Wednesday, August 19, 2009

HOLDING BREATH FOR SEVERAL MINUTES ELEVATES MARKER FOR BRAIN DAMAGE

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Divers who held their breath for several minutes had elevated levels of a protein that can signal brain damage, according to a new study from the Journal of Applied Physiology. However, the appearance of the protein, S100B, was transient and leaves open the question of whether lengthy apnea (breath-holding) can damage the brain over the long term.

“The results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system, and may have cumulative effects,” the Swedish researchers said. The release of S100B into the blood suggests that holding one’s breath for a long time disrupts the blood-brain barrier, they said.

The concern is that repetitive exposures to severe hypoxia (lowered oxygen supply), such as that experienced by individuals training and competing in static apnea diving events, could cause neurological damage over time. The researchers recommended further research on free divers that would begin early in their careers and follow them for years to monitor their neurological function.

The study is “Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations.” The researchers are Johan P.A. Andersson, Mats H. Linér and Henrik Jönsson, of Lund University in Sweden. The American Physiological Society published the study.

There is a tradition of breath-hold diving in Japan and some other parts of the world that goes back hundreds of years, although the occupation has been dying out. These divers harvest seaweed, shellfish and other growth from the sea bottom, diving dozens of times per day. Some divers routinely dive to depths of 90 feet on a single breath while others dive in the 15-30 foot range.

More recently, breath-hold diving has become a competitive sport. Competitive events include how long divers can remain underwater, how far they can swim underwater and how deep they can dive. Participants must undergo intense training to increase their lung capacity while learning crucial safety measures.

Breath-hold diving often leads to hypoxia, elevated blood pressure, slowed heartbeat and other physiological changes. However, whether the sport causes any long-term damage to the brain has remained a point of contention. Studies have produced conflicting results.

The authors of this study see cause for concern, noting that in six international competitions between 1998 and 2004, 10% of the contestants in the static apnea events were disqualified after they lost either motor control or consciousness. In this event, participants float face down on the water for as long as possible without coming up for air. The world record for the event is 11 minutes 35 seconds. Divers at international competitions routinely hold their breath 4-7 minutes.

“Whether such hypoxic episodes are associated with a risk for brain damage in these athletes remains to be established,” the researchers said. “Studying the changes in established biochemical markers of brain damage after such performances offers the possibility to address this question.”

Nine competitive breath-hold divers (eight men and one woman) took part in this study, along with six individuals who had limited experience with breath-hold diving. The nine competitive divers formed the experimental group, while the non-divers acted as the controls

The researchers told the participants to lie on their backs on a cot and hold their breath for as long as possible. The conditions were dry, but mimicked a static apnea dive in which the divers float face down holding their breath. The divers used whatever preparatory techniques they customarily use in competition, such as hyperventilating, insufflation (filling the lungs with as much air as possible) and breath-holding warm-ups.

The researchers took arterial blood samples from a catheter inserted into the artery that runs through the wrist. They took samples before the breath hold, at the end of the breath hold and at fixed intervals for the two hours following the end of the breath hold. The researchers also measured arterial blood gases. They did the same measurements on the individuals in the control group, but the controls rested on their backs for the entire experiment, without performing the breath hold or the warm-ups.

Among the findings of this experiment:

-The average breath-hold time was 5 minutes 35 seconds. The longest was 6 minutes 43 seconds and the shortest was 4 minutes 41 seconds.

-The marker for brain damage, S100B, rose in seven of the nine divers.

-The controls showed no change in S100B.

-On average, S100B rose 37% within 10 minutes after the apnea ended.

-S100B levels returned to normal within two hours for all the participants.

-The divers showed signs of asphyxia, that is, blood oxygen levels fell, while carbon dioxide levels rose.

The S100B levels, while elevated, were well below levels associated with brain injury. In brain-injured patients, the presence of S100B in the blood can increase by several hundred percent.

