Friday, August 28, 2009

ALL OF US - FROM SLIME MOULD TO MPS - ARE BORN TO CHEAT

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Organisms are genetically programmed to cheat the system and have to be policed to stop them putting their needs ahead of society and thus threatening its survival, say scientists.

University of Manchester researchers have shown that even the most-simple organisms have complex social behaviours. Dr Chris Thompson and Dr Jason Wolf’s study of slime moulds has shown that these microscopic organisms – which share many of their genes with humans – respond to competition, trying to get the upper hand with a variety of strategies including cheating. However the shift in behaviour is extremely complex. Individuals can cheat by promoting their own self interest or can coerce others to perform the altruistic act. Ultimately this balance may mean the species – or society – survives.

By illuminating general principles of how organisms cheat, their study could help us understand what drives – and what limits – selfish behaviour such as MPs fiddling their expenses.

Dr Thompson, of the Faculty of Life Sciences, explains: “Using slime mould allows us to look at social behaviour in its most basic form. They are single cell organisms that just divide; there is no experience, their social behaviour is simply genetically controlled.

“However they do work together and we have now shown for the first time they do have a complex social life that involves both cheating and coercion, which ensures the survival of the species. We are now working to identify the genes behind this.

“Since humans share many of the same genes, they will behave the same way.”

The paper, published in the latest Current Biology (23 July 2009) is the latest in a series that asks: why are organisms social? Why do they cooperate with one another when, according to natural selection, they should not do that? They should be fighting to get ahead.

Dr Thompson adds: “It was one of Darwin’s biggest challenges. If individuals did cheat and put themselves first all the time, the species would collapse.”

In slime mould, some amoeba make spores – thus gaining the reproductive advantage – while others make stalks and die. Making stalks is an altruistic act. So why do some make stalks, even though they do not enjoy the reproductive advantage? The trouble is that if everyone cheats, there would be no stalk, and everyone would suffer because fitness will be reduced.

Dr Thompson says: “This latest paper looks at whether organisms are cheating or just choosing the best strategy. If you use the analogy of two men in a sinking boat, with one man bailing more slowly than the other, it may be that he is cheating and allowing the other to do most of the work. Or it may be that he has a better or equally good strategy as bailing slower allows him to conserve energy and actually bail for a longer time.

“We looked at how slime moulds behaved when alone and found some were making more spores. So they were not cheating after all, they were simply following their chosen strategy.

“However we then looked at how these slime moulds behaved when they were mixed with others and found that they recognised that they were mixed with foreigners and changed their strategy: they did respond to competition.

“It is amazing how complex their ability is to recognise foreigners and shift their behaviour. Sometimes if one is making more spores then the other will make more spores in what we term self promotion. But if everyone did this, then over time you end up with no stalks – everyone is trying to make themselves better and better and better until it becomes spiteful and bloody minded. If everyone is making more spores and no stalks then the system collapses. You need policing or coercion to stop that happening. Somehow some cells are forced to make stalks.

“Now we want to know how organisms recognise foreigners and how they then force others to do something that benefits the species more than themselves.”

He adds: “Working with slime mould is fantastic. It allows us to look at social behaviour in its most basic form. We can us this to understand how organisms work together and form colonies. For example, with tooth decay is caused by colony forming bacteria, and organisms form biofilms and secrete group products to protect against antibiotics. So our findings have a wide application from the practical – why it can be difficult to stop tooth decay – to bigger issues such as evolution on the planet as we know it.

“People might wonder why bother studying slime mould but it could lead to a greater understanding of human behaviour. We know that human behaviour, at least in part, is influenced by our genes, so studying behaviour at a cellular level can improve our understanding of why some genes are associated with cooperation and others with conflict. Cooperation is a major driving force in evolution and understanding it is a huge challenge in biology. In society, people help each other; they work together within a social structure for a common good even if that means individual effort or sacrifice. I'm interested in finding out what keeps things fair and how cooperation is stabilized in the face of selfish cheats.”

University of Manchester

NANODIAMONDS DELIVER INSULIN FOR WOUND HEALING

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Bacterial infection is a major health threat to patients with severe burns and other kinds of serious wounds such as traumatic bone fractures. Recent studies have identified an important new weapon for fighting infection and healing wounds: insulin.

