Female Choice Key to Evolutionary Shift to Modern Family

It is a question that has puzzled evolutionary biologists for years: Why did we stop being promiscuous and decide to settle down to start families?

Sergey Gavrilets, professor of ecology and evolutionary biology at the University of Tennessee, Knoxville, may have found the answer, and it lies in the power of female choice. The study reveals how females chose their mates played a critical role in human evolution by leading to monogamous relationships, which laid the foundation for the institution of the modern family.

Using mathematical modeling, the associate director for scientific activities at the National Institute for Mathematical and Biological Synthesis (NIMBioS) at UT has discovered that the transformation may have occurred when early-hominid females started choosing males who were good providers.

Gavrilets' findings are published in the Proceedings of the National Academy of Sciences.

The "sexual revolution" entailed males first competing with other males for dominance, as a way to get matings. However, low-ranked males—and eventually all males except those with the highest societal stature—began supplying females with provisions in what is called "food-for-mating" to get a leg up on the competition. Females showed preference for the "provisioning" males, leading males' energy to be spent on providing for females and females becoming increasingly faithful. This spurred self-domestication and the modern family as we know it today.

"This change has confounded scientists for a long time because many species would be much better off evolutionarily if the effort spent on males competing for mates was redirected towards increasing female fertility or survivorship of their offspring," said Gavrilets.

The study demonstrates mathematically that the most commonly proposed theories for the transition to human pair bonding—or coupling—are not biologically feasible.

However, the study advances a new model showing that the transition to pair-bonding can occur when female choice and faithfulness, among other factors, are included. The result is an increased emphasis on males provisioning females over male competition for mating.

"The study reveals that female choice played a crucial role in human evolution," said Gavrilets.

According to Gavrilets, the transition to coupling has opened the path to intensified male parental investment, which was a breakthrough adaptation with multiple anatomical, behavioral and physiological consequences for early hominids and for all of their descendants. It shifted the dynamic away from males competing with each other for sex to males competing with each other to see who is a better provider to get better mates.

"Pair bonding laid the foundation for a later emergence of the institution of the modern family," said Gavrilets.

Source: University of Tennessee [May 30, 2012]

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16th-Century Korean Mummy Provides Clue to Hepatitis B Virus Genetic Code

The discovery of a mummified Korean child with relatively preserved organs enabled an Israeli-South Korean scientific team to conduct a genetic analysis on a liver biopsy which revealed a unique hepatitis B virus (HBV) genotype C2 sequence common in Southeast Asia.

The ancient Korean mummy of a child provides clues to the hepatitis B virus genome [Credit: Seoul National Univesity]

Additional analysis of the ancient HBV genomes may be used as a model to study the evolution of chronic hepatitis B and help understand the spread of the virus, possibly from Africa to East-Asia. It also may shed further light on the migratory pathway of hepatitis B in the Far East from China and Japan to Korea as well as to other regions in Asia and Australia where it is a major cause of cirrhosis and liver cancer.

The reconstruction of the ancient hepatitis B virus genetic code is the oldest full viral genome described in the scientific literature to date. It was reported in the May 21 edition of the scientific journal Hepathology by a research team from the Hebrew University of Jerusalem's Koret School of Veterinary Medicine, the Robert H. Smith Faculty of Agriculture, Food and Environment; the Hebrew University's Faculty of Medicine, the Hadassah Medical Center's Liver Unit; Dankook University and Seoul National University in South Korea.

Carbon 14 tests of the clothing of the mummy suggests that the boy lived around the 16th century during the Korean Joseon Dynasty. The viral DNA sequences recovered from the liver biopsy enabled the scientists to map the entire ancient hepatitis B viral genome.

Using modern-day molecular genetic techniques, the researchers compared the ancient DNA sequences with contemporary viral genomes disclosing distinct differences. The changes in the genetic code are believed to result from spontaneous mutations and possibly environmental pressures during the virus evolutionary process. Based on the observed mutations rates over time, the analysis suggests that the reconstructed mummy's hepatitis B virus DNA had its origin between 3,000 to 100,000 years ago.

The hepatitis B virus is transmitted through the contact with infected body fluids , i.e. from carrier mothers to their babies, through sexual contact and intravenous drug abuse. According to the World Health Organization, there are over 400 million carriers of the virus worldwide, predominantly in Africa, China and South Korea, where up to 15 percent of the population are cariers of the virus. In recent years, universal immunization of newborns against hepatitis B in Israel and in South Korea has lead to a massive decline in the incidence of infection.

The findings are the result of a collaborative effort between Dr. Gila Kahila Bar-Gal of the Hebrew University of Jerusalem's Koret School of Veterinary Medicine; Prof. Daniel Shouval of the Hadassah Medical Center's Liver Unit and Hebrew University; Dr. Myeung Ju Kim of Dankook University, Seok Ju Seon Memorial Museum; Dr. Dong Hoon Shin of Seoul National University, College of Medicine ; Prof Mark Spigelman of the Hebrew University's Dept. of Parasitology and Dr. Paul R. Grant of University College of London,Dept. of Virology.

Source: Hebrew University of Jerusalem [May 29, 2012]

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Nanoparticles Seen as Artificial Atoms

In the growth of crystals, do nanoparticles act as "artificial atoms" forming molecular-type building blocks that can assemble into complex structures? This is the contention of a major but controversial theory to explain nanocrystal growth. A study by researchers at the U.S. Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) may resolve the controversy and point the way to energy devices of the future.

These are sequential color TEM images showing the growth of Pt3Fe nanorods over time, displayed as minutes:seconds. At the far right, twisty nanoparticle chains straighten and stretch into nanorods [Credit:  Haimei Zheng]

Led by Haimei Zheng, a staff scientist in Berkeley Lab's Materials Sciences Division, the researchers used a combination of transmission electron microscopy and advanced liquid cell handling techniques to carry out real-time observations of the growth of nanorods from nanoparticles of platinum and iron. Their observations support the theory of nanoparticles acting like artificial atoms during crystal growth.

"We observed that as nanoparticles become attached they initially form winding polycrystalline chains," Zheng says. "These chains eventually align and attach end-to-end to form nanowires that straighten and stretch into single crystal nanorods with length-to-thickness ratios up to 40:1. This nanocrystal growth process, whereby nanoparticle chains as well as nanoparticles serve as the fundamental building blocks for nanorods, is both smart and efficient."

Zheng is the corresponding author of a paper describing this research in the journal Science. The paper is titled "Real-Time Imaging of Pt3Fe Nanorod Growth in Solution." Co-authors are Hong-Gang Liao, Likun Cui and Stephen Whitelam.

If the near limitless potential of nanotechnology is to even be approached, scientists will need a much better understanding of how nano-sized particles can assemble into hierarchical structures of ever-increasing organization and complexity. Such understanding comes from tracking nanoparticle growth trajectories and determining the forces that guide these trajectories.

