We were only able to see the trees, so to speak," said Sejnowski. "With breakthroughs in recording techniques including brain imaging, which gives us a global picture of brain activity, and advances in computational neurobiology, we can now take a more global perspective. We're looking at the entire forest, and we're asking the question: How has the forest evolved?"
As the brain has evolved over millions of years, according to Sejnowski, it has become amazingly efficient and powerful. He says that nature has "optimized the structure and function of cortical networks with design principles similar to those used in electronic networks." To illustrate the brain's tremendous capacity, Sejnowski and Laughlin state that the potential bandwidth of all of the neurons in the human cortex is "comparable to the total world backbone capacity of the Internet in 2002."
But they point out that simply comparing the brain to the digital computers of today does not adequately describe the way it functions and makes computations. The brain, according to Sejnowski, has more of the hallmarks of an "energy efficient hybrid device."
"These hybrids offer the ability of analog devices to perform arithmetic functions such as division directly and economically, combined with the ability of digital devices to resist noise," he writes in Science.
"This is an important era in our understanding of the brain," according to Sejnowski. "We are moving toward uncovering some of the fundamental principles related to how neurons in the brain communicate. There is a tremendous amount of information distributed throughout the far-flung regions of the brain. Where does it come from? Where does it go? And how does the brain deal with all of this information?
"These are questions we've not been able to address on a comprehensive basis until now. I believe that over the next decade, we will begin to develop some answers."
The Salk Institute for Biological Studies, located in La Jolla, Calif., is an independent, nonprofit organization dedicated to fundamental discoveries in the life sciences, the improvement of human health and conditions, and the training of future generations of researchers. The institute was founded in 1960 by Jonas Salk, M.D., with a gift of land from the City of San Diego and the financial support of the March of Dimes Birth Defects Foundation.
This story has been adapted from a news release issued by Salk Institute.
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