Now, using tiny nanodiamonds, researchers at Northwestern University have demonstrated an innovative method for delivering and releasing the curative hormone at a specific location over a period of time. The nanodiamond-insulin clusters hold promise for wound-healing applications and could be integrated into gels, ointments, bandages or suture materials.

Localized release of a therapeutic is a major challenge in biomedicine. The Northwestern method takes advantage of a condition typically found at a wound site -- skin pH levels can reach very basic levels during the repair and healing process. The researchers found that the insulin, bound firmly to the tiny carbon-based nanodiamonds, is released when it encounters basic pH levels, similar to those commonly observed in bacterially infected wounds. These basic pH levels are significantly greater than the physiological pH level of 7.4.

The results of the study were published online July 26 by the journal Biomaterials.

“This study introduces the concept of nanodiamond-mediated release of therapeutic proteins,” said Dean Ho, assistant professor of biomedical engineering and mechanical engineering at the McCormick School of Engineering and Applied Science. Ho led the research. “It’s a tricky problem because proteins, even small ones like insulin, bind so well to the nanodiamonds. But, in this case, the right pH level effectively triggers the release of the insulin.”

A substantial amount of insulin can be loaded onto the nanodiamonds, which have a high surface area. The nanodiamond-insulin clusters, by releasing insulin in alkaline wound areas, could accelerate the healing process and decrease the incidence of infection. Ho says this ability to release therapeutics from the nanodiamonds on demand represents an exciting strategy towards enhancing the specificity of wound treatment.

In their studies, Ho and his colleagues showed that the insulin was very tightly bound to the nanodiamonds when in an aqueous solution near the normal physiological pH level. Measurements of insulin function revealed that the protein was virtually inactive when bound to the nanodiamonds -- a beneficial property for preventing excess or unnecessary drug release.

Upon increasing the pH to the basic levels commonly observed in the skin during severe burns, the researchers confirmed the insulin was released from the nanodiamond clusters and retained its function. Exploiting this pH-mediated release mechanism may provide unique advantages for enhanced drug delivery methods.

The researchers also found the insulin slowly and consistently released from the nanodiamond clusters over a period of several days.

Insulin accelerates wound healing by acting as a growth hormone. It encourages skin cells to proliferate and divide, restores blood flow to the wound, suppresses inflammation and fights infection. Earlier investigations have confirmed an increase in alkalinity of wound tissue, due to bacterial colonization, to levels as high as pH 10.5, the pH level that promoted insulin release from the nanodiamonds in the Northwestern study.

Ho’s group next will work on integrating the nanodiamond-insulin complexes into a gel and conducting preclinical studies. The researchers also will investigate different areas of medicine in which the nanodiamond-insulin clusters could be used.

Nanodiamonds have many advantages for biomedical applications. The large surface area allows a large amount of therapeutic to be loaded onto the particles. They can be functionalized with nearly any type of therapeutic, including small molecules, proteins and antibodies. They can be suspended easily in water, an important property in biomedicine. The nanodiamonds, each being four to six nanometers in diameter, are minimally invasive to cells, biocompatible and do not cause inflammation, a serious complication. And they are very scalable and can be produced in large quantities in uniform sizes.

By harnessing the unique surface properties of the nanodiamonds, Ho and his colleagues have demonstrated that the nanodiamonds serve as platforms that can successfully bind, deliver and release several classes of therapeutics, which could impact a broad range of medical needs.

Ho’s research group also has studied nanodiamonds for applications in cancer therapy. They demonstrated that nanodiamonds are capable of releasing the chemotherapy agent Doxorubicin in a sustained and consistent manner. (Ho is a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.)

In addition to using the nanodiamonds in their particle form, Ho’s group has developed devices that harness the slow drug-release capabilities of the nanodiamonds. More recently, his team has shown that nanodiamonds are effective in dispersing insoluble drugs in water, boosting their potential for broader applications in medicine.

(Photo: Andrew Campbell)

Northwestern University

ORANG-UTANS UNIQUE IN MOVEMENT THROUGH TREE-TOPS

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Scientists at the Universities of Liverpool and Birmingham have found that orang-utans move through the canopy of tropical forests in a completely different way to all other tree-dwelling primates.