Through the use of transmission electron microscopy and liquid observation cells, scientists at Berkeley Lab and elsewhere have made significant progress in observing nanoparticle growth trajectories, including the oriented attachment of nanoparticles -- the chemical phenomenon that starts the growth of nanocrystals in solution. However, these observations have typically been limited to the first few minutes of crystal growth. In their study, Zheng and her colleagues were able to extend the time of observation from minutes to hours.

"The key to studying the growth of colloidal nanocrystals with different shapes and architectures is to maintain the liquid in the viewing window long enough to allow complete reactions," Zheng says. "We dissolved molecular precursors of platinum and iron in an organic solvent and used capillary pressure to draw the growth solution into a silicon-nitride liquid cell that we sealed with epoxy. The sealing of the cell was especially important as it helped keep the liquid from turning viscous over time. Previously, we'd often see the liquids become viscous and this would prevent the nanoparticle interactions that drive crystal growth from taking place."

Zheng and her colleagues chose to study the growth of platinum iron nanorods because of the electrocatalytic material's promising potential for use in next generation energy conversion and storage devices. They were able to observe these nanoparticles assemble into nanorod crystals using powerful transmission electron microscopes at Berkeley Lab's National Center for Electron Microscopy, including TEAM 0.5 (Transmission Electron Aberration-corrected Microscope), which can produce images with half‑angstrom resolution -- less than the diameter of a single hydrogen atom.

"From what we observed only single nanoparticles exist at the beginning of crystal growth, but, as growth proceeds, small chains of nanoparticles become dominant until, ultimately, only long chains of nanoparticles can be seen," Zheng says. "Our observations provide a link between the world of single molecules and hierarchical nanostructures, paving the way for the rational design of nanomaterials with controlled properties."

Source: DOE/Lawrence Berkeley National Laboratory [May 24, 2012]

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Drug Destroys Human Cancer Stem Cells but Not Healthy Ones

A team of scientists at McMaster University has discovered a drug, thioridazine, successfully kills cancer stem cells in the human while avoiding the toxic side-effects of conventional cancer treatments.

"The unusual aspect of our finding is the way this human-ready drug actually kills cancer stem cells; by changing them into cells that are non-cancerous," said Mick Bhatia, the principal investigator for the study and scientific director of McMaster's Stem Cell and Cancer Research Institute in the Michael G. DeGroote School of Medicine.

Unlike chemotherapy and radiation, thioridazine appears to have no effect on normal stem cells.

The research, published May 24 in the science journal Cell, holds the promise of a new strategy and discovery pipeline for the development of anticancer drugs in the treatment of various cancers. The research team has identified another dozen drugs that have good potential for the same response.

For 15 years, some researchers have believed stem cells are the source of many cancers. In 1997, Canadian researchers first identified cancer stem cells in certain types of leukemia. Cancer stem cells have since been identified in blood, breast, brain, lung, gastrointestinal, prostate and ovarian cancer.

To test more than a dozen different compounds, McMaster researchers pioneered a fully automated robotic system to identify several drugs, including thioridazine.

"Now we can test thousands of compounds, eventually defining a candidate drug that has little effect on normal stem cells but kills the cells that start the tumor," said Bhatia.

The next step is to test thioridazine in clinical trials, focusing on patients with acute myeloid leukemia whose disease has relapsed after chemotherapy. Bhatia wants to find out if the drug can put their cancer into remission, and by targeting the root of the cancer (cancer stem cells) prevent the cancer from coming back. Researchers at McMaster have already designed how these trials would be done.

Bhatia's team found thioridazine works through the dopamine receptor on the surface of the cancer cells in both leukemia and breast cancer patients. This means it may be possible to use it as a biomarker that would allow early detection and treatment of breast cancer and early signs of leukemia progression, he said.

The research team's next step is to investigate the effectiveness of the drug in other types of cancer. In addition, the team will explore several drugs identified along with thioridazine. In the future, thousands of other compounds will be analyzed with McMaster robotic stem cell screening system in partnership with collaborations that include academic groups as well as industry.

"The goal for all of the partners is the same -- to find unique drugs to change the way we tackle and treat cancer," he said.

The research was supported by grants from the Canadian Institute of Health Research (CIHR), the Canadian Cancer Society Research Institute (CCSRI) and the Ontario Ministry of Economic Development and Innovation (MEDI)'s Ontario Consortium of Regenerating inducing Therapeutics (OCRiT).

Source: McMaster University [May 24, 2012]

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Stressed Men Are More Social

Freiburg researchers have refuted the common belief that stress always causes aggressive behavior. A team of researchers led by the psychologists and neuroscientists Prof. Markus Heinrichs and Dr. Bernadette von Dawans at the University of Freiburg, Germany, examined in a study how men react in stressful situations -- and have refuted a nearly 100-year-old doctrine with their results.

According to this doctrine, humans and most animal species show the "fight-or-flight" response to stress. Only since the late 1990s have some scientists begun to argue that women show an alternate "tend-and-befriend" response to stress -- in other words, a protective ("tend") and friendship-offering ("befriend") reaction. Men, in contrast, were still assumed to become aggressive under stress. Von Dawans refuted this assumption, saying: "Apparently men also show social approach behavior as a direct consequence of stress."

With this study, the research team experimentally investigated male social behavior under stress for the first time. The results are published in the  journal Psychological Science. The economists Prof. Ernst Fehr of the University of Zurich, Switzerland, and Prof. Urs Fischbacher of the University of Konstanz, Germany, as well as the psychologist Prof. Clemens Kirschbaum from the Technical University of Dresden, Germany, also participated in the study. Last year, Heinrichs and von Dawans already developed a standardized procedure for inducing stress in groups using a public speaking task. The researchers examined the implications of this stressor for social behavior using specially designed social interaction games.. These games allowed them to measure positive social behavior -- for example, trust or sharing -- and negative social behavior -- for example, punishment.

In the study, subjects who were under stress showed significantly more positive social behavior than control subjects who were not in a stressful situation. Negative social behavior, on the other hand, was not affected by stress. For Markus Heinrichs, this has far-reaching consequences for our understanding of the social significance of stress: "From previous studies in our laboratory, we already knew that positive social contact with a trusted individual before a stressful situation reduces the stress response. Apparently, this coping strategy is anchored so strongly that people can also change their stress responses during or immediately after the stress through positive social behavior."

Source: Albert-Ludwigs-Universität Freiburg [May 21, 2012]

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Genetic Discovery Will Revolutionize Understanding Of Gene Expression

Over the past decade, research in the field of epigenetics has revealed that chemically modified bases are abundant components of the human genome and has forced us to abandon the notion we've had since high school genetics that DNA consists of only four bases.