In addition, the elevation of S100B was more transient in the divers, compared to people who suffered brain injury. The divers had a quick return to normal, while S100B levels peak in 24 hours in brain-injured patients.

The transient nature of the increase in S100B among the divers probably indicates the blood-brain barrier has been compromised, allowing the protein to escape from the fluid in the brain into the circulation. The blood-brain barrier controls what passes between the brain and the circulation. S100B would normally remain in the brain.

Other sports have also been associated with a similar transient increase in S100B, the researchers noted, including boxing, headings in soccer, running and long-distance swimming. One study also reported that individuals suffering sleep apnea had elevated levels of S100B in the morning, although another study indicated there had been no change in S100B overnight.

(Photo: JAP)

Journal of Applied Physiology

HIGHER CARBON DIOXIDE MAY GIVE PINES COMPETITIVE EDGE

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Pine trees grown for 12 years in air one-and-a-half times richer in carbon dioxide than today's levels produced twice as many seeds of at least as good a quality as those growing under normal conditions, a Duke University-led research team reported Monday, Aug. 3 at a national ecology conference.

Carbon dioxide readings that high are expected everywhere by mid-century. The findings suggest some woody tree species could, in the future, out-compete grasses and other herbaceous plants that scientists had previously found can also produce more seeds under high-CO2, but of inferior quality.

"Even if both groups were producing twice as many seeds, if the trees are producing high-quality seeds and the herbaceous species aren't, then competitively you can get a shift," said Danielle Way, a Duke post-doctoral researcher.

Way presented the results during the Ecological Society of America's 2009 annual meeting in Albuquerque, N.M. She is also first author of a report on the study scheduled for publication in the research journal Global Change Biology.

Way and her co-researchers collected, counted and analyzed seeds produced at the Duke Free Air CO2 Enrichment (FACE) site in Duke Forest, near the university's campus. There, growing parcels of loblolly pine trees have been receiving elevated amounts of CO2 around the clock since 1997 in a Department of Energy-funded project designed to simulate natural growing conditions.

Their analysis found the high-CO2 loblolly seeds were similar in nutrient content, germination and growth potential to seeds from trees growing under present-day CO2 concentrations. "If anything, they actually seem to be slightly better seeds rather than more seeds of poorer quality," Way said.

"The notion here is that if the trees are producing more high-quality seeds at high CO2 compared to grasses and herbs, then the trees may be at an advantage," added study participant Robert Jackson. Jackson is Way's advisor at Duke, where he is a biology professor, as well as professor of global environmental change at the university’s Nicholas School of the Environment.

The ultimate competitive outcome will depend on how other trees comparatively respond to high-CO2, said James Clark, another Duke biology professor and Nicholas School professor of the environment who also participated in the study. "We don't know that yet, because we only have estimates for loblolly pines," Clark said.

(Photo: Chris Hildreth)

Duke University

UNLOCKING THE KEY TO HUMAN FERTILITY

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BBSRC-funded scientists at University of Leeds and University of Bradford have discovered a unique ‘DNA signature’ in human sperm, which may act as a key that unlocks an egg’s fertility and triggers new life.

Dr David Miller and Dr David Iles from the University of Leeds, in collaboration with Dr Martin Brinkworth at the University of Bradford, have found that sperm writes a DNA signature that can only be recognised by an egg from the same species. This enables fertilisation and may even explain how a species develops its own unique genetic identity.

Dr Iles says, "What we have discovered is a previously unrecognised DNA packaging ‘signature’ in mammalian sperm that may be essential for successful fertilisation of the egg and development of the embryo. We think it may also be ancient in origin."

Without the right ‘key’, successful fertilisation either cannot occur, or if it does, development will not proceed normally. Notably, disturbances in human sperm DNA packaging are known to cause male infertility and pregnancy failures.

This ‘lock and key’ mechanism has other profound implications. Not only does it explain why some otherwise healthy men produce sperm that is sterile, but it also explains how different species evolve and retain their own identity.