Movement through a complex meshwork of small branches at the heights of tropical forests presents a unique challenge to animals wanting to forage for food safely. It can be particularly dangerous for large animals where a fall of up to 30m could be fatal. Scientists found that dangerous tree vibrations can be countered by the orang-utan’s ability to move with an irregular rhythm.

Professor Robin Crompton, from the University of Liverpool’s School of Biomedical Sciences, explained that these challenges were similar to the difficulties engineers encountered with London’s ‘wobbly’ Millennium Bridge: “The problems with the Millennium Bridge were caused by large numbers of people walking in sync with the slight sideways motion of the bridge. This regular pattern of movement made the swaying motion of the bridge even worse. We see a similar problem in the movement of animals through the canopy of tropical forests, where there are highly flexible branches.

“Most animals, such as the chimpanzee, respond to these challenges by flexing their limbs to bring their body closer to the branch. Orang-utans, however, are the largest arboreal mammal and so they are likely to face more severe difficulties due to weight. If they move in a regular fashion, like their smaller relatives, we get a ‘wobbly bridge’ situation, whereby the movement of the branches increases.”

Dr Susannah Thorpe, from the University of Birmingham’s School of Biosciences, added: “Orang-utans have developed a unique way of coping with these problems; they move in an irregular way which includes upright walking, four-limbed suspension from branches and tree-swaying, whereby they move branches backwards and forwards, with increasing magnitude, until they are able to cross large gaps between trees.”


The team studied orang-utans in Sumatra, where the animal is predicted to be the first great ape to become extinct. This new research could further understanding into the way orang-utans use their habitat, which could support new conservation programmes.

Dr Thorpe continued: “If the destruction of forest land does not slow down, the Sumatran orang-utan could be extinct within the next decade. Now that we know more about how they move through the trees and the unique way that they adapt to challenges in their environment we can better understand their needs. This could help with reintroducing rescued animals to the forests and efforts to conserve their environment.”

(Photo: U. Liverpool)

University of Liverpool

KEY FEATURE OF IMMUNE SYSTEM SURVIVED IN HUMANS, OTHER PRIMATES FOR 60 MILLION YEARS

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A new study has concluded that one key part of the immune system, the ability of vitamin D to regulate anti-bactericidal proteins, is so important that is has been conserved through almost 60 million years of evolution and is shared only by primates, including humans – but no other known animal species.

The fact that this vitamin-D mediated immune response has been retained through millions of years of evolutionary selection, and is still found in species ranging from squirrel monkeys to baboons and humans, suggests that it must be critical to their survival, researchers say.

Even though the "cathelicidin antimicrobial peptide" has several different biological activities in addition to killing pathogens, it's not clear which one, or combination of them, makes vitamin D so essential to its regulation.

The research also provides further evidence of the biological importance of adequate levels of vitamin D in humans and other primates, even as some studies and experts suggest that more than 50 percent of the children and adults in the U.S. are deficient in "the sunshine vitamin."

"The existence and importance of this part of our immune response makes it clear that humans and other primates need to maintain sufficient levels of vitamin D," said Adrian Gombart, an associate professor of biochemistry and a principal investigator with the Linus Pauling Institute at Oregon State University.

In a new study in the journal BMC Genomics, researchers from OSU and the Cedars-Sinai Medical Center describe the presence of a genetic element that's specific to primates and involved in the innate immune response. They found it not only in humans and their more recent primate ancestors, such as chimpanzees, but also primates that split off on the evolutionary tree tens of millions of years ago, such as old world and new world primates.

The genetic material – called an Alu short interspersed element – is part of what used to be thought of as "junk DNA" and makes up more than 90 percent of the human genome. That genetic material, however, is now understood to often play important roles in regulating and "turning on" the expression of other genes.

In this case, the genetic element is believed to play a major role in the proper function of the "innate" immune system in primates – an ancient, first line of defense against bacteria, viruses and other pathogens, in which the body recognizes something that probably doesn't belong there, even though the specific pathogen may never have been encountered before.