Over the past decade, research in the field of epigenetics has revealed that chemically modified bases are abundant components of the human genome and has forced us to abandon the notion we've had since high school genetics that DNA consists of only four bases. Now, researchers have made a discovery that once again forces us to rewrite our textbooks. This time, however, the findings pertain to RNA, which like DNA carries information about our genes and how they are expressed. The researchers have identified a novel base modification in RNA which they say will revolutionize our understanding of gene expression [Credit: © Attila Németh / Fotolia]

Now, researchers at Weill Cornell Medical College have made a discovery that once again forces us to rewrite our textbooks. This time, however, the findings pertain to RNA, which like DNA carries information about our genes and how they are expressed. The researchers have identified a novel base modification in RNA which they say will revolutionize our understanding of gene expression.

Their report, published in the journal Cell, shows that messenger RNA (mRNA), long thought to be a simple blueprint for protein production, is often chemically modified by addition of a methyl group to one of its bases, adenine. Although mRNA was thought to contain only four nucleobases, their discovery shows that a fifth base, N6-methyladenosine (m6A), pervades the transcriptome. The researchers found that up to 20 percent of human mRNA is routinely methylated. Over 5,000 different mRNA molecules contain m6A, which means that this modification is likely to have widespread effects on how genes are expressed.

"This finding rewrites fundamental concepts of the composition of mRNA because, for 50 years, no one thought mRNA contained internal modifications that control function," says the study's senior investigator, Dr. Samie R. Jaffrey, an associate professor of pharmacology at Weill Cornell Medical College.

"We know that DNA and proteins are routinely modified by chemical switches that have profound effects on their function in both health and disease. But biologists believed mRNA was simply an intermediate between DNA and protein," he says. "Now we know mRNA is much more complex, and defects in RNA methylation can lead to disease."

Indeed, as part of the study, the researchers demonstrated that the obesity risk gene, FTO (fat mass and obesity-associated), encodes an enzyme capable of reversing this modification, converting m6A residues in mRNA back to regular adenosine. Humans with FTO mutations have an overactive FTO enzyme, which results in low levels of m6A and causes abnormalities in food intake and metabolism that lead to obesity.

The researchers uncovered links between m6A and other diseases as well.

"We found that m6A is present in many mRNAs encoded by genes linked to human diseases, including cancer as well as several brain disorders, such as autism, Alzheimer's disease, and schizophrenia," says the study's lead investigator, Dr. Kate Meyer, a postdoctoral researcher in Dr. Jaffrey's laboratory. 

"Methylation in RNA is a reversible modification that appears to be a central step in a wide variety of biological pathways and physiological processes," she says.

The first time that m6A was detected in mRNA was in 1975, but at the time scientists were unsure whether this finding was a result of contamination by other RNA molecules, Dr. Jaffrey says. Over 90 percent of RNA is either transfer RNA (tRNA) or ribosomal RNA (rRNA), cellular workhorses that are routinely modified.

But Dr. Jaffrey says he has always been interested in the idea that mRNA may be modified - "DNA, proteins, other forms of RNA are modified, so why not mRNA?" he says - so he and investigators in his laboratory developed a technique to help them uncover methylation in mRNA taken from both mouse and human samples.

They used two different antibodies that recognize and bind to m6A in mRNA in order to selectively isolate the mRNAs that contain m6A. By subjecting these mRNAs to next-generation sequencing, they were able to identify the sequence of each individual mRNA they had isolated. Co-authors Dr. Christopher Mason and Dr. Olivier Elemento, assistant professors from the Department of Physiology and Biophysics and Computational Genomics in Computational Biomedicine at Weill Cornell Medical College, then developed computational algorithms to reveal the identity of each of these methylated mRNAs.

The Weill Cornell researchers don't know how the thousands of m6As they detected in humans work to control the function of mRNAs, but they do note that the m6As are located near "stop codons" in mRNA sequences. These areas signal the end of translation of the mRNA, suggesting that m6A might influence ribosomal function. "But we really don't know yet," says Dr. Mason, a co-lead investigator on the study. "It may allow other proteins to bind to mRNA, or subject these mRNAs to a whole new regulatory pathway. Our bioinformatics analyses are providing several hints about the possible impact of methylation on RNA function."

Indeed, in their study, the investigators have already found that m6A sites frequently occur in regions of mRNA that are highly conserved across several species of vertebrates. "This shows that m6A sites are not just important for humans, but rather are maintained under selection across hundreds of millions of years of evolution, and thus are likely of critical importance for all animals," Dr. Mason says.

"This is the first demonstration of an epitranscriptomic modification - alterations in RNA function that are not due to changes in the underlying sequence," he adds.

"These findings are very, very exciting, and amazing, really, when you consider that mRNA has been around for so long and that nobody realized, in all this time, that they were being regulated in this way," Dr. Jaffrey says. "It was right under our noses."

In addition to investigating how m6A regulates mRNAs within cells, the researchers are now focused on identifying the enzymes and pathways that control mRNA methylation.

Their study already demonstrates that FTO is capable of reversing adenosine methylation and suggests that it acts on a large proportion of cellular mRNA. "FTO mutations are estimated to occur in one billion people worldwide and are a leading cause of obesity and type 2 diabetes. Our studies link m6A levels in mRNA to these major health problems and identify for the first time the mRNAs which are potentially targeted by FTO," Dr. Meyer says.

The investigators are currently working to understand how defective regulation of m6A in patients with FTO mutations causes obesity and metabolic disorders, and they are also developing tests to rapidly identify compounds that inhibit FTO activity. These compounds are expected to inhibit the overactive FTO found in humans, potentially leading to novel therapeutics for diabetes and obesity.

Source: Medical News Today {May 19, 2012]

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Emotionally Intelligent People Are Less Good at Spotting Liars

People who rate themselves as having high emotional intelligence (EI) tend to overestimate their ability to detect deception in others. This is the finding of a paper published in the journal Legal and Criminological Psychology on18 May 2012.

Professor Stephen Porter, director of the Centre for the Advancement of Psychological Science and Law at University of British Columbia, Canada, along with colleagues Dr. Leanne ten Brinke and Alysha Baker used a standard questionnaire to measure the EI of 116 participants.

These participants were then asked to view 20 videos from around the world of people pleading for the safe return of a missing family member. In half the videos the person making the plea was responsible for the missing person's disappearance or murder.

The participants were asked to judge whether the pleas were honest or deceptive, say how much confidence they had in their judgements, report the cues they had used to make those judgements and rate their emotional response to each plea.

Professor Porter found that higher EI was associated with overconfidence in assessing the sincerity of the pleas and sympathetic feelings towards people in the videos who turned out to be responsible for the disappearance.

Although EI, in general, was not associated with being better or worse at discriminating between truths and lies, people with a higher ability to perceive and express emotion (a component of EI) were not so good at spotting when people were telling lies.

Professor Porter says: "Taken together, these findings suggest that features of emotional intelligence, and the decision-making processes they lead to, may have the paradoxical effect of impairing people's ability to detect deceit.

"This finding is important because EI is a well-accepted concept and is used in a variety of domains, including the workplace."

Source: British Psychological Society (BPS) [May 18, 2012]

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How Exercise Affects the Brain

Exercise clears the mind. It gets the blood pumping and more oxygen is delivered to the brain. This is familiar territory, but Dartmouth's David Bucci thinks there is much more going on.