Says Dr Miller, "Up until now, Doctors have struggled to understand idiopathic male infertility. Our latest research offers a plausible explanation for why some sperm malfunction or fail to function correctly."

If the DNA carried by a sperm cell was unwound and stretched out, it would actually measure more than a metre in length. In order to fit all this DNA into the microscopic space within the head of the sperm cell, the DNA needs to be very tightly coiled, or packaged. The Leeds study showed that in human and mouse sperm, not all of the DNA is packaged in the same way. Whilst most of the paternal DNA is compressed in an extremely compact fashion, some is packaged less tightly.

"There is a definite pattern to the way DNA is packaged in sperm cells and we can see that this pattern is the same in unrelated fertile men. It is different in the sperm of infertile men. This implies that there is a significance to the packaging of DNA that has a direct relevance to male fertility," says Dr Iles.

Detailed analyses of the DNA in the ‘open’, less tightly packaged conformation, showed this DNA carries much of the information critical for activating genes essential for directing the development of the embryo. Further investigations showed the same conformation to exist in the sperm of several unrelated human donors and remarkably, highly similar packaging patterns to exist in the sperm of mice.

DNA regions in the ‘open’ conformation may therefore be more vulnerable to damaging toxins, such as those in cigarette smoke and certain anti-cancer drugs, than those that are tightly packaged. As Dr Brinkworth says, "this might mean that anything capable of causing genetic damage to sperm could have particular significance for the development of the embryo".

The findings also help explain why inter-species breeding is so rarely successful. Where the locks and keys of two species do not match, however similar their DNA is, no viable offspring can be born. Occasionally, for example, with horses and donkeys, offspring are produced - but because the sperm and egg signatures are incompatible, their development as embryos is abnormal and any offspring are almost always infertile.

The research team believes that the same mechanism must also have played a role during human evolution. In the ancient history of mankind, Neanderthals co-existed with modern humans over many thousands of years. Sexual encounters between these two closely related species cannot be ruled out, yet there is no evidence in our DNA of a legacy from such couplings. It is possible that if offspring were produced, they either did not survive long or if they did, they were unable to breed.

Biotechnology and Biological Sciences Research Council (BBSRC)

TINY RIFTS CREATE FRAGILITY OF BRITTLE BONE DISEASE

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The weak tendons and fragile bones characteristic of osteogenesis imperfecta, or brittle bone disease, stem from a genetic mutation that causes the incorrect substitution of a single amino acid in the chain of thousands of amino acids making up a collagen molecule, the basic building block of bone and tendon.

According to researchers at MIT, that minuscule encoding error creates a defective collagen molecule that, at the site of the amino acid substitution, repels rather than attracts the collagen molecule alongside it. This creates a tiny rift in the tissue, which when repeated in many molecules, leads to brittle tissue, broken bones, deformity and, in the most severe form of the disease, death. For example, if healthy collagen tissue looked like a sheet of paper, diseased collagen tissue would look more like a sheet of paper full of tiny perforations. At each of these perforations, the sheet would be considerably more prone to tearing.

In what may be the first detailed molecular-based multi-scale analysis of the role of a materials' failure in human disease, a paper in the Aug. 5 issue of Biophysical Journal describes exactly how the substituted amino acid repels other amino acids rather than forming chemical bonds with them, creating a radically altered structure at the nanoscale that results in severely compromised tissue at the macroscale. This approach to the study of disease, referred to as "materiomics" by the lead researcher on the project, Professor Markus Buehler of MIT's Department of Civil and Environmental Engineering, could prove valuable in the study of other diseases - particularly collagen- and other protein-based diseases - where a material's behavior and breakdown play a critical role.

"The consideration of how material properties change in diseases could lead to a new paradigm in the study of genetic disorders that expands beyond the biochemical approach," said Buehler.