"Many people are familiar with the role of our adaptive immune system, which is what happens when we mount a defense against a new invader and then retain antibodies and immunity in the future," Gombart said. "That's what makes a vaccine work. But also very important is the innate immune system, the almost immediate reaction your body has, for instance, when you get a cut or a skin infection."

In primates, this action of "turning on" an optimal response to microbial attack only works properly in the presence of adequate vitamin D, which is actually a type of hormone that circulates in the blood and signals to cells through a receptor. Vitamin D is produced in large amounts as a result of sun exposure, and is available in much smaller amounts from dietary sources.

Vitamin D prevents the "adaptive" immune response from over-reacting and reduces inflammation, and appears to suppress the immune response. However, the function of the new genetic element this research explored allows vitamin D to boost the innate immune response by turning on an antimicrobial protein. The overall effect may help to prevent the immune system from overreacting.

"It's essential that we have both an innate immune response that provides an immediate and front line of defense, but we also have protection against an overreaction by the immune system, which is what you see in sepsis and some autoimmune or degenerative diseases," Gombart said. "This is a very delicate balancing act, and without sufficient levels of vitamin D you may not have an optimal response with either aspect of the immune system."

After years of research, scientists are continuing to find new roles that vitamin D plays in the human body. It can regulate the actions of genes that are important to bone health, calcium uptake, and inhibition of cell growth. It helps regulate cell differentiation and, of course, immune function.

"The antimicrobial peptide that we're studying seems to be involved not just in killing bacteria, but has other biological roles," Gombart said. "It recruits other immune cells and sort of sounds the alarm that something is wrong. It helps promote development of blood vessels, cell growth and healing of wounds. And it seems to have important roles in barrier tissues such as skin and the digestive system. Vitamin D is very important for the health of the skin and digestive system, and putting the cathelicidin antimicrobial peptide gene under its regulation may be important in this function."

Any one, or some combination of those biological roles may be why vitamin D-mediated regulation of the antimicrobial peptide has been conserved in every primate species ever examined for its presence, researchers said, and did not disappear long ago through evolutionary variation and mutation. The evolution of primates into many different families and hundreds of species has been carefully tracked through genetic, molecular sequence and fossil studies, but the presence of this regulatory element in primates is still largely the same as it's been for more than 50 million years.

The evolutionary survival of this genetic element and the placement of the cathelicidin antimicrobial peptide gene under the regulation of the vitamin D pathway "may enable suppression of inflammation while potentiating innate immunity, thus maximizing the overall immune response to a pathogen and minimizing damage to the host," the researchers wrote in their conclusion.

Vitamin D deficiency is an issue of growing concern among many scientists, due to changing lifestyle or cultural trends in which many people around the world get less sun exposure and often inadequate dietary levels of the vitamin. It's a special problem with the elderly, which often have reduced exposure to sunlight and less ability to produce vitamin D in their skin – and at least partly as a result, are more susceptible to bone fractures, chronic inflammation and infectious disease.

Oregon State University

THE GREENHOUSE GAS THAT SAVED THE WORLD

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When Planet Earth was just cooling down from its fiery creation, the sun was faint and young. So faint that it should not have been able to keep the oceans of earth from freezing. But fortunately for the creation of life, water was kept liquid on our young planet. For years scientists have debated what could have kept earth warm enough to prevent the oceans from freezing solid. Now a team of researchers from Tokyo Institute of Technology and University of Copenhagen's Department of Chemistry have coaxed an explanation out of ancient rocks, as reported in this week's issue of PNAS.

"The young sun was approximately 30 percent weaker than it is now, and the only way to prevent earth from turning into a massive snowball was a healthy helping of greenhouse gas," Associate Professor Matthew S. Johnson of the Department of Chemistry explains. And he has found the most likely candidate for an archean atmospheric blanket. Carbonyl Sulphide: A product of the sulphur disgorged during millennia of volcanic activity.

"Carbonyl Sulphide is and was the perfect greenhouse gas. Much better than Carbon Dioxide. We estimate that a blanket of Carbonyl Sulphide would have provided about 30 percent extra energy to the surface of the planet. And that would have compensated for what was lacking from the sun", says Professor Johnson.