Exercise clears the mind. It gets the blood pumping and more oxygen is delivered to the brain. This is familiar territory, but Dartmouth's David Bucci thinks there is much more going on [Credit: Web]

"In the last several years there have been data suggesting that neurobiological changes are happening -- [there are] very brain-specific mechanisms at work here," says Bucci, an associate professor in the Department of Psychological and Brain Sciences.

From his studies, Bucci and his collaborators have revealed important new findings:

• The effects of exercise are different on memory as well as on the brain, depending on whether the exerciser is an adolescent or an adult.

• A gene has been identified which seems to mediate the degree to which exercise has a beneficial effect. This has implications for the potential use of exercise as an intervention for mental illness.

Bucci began his pursuit of the link between exercise and memory with attention deficit hyperactivity disorder (ADHD), one of the most common childhood psychological disorders. Bucci is concerned that the treatment of choice seems to be medication.

"The notion of pumping children full of psycho-stimulants at an early age is troublesome," Bucci cautions. "We frankly don't know the long-term effects of administering drugs at an early age -- drugs that affect the brain -- so looking for alternative therapies is clearly important."

Anecdotal evidence from colleagues at the University of Vermont started Bucci down the track of ADHD. Based on observations of ADHD children in Vermont summer camps, athletes or team sports players were found to respond better to behavioral interventions than more sedentary children. While systematic empirical data is lacking, this association of exercise with a reduction of characteristic ADHD behaviors was persuasive enough for Bucci.

Coupled with his interest in learning and memory and their underlying brain functions, Bucci and teams of graduate and undergraduate students embarked upon a project of scientific inquiry, investigating the potential connection between exercise and brain function. They published papers documenting their results, with the most recent now available in the online version of the journal Neuroscience.

Bucci is quick to point out that "the teams of both graduate and undergraduates are responsible for all this work, certainly not just me." Michael Hopkins, a graduate student at the time, is first author on the papers.

Early on, laboratory rats that exhibit ADHD-like behavior demonstrated that exercise was able to reduce the extent of these behaviors. The researchers also found that exercise was more beneficial for female rats than males, similar to how it differentially affects male and female children with ADHD.

Moving forward, they investigated a mechanism through which exercise seems to improve learning and memory. This is "brain derived neurotrophic factor" (BDNF) and it is involved in growth of the developing brain. The degree of BDNF expression in exercising rats correlated positively with improved memory, and exercising as an adolescent had longer lasting effects compared to the same duration of exercise, but done as an adult.

"The implication is that exercising during development, as your brain is growing, is changing the brain in concert with normal developmental changes, resulting in your having more permanent wiring of the brain in support of things like learning and memory," says Bucci. "It seems important to [exercise] early in life."

Bucci's latest paper was a move to take the studies of exercise and memory in rats and apply them to humans. The subjects in this new study were Dartmouth undergraduates and individuals recruited from the Hanover community.

Bucci says that, "the really interesting finding was that, depending on the person's genotype for that trophic factor [BDNF], they either did or did not reap the benefits of exercise on learning and memory. This could mean that you may be able to predict which ADHD child, if we genotype them and look at their DNA, would respond to exercise as a treatment and which ones wouldn't."

Bucci concludes that the notion that exercise is good for health including mental health is not a huge surprise. "The interesting question in terms of mental health and cognitive function is how exercise affects mental function and the brain." This is the question Bucci, his colleagues, and students continue to pursue.

Author: Joseph Blumberg | Source: Dartmouth College [May 18, 2013]

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Are character traits determined genetically?

Genes play a greater role in forming character traits -- such as self-control, decision making or sociability -- than was previously thought, new research suggests.

Genes play a greater role in forming character traits -- such as self-control, decision making or sociability -- than was previously thought, new research suggests [Credit: Web]

A study of more than 800 sets of twins found that genetics were more influential in shaping key traits than a person's home environment and surroundings.

Psychologists at the University of Edinburgh who carried out the study, say that genetically influenced characteristics could well be the key to how successful a person is in life.

The study of twins in the US -- most aged 50 and over- used a series of questions to test how they perceived themselves and others. Questions included "Are you influenced by people with strong opinions?" and "Are you disappointed about your achievements in life?"

The results were then measured according to the Ryff Psychological Well-Being Scale which assesses and standardizes these characteristics.

By tracking their answers, the research team found that identical twins -- whose DNA is [presumed to be] exactly the same -- were twice as likely to share traits compared with non-identical twins.

Psychologists say the findings are significant because the stronger the genetic link, the more likely it is that these character traits are carried through a family.

Professor Timothy Bates, of the University of Edinburgh's School of Philosophy, Psychology and Language Sciences, said that the genetic influence was strongest on a person's sense of self-control.

Researchers found that genes affected a person's sense of purpose, how well they get on with people and their ability to continue learning and developing.

Professor Bates added: "Ever since the ancient Greeks, people have debated the nature of a good life and the nature of a virtuous life. Why do some people seem to manage their lives, have good relationships and cooperate to achieve their goals while others do not? Previously, the role of family and the environment around the home often dominated people's ideas about what affected psychological well-being. However, this work highlights a much more powerful influence from genetics."

The study, which builds on previous research that found that happiness is underpinned by genes, is published online in the Journal of Personality.

Source: University of Edinburgh [May 16, 2013]

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In the Genes, but Which Ones? Studies That Linked Specific Genes to Intelligence Were Largely Wrong, Experts Say

For decades, scientists have understood that there is a genetic component to intelligence, but a new Harvard study has found both that most of the genes thought to be linked to the trait are probably not in fact related to it, and identifying intelligence's specific genetic roots may still be a long way off.

For decades, scientists have understood that there is a genetic component to intelligence, but a new study has found both that most of the genes thought to be linked to the trait are probably not in fact related to it, and identifying intelligence's specific genetic roots may still be a long way off [Credit: Web]

Led by David I. Laibson '88, the Robert I. Goldman Professor of Economics, and Christopher F. Chabris '88, Ph.D. '99, assistant professor of psychology at Union College in Schenectady, N.Y., a team of researchers examined a dozen genes using large data sets that included both intelligence testing and genetic data. As reported in a forthcoming article in the journal Psychological Science, they found that in nearly every case, the hypothesized genetic pathway failed to replicate. In other words, intelligence could not be linked to the specific genes that were tested.

"It is only in the past 10 or 15 years that we have had the technology for people to do studies that involved picking a particular genetic variant and investigating whether people who score higher on intelligence tests tend to have that genetic variant," said Chabris. "In all of our tests we only found one gene that appeared to be associated with intelligence, and it was a very small effect. This does not mean intelligence does not have a genetic component, it means it's a lot harder to find the particular genes, or the particular genetic variants, that influence the differences in intelligence."

To get at the question of how genes influence intelligence, researchers first needed data, and plenty of it.