"We wanted to see how a single-point genetic mutation in a collagen molecule could cause entire tissue to become brittle, soft and even fail. The medical community finds correlations between genetics and patients; our interest is in finding the correlation between genetics and a material's behavior," he said.

Buehler first described the materiomics approach in an article appearing in the March 2009 issue of Nature Materials. He sees the application of this approach to collagen-based diseases as a starting point that could lead to a similar analysis of the mechanical properties of tissue involved in other protein-based diseases. About one in 10,000 people are diagnosed with brittle bone disease annually, and defective collagen is implicated in many other medical conditions, including Alport syndrome (kidney disease) and Ehlers-Danlos syndrome (overly-flexible skin and joints). The broader category of protein-based diseases contains even neuronal disorders such as Alzheimer's disease.

Three years ago, Buehler used atomistic-based multi-scale modeling to describe in detail the hierarchical structure of collagen, the tissue comprising most structural material in mammalian bodies. His model incorporates a bottom-up description of collagen, accounting for the hierarchical assembly of molecules, each of which consists of three helical threads of amino acids. The molecules are arranged in packets called fibrils that collectively make up whole tissue.

In new research, Buehler and Sebastien Uzel, a graduate student at MIT, and Alfonso Gautieri, Alberto Redaelli and Simone Vesentini of Politecnico di Milano modeled type I collagen's behavior at the atomistic level all the way up to the scale of the fibrils that make up whole tissue.

The different forms of severity in brittle bone disease correlate with a particular genetic mutation; some amino acid substitutions for glycine create more severe forms of osteogenesis imperfecta.

Using atomistic modeling, the researchers demonstrate exactly how the substitution of eight different amino acids in place of glycine changes the electrochemical behavior of the collagen molecules and affects the mechanical properties of the collagen tissue. They learned that the mutations creating the most severe form of the disease also correlate with the greatest magnitude of adverse effects in creating more pronounced rifts in the tissue, which lead to the deterioration and failure of the tissue.

"The study of how the nature of the genetic makeup influences the mechanical behavior of materials is an important frontier in bioengineering," said Uzel. "It could potentially revolutionize the way we understand, model and treat medical disorders, and may also lead to the development of new biomaterials for applications in tissue engineering and regenerative medicine."

(Photo: Sebastien Uzel and Markus Buehler)

Massachusetts Institute of Technology

FRIENDSHIP INFLUENCES EATING BEHAVIOR, PARTICULARLY WHEN FRIENDS ARE OVERWEIGHT

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A new study of childhood obesity in the United States has found that some social factors, such as the presence of friends, may put overweight youths at greater risk of overeating.

The research, published in the August issue of the American Journal of Clinical Nutrition, demonstrates that friends may act as "permission givers" on children's food intake.

"These results are important, considering the role of friends as agents of change in childhood and adolescence," said Sarah Salvy, Ph.D., assistant professor in the Division of Behavioral Medicine, Department of Pediatrics, University at Buffalo School of Medicine and Biomedical Sciences.

"Overweight children are more likely to find food more reinforcing than non-overweight youth," she continued. "Being in the company of overweight peers may give them the permission to eat more or may decrease their inhibitions, increasing what are seen as the norms of appropriate eating, or how much one should eat."

The study involved 23 overweight and 42 normal weight children between the ages of 9 and 15, who were randomized to participate with either a friend or an unfamiliar person of a similar age. After randomization, there were 33 friend pairs and 39 "unfamiliar" pairs.

Before taking part in the study experiment, participants listed what they had eaten in the past 24 hours to make sure they hadn't eaten anything during the previous two hours, and rated their hunger level.

Each participant pair spent 45 minutes in a room equipped with games, puzzles and individual bowls of low-calorie, "nutrient dense" baby carrots and grapes, and high-calorie "energy-dense" potato chips and cookies. The children were told they could eat as much or as little as they wanted, but were asked to eat from their own bowls only.