To discover what could have helped the faint young sun warm early earth, Professor Johnson and his colleagues in Tokyo examined the ratio of sulphur isotopes in ancient rocks. And what they saw was a strange signal; A mix of isotopes that couldn't very well have come from geological processes.

"There is really no process in the rocky mantle of earth that would explain this distribution of isotopes. You would need something happening in the atmosphere," says Johnson. The question was what. Painstaking experimentation helped them find a likely atmospheric process. By irradiating sulphur dioxide with different wavelengths of sunlight, they observed that sunlight passing through Carbonyl Sulphide gave them the wavelengths that produced the weird isotope mix.

"Shielding by Carbonyl Sulphide is really a pretty obvious candidate once you think about it, but until we looked, everyone had missed it," says Professor Johnson, and he continues.

"What we found is really an archaic analogue to the current ozone layer. A layer that protects us from ultraviolet radiation. But unlike ozone, Carbonyl Sulphide would also have kept the planet warm. The only problem is: It didn't stay warm".

As life emerged on earth it produced increasing amounts of oxygen. With an increasingly oxidizing atmosphere, the sulphur emitted by volcanoes was no longer converted to Carbonyl Sulphide. Instead it got converted to sulphate aerosols: A powerful climate coolant. Johnson and his co-workers created a Computer model of the ancient atmosphere. And the models in conjunction with laboratory experiments suggest that the fall in levels of Carbonyl Sulphide and rise of sulphate aerosols taken together would have been responsible for creating snowball earth, the planetwide ice-age hypothesised to have taken place near the end of the Archean eon 2500 million years ago. And the implications to Johnson are alarming:

"Our research indicates that the distribution and composition of atmospheric gasses swung the planet from a state of life supporting warmth to a planet-wide ice-age spanning millions of years. I can think of no better reason to be extremely cautious about the amounts of greenhouse gasses we are currently emitting to the atmosphere".

(Photo: U. Copenhagen)

ADVANCE TOWARD AN 'ELECTRONIC TONGUE' WITH A TASTE FOR SWEETS

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In a new approach to an effective "electronic tongue" that mimics human taste, scientists in Illinois are reporting development of a small, inexpensive, lab-on-a-chip sensor that quickly and accurately identifies sweetness — one of the five primary tastes. It can identify with 100 percent accuracy the full sweep of natural and artificial sweet substances, including 14 common sweeteners, using easy-to-read color markers.

This sensory "sweet-tooth" shows special promise as a simple quality control test that food processors can use to ensure that soda pop, beer, and other beverages taste great, — with a consistent, predictable flavor. Their study was described at the American Chemical Society's 238th National Meeting.

The new sensor, which is about the size of a business card, can also identify sweeteners used in solid foods such as cakes, cookies, and chewing gum. In the future, doctors and scientists could use modified versions of the sensor for a wide variety of other chemical-sensing applications ranging from monitoring blood glucose levels in people with diabetes to identifying toxic substances in the environment, the researchers say.

"We take things that smell or taste and convert their chemical properties into a visual image," says study leader Kenneth Suslick, Ph.D., of the University of Illinois at Urbana-Champaign. "This is the first practical "electronic tongue" sensor that you can simply dip into a sample and identify the source of sweetness based on its color."

Researchers have tried for years to develop "electronic tongues" or "electronic noses" that rival or even surpass the sensitivity of the human tongue and nose. But these devices can generally have difficulty distinguishing one chemical flavor from another, particularly in a complex mixture. Those drawbacks limit the practical applications of prior technology.

Suslick's team has spent a decade developing "colorimetric sensor arrays" that may fit the bill. The "lab-on-a-chip" consists of a tough, glass-like container with 16 to 36 tiny printed dye spots, each the diameter of a pencil lead. The chemicals in each spot react with sweet substances in a way that produces a color change. The colors vary with the type of sweetener present, and their intensity varies with the amount of sweetener.

To the scientists' delight, the sensor identified 14 different natural and artificial sweeteners, including sucrose (table sugar), xylitol (used in sugarless chewing gum), sorbitol, aspartame, and saccharin with 100 percent accuracy in 80 different trials.