Though it had long been understood, based on studies of twins, that intelligence was a heritable trait, it wasn't until relatively recently that the technology emerged to allow scientists to directly probe DNA in a search for genes that affected intelligence.

The problem, Chabris said, was that early technology for assaying genes was very expensive, meaning that such studies were typically limited to, at most, several hundred subjects, who would take IQ tests and provide DNA samples for testing.

As part of their study, Chabris and his colleagues relied on several pre-existing data sets -- a massive study of Wisconsin high school graduates that began in the 1950s, the Framingham Heart Study, and an ongoing survey of all twins born in Sweden -- to expand that subject pool from a few hundred to many thousands.

"What we want to emphasize is that we are not saying the people who did earlier research in this area were foolish or wrong," Chabris said. "They were using the best technology they had available. At the time it was believed that individual genes would have a much larger effect -- they were expecting to find genes that might each account for several IQ points."

To identify genes that might play a role in intelligence, previous researchers used the "candidate gene approach," which requires identifying a gene that is already linked with a known biological function -- such as Alzheimer's disease or the production of a specific neurotransmitter. If people who scored high on intelligence tests shared a particular variant of that gene, it was believed, that demonstrated the gene's role in intelligence.

"These were reasonable hypotheses," said study co-author Daniel J. Benjamin '99, Ph.D. '06, assistant professor of economics at Cornell University. "But in retrospect, either the findings were false positives or the effects of the genes are much, much smaller than anyone had anticipated."

Chabris, however, emphasized that the results don't point to the idea that the dozen genes examined in the study play no role in intelligence, but rather suggest that intelligence may be tied to many genes and the ways in which they interact.

"As is the case with other traits, like height, there are probably thousands of genes and their variants that are associated with intelligence," he said. "And there may be other genetic effects beyond the single gene effects -- there could be interactions between genes, there could be interactions between genes and the environment. What our results show is that the way researchers have been looking for genes that may be related to intelligence -- the candidate gene method -- is fairly likely to result in false positives, so other methods should be used."

Author: Peter Reuell | Source: Harvard University [February 24, 2012]

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A walk in the park gives mental boost to people with depression

A walk in the park may have psychological benefits for people suffering from depression. In one of the first studies to examine the effect of nature walks on cognition and mood in people with major depression, researchers in Canada and the U.S. have found promising evidence that a walk in the park may provide some cognitive benefits.

The study was led by Marc Berman, a post-doctoral fellow at Baycrest's Rotman Research Institute in Toronto, with partners from the University of Michigan and Stanford University. It is published online this week, ahead of print publication, in the Journal of Affective Disorders.

"Our study showed that participants with clinical depression demonstrated improved memory performance after a walk in nature, compared to a walk in a busy urban environment," said Dr. Berman, who cautioned that such walks are not a replacement for existing and well-validated treatments for clinical depression, such as psychotherapy and drug treatment.

"Walking in nature may act to supplement or enhance existing treatments for clinical depression, but more research is needed to understand just how effective nature walks can be to help improve psychological functioning," he said.

Dr. Berman's research is part of a cognitive science field known as Attention Restoration Theory (ART) which proposes that people concentrate better after spending time in nature or looking at scenes of nature. The reason, according to ART, is that people interacting with peaceful nature settings aren't bombarded with external distractions that relentlessly tax their working memory and attention systems. In nature settings, the brain can relax and enter a state of contemplativeness that helps to restore or refresh those cognitive capacities.

In a research paper he published in 2008 in Psychological Science, Dr. Berman showed that adults who were not diagnosed with any illness received a mental boost after an hour-long walk in a woodland park – improving their performance on memory and attention tests by 20 percent – compared to an hour-long stroll in a noisy urban environment. The findings were reported by The Wall Street Journal, The Boston Globe, The New York Times, and in the Pulitzer Prize finalist book by Nicholas Carr, The Shallows: What the internet is doing to our brains.

In this latest study, Dr. Berman and his research team explored whether a nature walk would provide similar cognitive benefits, and also improve mood for people with clinical depression. Given that individuals with depression are characterized by high levels of rumination and negative thinking, the researchers were skeptical at the outset of the study that a solitary walk in the park would provide any benefit at all and may end up worsening memory and exacerbating depressed mood.

For the study, 20 individuals were recruited from the University of Michigan and surrounding Ann Arbor area; all had a diagnosis of clinical depression. The 12 females and eight males (average age 26) participated in a two-part experiment that involved walking in a quiet nature setting and in a noisy urban setting.

Prior to the walks, participants completed baseline testing to determine their cognitive and mood status. Before beginning a walk, the participants were asked to think about an unresolved, painful autobiographical experience. They were then randomly assigned to go for an hour-long walk in the Ann Arbor Arboretum (woodland park) or traffic heavy portions of downtown Ann Arbor. They followed a prescribed route and wore a GPS watch to ensure compliance.

After completing their walk, they completed a series of mental tests to measure their attention and short-term/working memory and were re-asssessed for mood. A week later the participants repeated the entire procedure, walking in the location that was not visited in the first session.

Participants exhibited a 16 percent increase in attention and working memory after the nature walk relative to the urban walk. Interestingly, interacting with nature did not alleviate depressive mood to any noticeable degree over urban walks, as negative mood decreased and positive mood increased after both walks to a significant and equal extent. Dr. Berman says this suggests that separate brain mechanisms may underlie the cognitive and mood changes of interacting with nature. 

Source: Baycrest Centre for Geriatric Care [May 14, 2012]

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Powerful Function of Single Protein That Controls Neurotransmission Discovered

Scientists at Weill Cornell Medical College have discovered that the single protein -- alpha 2 delta -- exerts a spigot-like function, controlling the volume of neurotransmitters and other chemicals that flow between the synapses of brain neurons. The study, published online in Nature, shows how brain cells talk to each other through these signals, relaying thoughts, feelings and action, and this powerful molecule plays a crucial role in regulating effective communication.

In the study, the investigators also suggest how the widely used pain drug Lyrica might work. The alpha 2 delta protein is the target of this drug and the new work suggests an approach to how other drugs could be developed that effectively twist particular neurotransmitter spigots on and off to treat neurological disorders. The research findings surprised the research team, which includes scientists from University College London.

"We are amazed that any single protein has such power," says the study's lead investigator Dr. Timothy A. Ryan, professor of Biochemistry and associate professor of Biochemistry in Anesthesiology at Weill Cornell Medical College. "It is indeed rare to identify a biological molecule's function that is so potent, that seems to be controlling the effectiveness of neurotransmission."

The researchers found that alpha 2 delta determines how many calcium channels will be present at the synaptic junction between neurons. The transmission of chemical signals is triggered at the synapse by the entry of calcium into these channels, so the volume and speed of neurotransmission depends on the availability of these channels.

Researchers discovered that taking away alpha 2 delta from brain cells prevented calcium channels from getting to the synapse. "But if you add more alpha 2 delta, you can triple the number of channels at synapses," Dr. Ryan says. "This change in abundance was tightly linked to how well synapses carry out their function, which is to release neurotransmitters."