Researchers observed the children via closed-circuit television and recorded their activities. At the end of the session, they weighed the snacks that weren't eaten to determine how much each participant had consumed and to calculate calories.

Results showed that friends who ate together consumed more food than participants who were paired with someone they didn't know, and that friends were more likely to eat similar amounts than participants paired with a stranger.

However, overweight children who were paired with an overweight peer, whether friend or stranger, ate more than the overweight participants who were paired with a normal weight youth.

"These findings indicate that both overweight and normal weight participants eating with a friend ate significantly more than did participants eating in the presence of an unfamiliar peer," Salvy said. "These results are consistent with research in adults, which showed that eating among friends and family is distinctly different than eating among strangers.

"Given the impact of friends on eating behavior, it appears that if we hope to change the growing obesity epidemic among children, friends and family need to be involved," said Salvy. "If the environment in which children live doesn't change -- if family meals remain high calorie and overeating is the norm -- any progress children may make in their eating behavior won't last."

Salvy currently is investigating the influence of a parent versus a friend on children's and adolescents' eating behavior.

(Photo: U. Buffalo)

University at Buffalo

TOO MANY WAYS TO SAY 'IT HURTS'

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There are at least 100 ways to say, "It hurts!" And that is the problem.

David Cella is on mission -- backed by nearly $10 million in National Institutes of Health funds -- to revolutionize the language of pain, as well as fatigue, depression and anxiety. These are some of the important symptoms researchers measure when they try to figure out if a medical treatment improves the quality of life for a patient with a chronic disease.

Are they in too much pain to unload groceries from the car? Are they too tired or depressed to go out to lunch with a friend? The answers are vital for researchers to know if new treatments are useful or useless.

But the glitch is every group of researchers asks patients different questions to measure their symptoms. Thus, one group's measurement of severe pain or fatigue or depression may be different than another's. Because researchers aren't speaking a common language, doctors and other health care providers can’t compare the results across studies to decide which is the best approach. Instead, study results remain separate puzzle pieces that never fit together into a whole picture.

“Can you imagine if a doctor wanted to check your hemoglobin and there weren’t any numbers to measure whether it was normal?” asked Cella , professor and chair of the new department of medical social sciences at Northwestern University Feinberg School of Medicine and a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. “When you say a patient's hemoglobin is 11, everybody knows what it means, but nobody knows what a pain of 36 means or a fatigue of 32 because we don’t use common measures."

That’s about to change. Cella is leading a far-reaching new national project that establishes a common scientific vocabulary. In August, he and colleagues from six other institutions and the NIH will release a set of free publicly available computerized tests for researchers to measure pain, fatigue, depression, anxiety and physical and social functioning. Now there will be a pain measurement of 75, for example, that will mean the same thing to every doctor and scientist.

The new project is called Patient-Reported Outcome Measurement Information System (PROMIS). More than 1,000 researchers have already registered to try the new tools.

Cella’s project addresses President Obama’s call for greater accountability in medical treatment. "In order to have a system that works that way you need a consistent measure of outcomes that people can understand and relate to," Cella said. “That’s what we have developed.”

The lack of a common vocabulary has hurt research, Cella noted. “"It's a Tower of Babel, a hodge-podge of language. It’s a big problem because you can't migrate the results of one study to a broader understanding,” he said. “We keep having to learn the same things over and over. We are not building on a foundation of knowledge.”

Not only have Cella and his team created a new language and tool for researchers, but the PROMIS project also represents a shift in the way researchers evaluate the benefits of treatments. The goal is not just to help people live longer but also live better.

X-rays, CT scans and lab tests may have minimal relevance to the day-to-day functioning of patients with chronic diseases. "We help measure directly if people are living better by asking them,” Cella said. “Sometimes it's as simple as asking, 'Do you think this treatment has made your life better?' That question is surprisingly absent from many studies."

(Photo: Northwestern University)

Northwestern University

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