Many food processors use a test called high-pressure liquid chromatography to measure sweeteners for quality control. But it requires an instrument the size of a desk that costs tens of thousands of dollars and needs a highly trained technician to operate. The process is also relatively slow, taking up to 30 minutes. The new sensor, in contrast, is small, inexpensive, disposable, and produces results in about 2 minutes.

Those minutes can be critical. Suclick noted that the food and beverage industry takes great care to ensure consistent quality of the many products that use sweeteners. At present, when a product's taste falls below specifications, then samples must be taken to the lab for analysis. Meanwhile, the assembly lines continue to whirl, with thousands of packages moving along each minute.

"With this device, manufacturers can fix the problem immediately — on location and in real-time," Suslick says.

Christopher Musto, a doctoral student in Suslick's lab, says it will take more work to develop the technology into a complete electronic tongue. "To be considered a true electronic tongue, the device must detect not just sweet, but sour, salty, bitter, and umami — the five main human tastes," he says. Umami means meaty or savory.

(Photo: Kenneth Suslick, Ph.D., University of Illinois at Urbana-Champaign)
American Chemical Society

THE BUZZ ON AN AMAZING NEW MOSQUITO REPELLENT: WILL IT FLY?

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After searching for more than 50 years, scientists finally have discovered a number of new mosquito repellents that beat DEET, the gold standard for warding off those pesky, sometimes disease-carrying insects. The stuff seems like a dream come true. It makes mosquitoes buzz off three times longer than DEET, the active ingredient in many of today's bug repellents. It does not have the unpleasant odor of DEET. And it does not cause DEET's sticky-skin sensation.

But there's a fly in the ointment: The odds may be stacked against any of the new repellents finding a place on store shelves this year or next — or ever.

Ulrich Bernier, Ph.D., lead researcher for the repellent study, said the costly, time-consuming pre-market testing and approval process is a hurdle that will delay availability of the repellents, which were discovered last year. The results of his team's work were presented at the 238th National Meeting of the American Chemical Society (ACS) by Maia Tsikoli, Ph.D., a post-doctoral researcher working with Bernier.

"Commercial availability of topical repellents can take years and a significant investment to achieve that end goal," Bernier said. "The cost will be several hundred thousand dollars. Once you determine that the repellent works through some screening process, we then have to go through a toxicological hazard evaluation involving numerous toxicological tests."

Provided the repellents continue to work well when tested in the laboratory on human skin, and if they pass the battery of toxicological tests, they would still face a series of tests to prove their effectiveness in making mosquitoes bug off, Bernier said.

"Clearly, the odds are stacked against new repellent products making it to market," he noted.

Bernier and his team discovered the repellents with what they say is the first successful application of a computer model using the molecular structures of more than 30,000 chemical compounds tested as repellents over the last 60 years. Using 11 known compounds, they synthesized 23 new ones. Of those, 10 gave about 40 days protection, compared to 17.5 days for DEET, when a soaked cloth was worn by a human volunteer. When applied to the skin, however, DEET lasts about five hours.

Bernier routinely participates in repellency studies, which involve about 500 mosquitoes trying to land on his arm and bite through a repellent-soaked cloth. "If the mosquitoes don't even land, we know the repellent is surely working," he explained. "If they walk around on the cloth-covered-arm, they are on the verge of being repelled. If they bite… on to the next repellent."

Overall, in addition to lasting longer than current products, including DEET, the new repellents don't have the stickiness or unpleasant smell common with today's insect sprays and liquids, said Bernier. He said that extended studies are now evaluating the effectiveness of the repellents against flies and ticks.

"This was quite an ambitious project," Bernier said. "The USDA historical archives and repellents database we used consisted of more than 30,000 chemical structures tested over the past six decades."

To search for the best repellents, the team devised software that recognized structural features of a chemical that would make it effective in keeping the bugs away. They trained it by feeding it the molecular structures of 150 known repellents. Based on this information, the program learned to identify the chemical traits of a good repellent without the chemists even having to know what those traits were. For example, the team checked out 2,000 variants of a compound found in black pepper that repels insects.