Before this study, it was known that Lyrica, which is used for neuropathic pain, seizures and fibromyalgia, binds to alpha 2 delta, but little was understood about how this protein works to control synapses.

Lifting up the Hood

Dr. Ryan is building what he calls a "shop manual" of neurological function, much of which centers on synaptic neurotransmission. In 2007 and 2008, he discovered crucial clues to how neurons repackage the chemicals used to signal across synapses. In 2011, Dr. Ryan discovered that distinct neurons differently tune the speed by which they package these chemicals. And in a recent study published April 29 in Nature Neuroscience, he described, for the first time, the molecular mechanisms at the synapse that control the release of dopamine, a crucial neurotransmitter.

"We are looking under the hood of these machines for the first time," he says. "Many neurological diseases are considered to arise from pathologies of synaptic function. The synapse is so complex; at least a few thousand genes control how they work. Repairing them through treatment requires that we understand how they work."

Dr. Ryan and his team often use two tools to conduct these studies -- they pin fluorescent tags on to molecules involved in synaptic function, and use ultra sensitive microscopy technology to watch these molecules up close and in real-time.

The researchers used the same toolkit to examine the function of calcium channels, which triggers neurotransmission. "At all synapses, the secretion of a neurotransmitter is driven by the arrival of an electric impulse, initiated by another neuron," Dr. Ryan says. When this impulse arrives at the nerve terminal it triggers the opening of calcium channels. The calcium that rushes in is the key trigger that drives a synapse to secrete its neurotransmitter.

"We have known for the past half century that calcium is a key controller of neurotransmission," he says. "Any small change in calcium influx has a big impact on neurotransmission."

Protein Acts like a Shipping Label

But the number of calcium channels at the synapse is not static. Neurons constantly replace worn out channels, and to do this, they build the channels in the neuron's cell body and then package them up and ship them to the nerve terminal. In some cases, that is a very long journey -- as much as a few feet, such as the distance between the brain and the base of the spinal cord or the length of a leg.

In the study, researchers tagged fluorescent proteins onto a gene that encodes protein that makes a calcium channel and delivered it to neurons. They then watched the progress of the newly formed channels as they made their way, from day four to day seven, from the bodies of neurons to the synapse.

They also manipulated the levels of alpha 2 delta, a suspected calcium channel partner, and discovered that when the protein was increased, more calcium channels were moved to the synapse. Less alpha 2 delta reduced the flow. "We discovered that alpha 2 delta made the decision of how many calcium channels should be shipped the length of the neuron to the synapse," Dr. Ryan says. "It's like the channels couldn't be transported without an alpha 2 delta shipping label."

The research team found however that alpha 2 delta must work in at least two steps. When they impaired a piece of alpha 2 delta that resembles proteins that are involved in how cells bind to each other, they found that this broken alpha 2 delta could still help get calcium channels shipped down to synapses. But once there, they no longer helped drive neurotransmitter release. "This means that not only does alpha 2 delta help to get calcium channels shipped out, but it also implies that something at the synapse has to sign-off on receiving the calcium channels, putting them in the right place for them to do their job," Dr. Ryan says.

The researchers suggest that Lyrica might work by interfering with this final step since the piece of alpha 2 delta they "broke" that prevents the signing-off resembles parts of proteins that allows them to stick to each other in a kind of handshake.

These findings suggest that future therapies designed to manipulate neurotransmission could try to target this handshaking process, Dr. Ryan says. To do this will require that researchers identify the missing partner in the handshake.

"We hope these exciting findings are providing a new direction in how to make better drugs to control communication between brain cells," Dr. Ryan says.

The study was funded by the National Institutes of Mental Health and the Welcome Trust. Co-authors of the study include Dr. Michael B. Hoppa from Weill Cornell Medical College, and Dr. Beatrice Lana, Dr. Wojciech Margas, and Dr. Annette C. Dolphin from University College London.

Source: NewYork-Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College [May 13, 2012]

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DNA replication protein also has a role in mitosis, cancer

The foundation of biological inheritance is DNA replication – a tightly coordinated process in which DNA is simultaneously copied at hundreds of thousands of different sites across the genome. If that copying mechanism doesn't work as it should, the result could be cells with missing or extra genetic material, a hallmark of the genomic instability seen in most birth defects and cancers.

Mitotic spindle-chromosome attachments, marked in green, become unstable (on the right) compared to normal (on the left) [Credit: Cook and Salmon labs, UNC School of Medicine]

University of North Carolina School of Medicine scientists have discovered that a protein known as Cdt1, which is required for DNA replication, also plays an important role in a later step of the cell cycle, mitosis. The finding presents a possible explanation for why so many cancers possess not just genomic instability, but also more or less than the usual 46 DNA-containing chromosomes.

The new research, which was published online ahead of print by the journal Nature Cell Biology, is the first to definitively show such a dual role for a DNA replication protein.

"It was such a surprise, because we thought we knew what this protein's job was – to load proteins onto the DNA in preparation for replication," said Jean Cook, PhD, associate professor of biochemistry and biophysics and pharmacology at the UNC School of Medicine and senior study author. "We had no idea it also had a night job, in a completely separate part of the cell cycle."

The cell cycle is the series of events that take place in a cell leading to its growth, replication and division into two daughter cells. It consists of four distinct phases: G1 (Gap 1), S (DNA synthesis), M (mitosis) and G2 (Gap 2). Cook's research focuses on G1, when Cdt1 places proteins onto the genetic material to get it ready to be copied.

In this study, Cook ran a molecular screen to identify other proteins that Cdt1 might be interacting with inside the cell. She expected to just find more entities that controlled replication, and was surprised to discover one that was involved in mitosis. That protein, called Hec1 for "highly expressed in cancer," helps to ensure that the duplicated chromosomes are equally divided into daughter cells during mitosis, or cell division. Cook hypothesized that either Hec1 had a job in DNA replication that nobody knew about, or that Cdt1 was the one with the side business.

Cook partnered with Hec1 expert Edward (Ted) D. Salmon, PhD, professor of biology and co-senior author in this study, to explore these two possibilities. After letting Cdt1 do its replication job, the researchers interfered with the protein's function to see if it adversely affected mitosis. Using a high-powered microscope that records images of live cells, they showed that cells where Cdt1 function had been blocked did not undergo mitosis properly.

Once the researchers knew that Cdt1 was involved in mitosis, they wanted to pinpoint its role in that critical process. They further combined their genetic, microscopy and computational methods to demonstrate that without Cdt1, Hec1 fails to adopt the conformation inside the cells necessary to connect the chromosomes with the structure that pulls them apart into their separate daughter cells.

Cook says cells that make aberrant amounts of Cdt1, like that seen in cancer, can therefore experience problems in both replication and mitosis. One current clinical trial is actually trying to ramp up the amount of Cdt1 in cancer cells, in the hopes of pushing them from an already precarious position into a fatal one.

Source: University of North Carolina Health Care [May 13, 2012]

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Scientists generate electricity from viruses

Imagine charging your phone as you walk, thanks to a paper-thin generator embedded in the sole of your shoe. This futuristic scenario is now a little closer to reality. Scientists from the U.S. Department of Energy's Lawrence Berkeley National Laboratory (Berkeley Lab) have developed a way to generate power using harmless viruses that convert mechanical energy into electricity.

The scientists tested their approach by creating a generator that produces enough current to operate a small liquid-crystal display. It works by tapping a finger on a postage stamp-sized electrode coated with specially engineered viruses. The viruses convert the force of the tap into an electric charge.

Their generator is the first to produce electricity by harnessing the piezoelectric properties of a biological material. Piezoelectricity is the accumulation of a charge in a solid in response to mechanical stress.

The milestone could lead to tiny devices that harvest electrical energy from the vibrations of everyday tasks such as shutting a door or climbing stairs.

It also points to a simpler way to make microelectronic devices. That's because the viruses arrange themselves into an orderly film that enables the generator to work. Self-assembly is a much sought after goal in the finicky world of nanotechnology.

The scientists describe their work in a May 13 advance online publication of the journal Nature Nanotechnology.

"More research is needed, but our work is a promising first step toward the development of personal power generators, actuators for use in nano-devices, and other devices based on viral electronics," says Seung-Wuk Lee, a faculty scientist in Berkeley Lab's Physical Biosciences Division and a UC Berkeley associate professor of bioengineering.

He conducted the research with a team that includes Ramamoorthy Ramesh, a scientist in Berkeley Lab's Materials Sciences Division and a professor of materials sciences, engineering, and physics at UC Berkeley; and Byung Yang Lee of Berkeley Lab's Physical Biosciences Division.

The piezoelectric effect was discovered in 1880 and has since been found in crystals, ceramics, bone, proteins, and DNA. It's also been put to use. Electric cigarette lighters and scanning probe microscopes couldn't work without it, to name a few applications.

But the materials used to make piezoelectric devices are toxic and very difficult to work with, which limits the widespread use of the technology.

Lee and colleagues wondered if a virus studied in labs worldwide offered a better way. The M13 bacteriophage only attacks bacteria and is benign to people. Being a virus, it replicates itself by the millions within hours, so there's always a steady supply. It's easy to genetically engineer. And large numbers of the rod-shaped viruses naturally orient themselves into well-ordered films, much the way that chopsticks align themselves in a box.

These are the traits that scientists look for in a nano building block. But the Berkeley Lab researchers first had to determine if the M13 virus is piezoelectric. Lee turned to Ramesh, an expert in studying the electrical properties of thin films at the nanoscale. They applied an electrical field to a film of M13 viruses and watched what happened using a special microscope. Helical proteins that coat the viruses twisted and turned in response—a sure sign of the piezoelectric effect at work.

Next, the scientists increased the virus's piezoelectric strength. They used genetic engineering to add four negatively charged amino acid residues to one end of the helical proteins that coat the virus. These residues increase the charge difference between the proteins' positive and negative ends, which boosts the voltage of the virus.

The scientists further enhanced the system by stacking films composed of single layers of the virus on top of each other. They found that a stack about 20 layers thick exhibited the strongest piezoelectric effect.

The only thing remaining to do was a demonstration test, so the scientists fabricated a virus-based piezoelectric energy generator. They created the conditions for genetically engineered viruses to spontaneously organize into a multilayered film that measures about one square centimeter. This film was then sandwiched between two gold-plated electrodes, which were connected by wires to a liquid-crystal display.

When pressure is applied to the generator, it produces up to six nanoamperes of current and 400 millivolts of potential. That's enough current to flash the number "1" on the display, and about a quarter the voltage of a triple A battery.

"We're now working on ways to improve on this proof-of-principle demonstration," says Lee. "Because the tools of biotechnology enable large-scale production of genetically modified viruses, piezoelectric materials based on viruses could offer a simple route to novel microelectronics in the future."

Source: DOE/Lawrence Berkeley National Laboratory [May 13, 2012]

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Gene therapy for hearing loss: Potential and limitations

Regenerating sensory hair cells, which produce electrical signals in response to vibrations within the inner ear, could form the basis for treating age- or trauma-related hearing loss. One way to do this could be with gene therapy that drives new sensory hair cells to grow.

Researchers at Emory University School of Medicine have shown that introducing a gene called Atoh1 into the cochleae of young mice can induce the formation of extra sensory hair cells.

Their results show the potential of a gene therapy approach, but also demonstrate its current limitations. The extra hair cells produce electrical signals like normal hair cells and connect with neurons. However, after the mice are two weeks old, which is before puberty, inducing Atoh1 has little effect. This suggests that an analogous treatment in adult humans would also not be effective by itself.

The findings were published May 9 in the Journal of Neuroscience.

"We've shown that hair cell regeneration is possible in principle," says Ping Chen, PhD, associate professor of cell biology at Emory University School of Medicine. "In this paper, we have identified which cells are capable of becoming hair cells under the influence of Atoh1, and we show that there are strong age-dependent limitations on the effects of Atoh1 by itself."

The first author of the paper, Michael Kelly, now a postdoctoral fellow at the National Institute on Deafness and Other Communication Disorders, was a graduate student in Emory's Neuroscience program.

Kelly and his coworkers engineered mice to turn on the Atoh1 gene in the inner ear in response to the antibiotic doxycycline. Previous experimenters had used a virus to introduce Atoh1 into the cochleae of animals. This approach resembles gene therapy, but has the disadvantage of being slightly different each time, Chen says. In contrast, the mice have the Atoh1 gene turned on in specific cells along the lining of the inner ear, called the cochlear epithelium, but only when fed doxycycline.

Young mice given doxycycline for two days had extra sensory hair cells, in parts of the cochlea where developing hair cells usually appear, and also additional locations (see accompanying image).

The extra hair cells could generate electrical signals, although those signals weren't as strong as mature hair cells. Also, the extra hair cells appeared to attract neuronal fibers, which suggests that those signals could connect to the rest of the nervous system.

"They can generate electrical signals, but we don't know if they can really function in the context of hearing." Chen says. "For that to happen, the hair cells' signals need to be coordinated and integrated."

Although doxycycline could turn on Atoh1 all over the surface of the cochlea, extra sensory hair cells did not appear everywhere. When they removed cochleae from the mice and grew them in culture dishes, her team was able to provoke even more hair cells to grow when they added a drug that inhibits the Notch pathway.

Manipulating the Notch pathway affects several aspects of embryonic development and in some contexts appears to cause cancer, so the approach needs to be refined further. Chen says that it may be possible to unlock the age-related limits on hair cell regeneration by supplying additional genes or drugs in combination with Atoh1, and the results with the Notch drug provide an example.

"Our future goals are to develop approaches to stimulate hair cell formation in older animals, and to examine functional recovery after Atoh1 induction," she says.