(Photo: Greg Allen, U.S. Department of Agriculture, Agricultural Research Service)

American Chemical Society

FIRST HUMAN GENE IMPLICATED IN REGULATING LENGTH OF HUMAN SLEEP

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Scientists have discovered the first gene involved in regulating the optimal length of human sleep, offering a window into a key aspect of slumber, an enigmatic phenomenon that is critical to human physical and mental health.

The team, reporting in the Aug. 14, 2009 issue of Science, identified a mutated gene that allows two members of an extended family to thrive on six hours of sleep a day rather than the eight to eight-and-a-half hours that studies have shown humans need over time to maintain optimal health. Working from this discovery, the scientists genetically engineered mice and fruit flies to express the mutated gene and study its impact.

While most Americans obtain less than eight hours of sleep a night (the average on non-work days is 7.4 hours), and some may feel they succeed with less when engaged in exhilarating work, domestic life or recreation, scientific evidence indicates that, over time, the body suffers from this regimen, the researchers say.

"Short term and chronic disruptions in the length of optimal sleep can have serious consequences on cognition, mood and physical health, including cancer and endocrine function," says the senior author of the study, Ying-Hui Fu, PhD, UCSF professor of neurology. However, teasing out this impact can be challenging, she says, given access to such stimuli as coffee and chocolate.

The finding, she says, offers an opportunity to unravel the regulatory mechanism of sleep. While the mutation may be rare, it could offer a probe more generally into the regulatory mechanisms of sleep quality and quantity. Understanding these mechanisms could lead to interventions to alleviate pathologies associated with sleep disturbance.

Sleep remains a relatively inscrutable biological phenomenon. Scientists know that it is regulated in large part by two processes: 1) circadian rhythms -- genetic, biochemical and physiological mechanisms that wax and wane during a 24 hour period to regulate the timing of sleep, 2) and homeostasis – unknown mechanisms that ensure that the body acquires over time the necessary amount of sleep, nudging it toward sleep when it has been deprived, prompting it out of sleep when it has received enough. This regulation of sleep intensity is measured in non rapid eye movement sleep and REM sleep. Interactions between the circadian rhythms and homeostatic mechanisms influence the timing, duration and quality of sleep and wakefulness.

But "the details in the process are really completely unknown," says Fu.

In 2001, the team discovered a mutated gene that caused some members of several families to be "morning larks," awaking around 3:30 a.m. and going to bed around 7:30 p.m. The condition, which the researchers named "familial advanced sleep phase syndrome," is believed to be primarily a variant, or mutated, form of a gene involved in regulating circadian rhythms. The total daily sleep time in people with this condition is normal.

In the current study, the team identified a small extended family in which a mother and her adult daughter had life-long shorter daily sleep requirements than most individuals. Fu's lab then studied blood samples from these women and their extended family. They identified a mutation in a gene known as hDEC2, which is a transcription factor that represses expression of certain other genes and is implicated in the regulation of circadian rhythms.

Next, the team genetically engineered mice and fruit flies to express the mutated human gene, and Ying He, PhD, a postdoctoral fellow in the Fu lab, studied its impact on their behavior and sleep patterns. Mice slept less, as seen in the extent of their scampering about in the dark (mouse preference) over the course of 24 hours and in electroencephalography (EEG) and electromyography (EMG) measurements indicating reduced nonREM and REM sleep. While lacking a Lilliputian size EEG to monitor the fruit flies, He studied the miniscule creatures' activity and sleep patterns by tracking the frequency of their movements through infrared light.

Next, the team compared the response of the genetically engineered mice and normal mice to the consequence of six hours of sleep deprivation. The engineered mice needed to compensate for their lost sleep to a much lesser extent – as seen in nonREM and REM measures – than their normal counterparts.

"These changes in sleep homeostasis in the mutant mice could provide an explanation for why human subjects with the mutation are able to live unaffected by shorter amounts of sleep throughout their lives," says Fu.

The next step, she says, is determining the DEC2's precise role. "We know the gene encodes a protein that is a transcriptional repressor and we know it makes the repressor's activity weaker. But we don't know if the weaker repressor is directly related to the shorter amount of sleep, because proteins can have many functions. It could be the protein functions as part of a larger transcriptional machinery, not necessarily as a repressor."