Source: Emory University [May 11, 2012]

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New twist on ancient math problem could improve medicine, microelectronics

A hidden facet of a math problem that goes back to Sanskrit scrolls has just been exposed by nanotechnology researchers at the University of Michigan and the University of Connecticut.

A hidden facet of a math problem that goes back to Sanskrit scrolls has just been exposed by nanotechnology researchers [Credit: © bivainis/Fotolia]

It turns out we've been missing a version of the famous "packing problem," and its new guise could have implications for cancer treatment, secure wireless networks, microelectronics and demolitions, the researchers say.

Called the "filling problem," it seeks the best way to cover the inside of an object with a particular shape, such as filling a triangle with discs of varying sizes. Unlike the traditional packing problem, the discs can overlap. It also differs from the "covering problem" because the discs can't extend beyond the triangle's boundaries.

"Besides introducing the problem, we also provided a solution in two dimensions," said Sharon Glotzer, U-M professor of chemical engineering.

That solution makes it immediately applicable to treating tumors using fewer shots with radiation beams or speeding up the manufacturing of silicon chips for microprocessors.

The key to solutions in any dimension is to find a shape's "skeleton," said Carolyn Phillips, a postdoctoral fellow at Argonne National Laboratory who recently completed her Ph.D. in Glotzer's group and solved the problem as part of her dissertation.

"Every shape you want to fill has a backbone that goes through the center of the shape, like a spine," she said.

For a pentagon, the skeleton looks like a stick-drawing of a starfish. The discs that fill the pentagon best will always have their centers on one of those lines.

Junctions between lines in the skeleton are special points that Glotzer's team refers to as "traps." The pentagon only has one trap, right at its center, but more complicated shapes can contain multiple traps. In most optimal solutions, each trap has a disc centered over it, Phillips said.

Other discs in the pattern change size and move around, depending on how many discs are allowed, but those over the traps are always the same. Phillips suspects that if a design uses enough discs, every trap will have a disc centered over it.

In their paper, published online today in Physical Review Letters, the researchers report the rules for how to find the ideal size and spacing of the discs that fill a shape. In the future, they expect to reveal an algorithm that can take the desired shape and the number of discs, or the shape and percentage of the area to be filled, and spit out the best pattern to fill it.

Extending the approach into three dimensions, Glotzer proposes that it could decide the placement of wireless routers in a building where the signal must not be available to a potential hacker in the parking lot. Alternatively, it could help demolition workers to set off precision explosions, ensuring that the blast covers the desired region but doesn't extend beyond a building's outer walls.

Phillips expects filling solutions to be scientifically useful as well. Glotzer's team developed the new problem by trying to find a way to represent many-sided shapes for their computer models of nanoparticles. In addition to nanotechnology, biology and medicine often need models for complex shapes, such as those of proteins.

"You don't want to model every single one of the thousands of atoms that make up this protein," Phillips said. "You want a minimal model that gives the shape, allowing the proteins to interact in a lock-and-key way, as they do in nature."

The filling approach may prove a perfect fit for a variety of fields.

Author: Katherine McAlpine | Source: University of Michigan [May 10, 2012]

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Genes and Vascular Risk Modify Effects of Aging On Brain and Cognition

Efforts to understand how the aging process affects the brain and cognition have expanded beyond simply comparing younger and older adults.

"Everybody ages differently. By looking at genetic variations and individual differences in markers of vascular health, we begin to understand that preventable factors may affect our chances for successful aging," said Wayne State University psychology doctoral student Andrew Bender, lead author of a study supported by the National Institute on Aging of the National Institutes of Health and now in press in the journal Neuropsychologia.

The report, "Age-related Differences in Memory and Executive Functions in Healthy APOE ε4 Carriers: The Contribution of Individual Differences in Prefrontal Volumes and Systolic Blood Pressure," focuses on carriers of the ε4 variant of the apolipoprotein (APOE) gene, present in roughly 25 percent of the population. Compared to those who possess other forms of the APOE gene, carriers of the ε4 allele are at significantly greater risk for Alzheimer's, dementia and cardiovascular disease.

Many studies also have shown that nondemented carriers of the APOE ε4 variant have smaller brain volumes and perform less well on cognitive tests than carriers of other gene variants. Those findings, however, are not consistent, and a possible explanation may come from examining interactions between the risky genes and other factors, such as markers of cardiovascular health. Prior research in typical samples of older adults has shown that indeed other vascular risk factors -- such as elevated cholesterol, hypertension or diabetes -- can exacerbate the impact of the APOE ε4 variant on brain and cognition, but it is unclear if such synergy of risks is present in healthy adults.

Thus, Wayne State researchers evaluated a group of volunteers from 19 to 77 years of age who self-reported as exceptionally healthy on a questionnaire that screened for a number of conditions, representing a "best case scenario" of healthy aging. The research project, led by Naftali Raz, Ph.D., professor of psychology and director of the Lifespan Cognitive Neuroscience Research Program at WSU's Institute of Gerontology, tested different cognitive abilities known for their sensitivity to aging and the effects of the APOE ε4 variant. Those abilities include speed of information processing, working memory (holding and manipulating information in one's mind) and episodic memory (memory for events).

Researchers also measured participants' blood pressure, performed genetic testing to determine which APOE variant participants carried, and measured the volumes of several critical brain regions using a high-resolution structural magnetic resonance imaging brain scan. Bender and Raz showed that for older APOE ε4 carriers, even minor increases in systolic blood pressure (the higher of the two numbers that are reported in blood pressure measures) were linked with smaller volumes of the prefrontal cortex and prefrontal white matter, slower speed of information processing, reduced working memory capacity and worse verbal memory. Notably, they said, that pattern was not evident in those who lacked the ε4 gene variant.

The study concludes that the APOE ε4 gene may make its carriers sensitive to negative effects of relatively subtle elevations in systolic blood pressure, and that the interplay between two risk factors, genetic and physiological, is detrimental to the key brain structures and associated cognitive functions.

"Although genes play a significant role in shaping the effects of age and vascular risk on the brain and cognition, the impact of single genetic variants is relatively small, and there are quite a few of them. Thus, one's aging should not be seen through the lens of one's genetic profile," cautioned the study's authors. They continued, "The negative impact of many genetic variations needs help from other risk factors, and while there isn't much one can do about genes, a lot can be done about vascular risk factors such as blood pressure or cholesterol."

"Everybody should try to keep those in check, although people with certain genetic variants more so than others." Raz said. "Practically speaking, even with the best deck of genetic cards dealt to you, it still makes sense to reduce risk through whatever works: exercise, diet or, if those fail, medication."

Because the study is part of a longitudinal project, he and Bender said the immediate future task now is to determine how the interaction between risky genes and vascular risk factors affect the trajectory of age-related changes -- not differences, as in this cross-sectional study -- in brain and cognition.

Source: Wayne State University - Office of the Vice President for Research [May 09, 2012]

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