DEC2 could be involved in modulating "sleep quantity" alone, or it could be mediating both "sleep quantity" and "wakefulness-behavioral drive," according to Fu. The latter drive, she says, is critical for the procurement of food, shelter, and mates and could be more potent in individuals with this mutation.

"The mouse model also provides an opportunity to investigate whether there are other behaviors or physiological conditions associated with a short sleep syndrome," says Fu. She suspects there will be.

(Photo: UCSF)

UCSF

WHY ARE AUTUMN LEAVES RED IN AMERICA AND YELLOW IN EUROPE?

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Walking outdoors in the fall, the splendidly colorful leaves adorning the trees are a delight to the eye. In Europe these autumn leaves are mostly yellow, while the United States and East Asia boast lustrous red foliage. But why is it that there are such differences in autumnal hues around the world?

A new theory provided by Prof. Simcha Lev-Yadun of the Department of Science Education- Biology at the University of Haifa-Oranim and Prof. Jarmo Holopainen of the University of Kuopio in Finland and published in the Journal New Phytologist proposes taking a step 35 million years back to solve the color mystery.

The green of a tree's leaves is from the larger proportion of the chlorophyll pigment in the leaves. The change in color to red or yellow as autumn approaches is not the result of the leaves' dying, but of a series of processes – which differ between the red and yellow autumn leaves. When the green chlorophyll in leaves diminishes, the yellow pigments that already exist become dominant and give their color to the leaves. Red autumn leaves result from a different process: As the chlorophyll diminishes, a red pigment, anthocyanin, which was not previously present, is produced in the leaf. These facts were only recently discovered and led to a surge of research studies attempting to explain why trees expend resources on creating red pigments just as they are about to shed their leaves.

Explanations that have been offered vary and there is no agreement on this as of yet. One discipline suggests that the red pigment is produced as a result of physiological functions that make the re-translocation of amino acids to the woody parts of the tree more efficient in setting up its protection against the potential damage of light and cold. Other explanations suggest that the red pigment is produced as part of the tree's strategy for protecting itself against insects that thrive on the flow of amino acids. But whatever the answer is, these explanations do not help us understand why the process of creating anthocyanin, the red pigment, does not occur in Europe.

An evolutionary ecology approach infers that the strong autumn colors result from the long evolutionary war between the trees and the insects that use them as hosts. During the fall season, which is when the insects suck the amino acids from the leaves and later lay their eggs, the tree colors its leaves in red because aphids are attracted to yellow ones, so as to advertise to the insects as to the defensive quality of the tree in order to lower the tendency of the insects to occupy the leaves for nutrition and the bark for breeding. In this case too, the protective logic of red pigmentation may be sound, but the yellow leaves cannot be reconciled with this approach. But to settle this point, the new theory can be applied.

According to the theory provided by Prof. Lev-Yadun and Prof. Holopainen, until 35 million years ago, large areas of the globe were covered with evergreen jungles or forests composed of tropical trees. During this phase, a series of ice ages and dry spells transpired and many tree species evolved to become deciduous. Many of these trees also began an evolutionary process of producing red deciduous leaves in order to ward off insects. In North America, as in East Asia, north-to-south mountain chains enabled plant and animal 'migration' to the south or north with the advance and retreat of the ice according to the climatic fluctuations. And, of course, along with them migrated their insect 'enemies' too. Thus the war for survival continued there uninterrupted. In Europe, on the other hand, the mountains – the Alps and their lateral branches – reach from east to west, and therefore no protected areas were created. Many tree species that did not survive the severe cold died, and with them the insects that depended on them for survival. At the end of the repeated ice ages, most tree species that had survived in Europe had no need to cope with many of the insects that had become extinct, and therefore no longer had to expend efforts on producing red warning leaves.
According to the scientists, evidence supporting this theory can be found in the dwarf shrubs that grow in Scandinavia, which still color their leaves red in autumn. Unlike trees, dwarf shrubs have managed to survive the ice ages under a layer of snow that covered them and protected them from the extreme condition above. Under the blanket of snow, the insects that fed off the shrubs were also protected – so the battle with insects continued in these plants, making it necessary for them to color their leaves red.

University of Haifa-Oranim

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