Health Matters Today!

Tests on Hereditary Diseases

noreply@blogger.com (Anonymous) — Sat, 27 Apr 2013 18:06:00 +0000

Scientists at the University of Medicine and Dentistry of New Jersey-New Jersey Medical School (UMDNJ-NJMS) have developed new DNA sequencing tests that hold significant promise for decreasing costs associated with diagnosing cancer and hereditary diseases, including cystic fibrosis.

According to the Cystic Fibrosis Foundation web site, "More than 10 million Americans are symptomless carriers of the defective CF gene." This chronic disease impacts the lungs and the digestive system. It occurs when a child inherits one defective CF gene from each parent. Statistics show New Jersey averages 125,000 births of children who are diagnosed with cystic fibrosis annually.Officials at the New Jersey Department of Health approved the use of the new Cystic Fibrosis (CF) Carrier and Diagnosis Test, which was created at the Institute for Genomic Medicine at UMDNJ-NJMS. Using a semiconductor mechanism that was developed by San Francisco-based Ion Torrent, the microchip tests the entire gene for mutations. IGM now offers this certified Clinical Diagnostic Laboratory service for hospitals as well as obstetrics and gynecology practices throughout the Garden State.

"We believe the adaptation of this new sequencing technology will drastically improve our ability to analyze genetic disorders," said Marvin N. Schwalb, PhD, director of the Institute for Genomic Medicine. "Traditional CF sequencing testing costs thousands of dollars making the test unavailable for carrier screening. This new test costs less than $200. Most importantly, the genetic carrier test we developed improves the diagnosis rate to 98 percent. While the test provides significant improvement for all populations, the improved rate is particularly valuable for minorities because current carrier screening methods only detects approximately 65% of mutations in these populations."

The new technology provides many advances including the ability to test as many as 96 samples on a single platform and the fact that the equipment cost 1/10 as much as the previous technology.

IGM has developed another test, which was also approved by the NJHSS, for mitochondrial DNA. Mutations in mitochondria cause a wide variety of diseases, such eye and neuromuscular system disorders and possible cancer.

Schwalb, a professor of Pediatrics, Microbiology and Molecular Genetics at NJMS, said, "We are proud of the fact that the IGM is a world leader in the advancement of genetic diagnosis. DNA sequencing will keep us very busy for a while. In the state of New Jersey, there is nothing that compares to this advancement and this is just the beginning."

Source: University of Medicine and Dentistry of New Jersey (UMDNJ) (2012, August 16). Researchers develop DNA sequencing tests for hereditary diseases. ScienceDaily. Retrieved April 27, 2013, from http://www.sciencedaily.com/releases/2012/08/120816170309.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%29

Gut bacteria linked to obesity

noreply@blogger.com (Anonymous) — Thu, 25 Apr 2013 15:58:00 +0000

Researchers at the University of Maryland School of Medicine have identified 26 species of bacteria in the human gut microbiota that appear to be linked to obesity and related metabolic complications. These include insulin resistance, high blood sugar levels, increased blood pressure and high cholesterol, known collectively as "the metabolic syndrome," which significantly increases an individual’s risk of developing diabetes, cardiovascular disease and stroke.

"We identified 26 species of bacteria that were correlated with obesity and metabolic syndrome traits such as body mass index (BMI), triglycerides, cholesterol, glucose levels and C-reactive protein, a marker for inflammation," says the senior author, Claire M. Fraser, Ph.D., professor of medicine and microbiology and immunology and director of the Institute for Genome Sciences (IGS) at the University of Maryland School of Medicine. "We can’t infer cause and effect, but it’s an important step forward that we're starting to identify bacteria that are correlated with clinical parameters, which suggests that the gut microbiota could one day be targeted with medication, diet or lifestyle changes."The results of the study, which analyzed data from the Old Order Amish in Lancaster County, Pa., are being published online on Aug. 15, 2012, in PLOS ONE, which is published by the Public Library of Science (PLOS One). The study was funded by the National Institutes of Health (NIH). (UH2/UH3 DK083982, U01 GM074518 and P30 DK072488)

Dr. Fraser says that additional research, including an interventional study with the Amish, is essential. "We can look at whether these bacteria change over time in a given individual or in response to diet or medication," she says.

Dr. Fraser notes that the research team, led by Margaret L. Zupancic, Ph.D., then a postdoctoral fellow at IGS, also found an apparent link between the gut bacteria and inflammation, which is believed to be a factor in obesity and many other chronic diseases. "This is one of the first studies of obesity in humans to make a link between inflammatory processes and specific organisms that are present in the GI tract," Dr. Fraser says, noting that participants with metabolic syndrome who had elevated serum markers associated with inflammation tended to have the lowest levels of good bacteria that have been reported previously to have anti-inflammatory properties.

The study is the result of an ongoing collaboration between Dr. Fraser and Alan R. Shuldiner, M.D., in connection with the NIH’s Human Microbiome Project, which seeks to characterize microbial communities in the body. Dr. Shuldiner, associate dean for personalized medicine and director of the Program in Personalized and Genomic Medicine at the University of Maryland School of Medicine, operates an Amish research clinic in Lancaster Pa. Over the past 20 years, he and his research team have conducted more than a dozen studies with the Amish, looking for genes that may cause common diseases, such as diabetes, osteoporosis and cardiovascular disease.

"The Old Order Amish are ideal for such studies because they are a genetically homogenous population descended from a few founder families and have a similar rural lifestyle," Dr. Shuldiner, the John L. Whitehurst Professor of Medicine, says. "We believe the results of this study are relevant to a broader population because the clinical characteristics of obesity and its complications in the Amish are no different from the general Caucasian population," he says.

E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and the John Z. and Akiko K. Bowers Distinguished Professor and dean of the University of Maryland School of Medicine, says, "Obesity and its related complications have become a critical public health concern, and the number of people who are now considered obese or overweight has skyrocketed. Dr. Fraser and Dr. Shuldiner are two of our most senior research-scientists and leaders in their respective fields. This study provides valuable insights into the role the bacteria in our bodies may play in obesity and the metabolic syndrome. We may ultimately be able to target the gut microbiome to help prevent or mitigate risk factors for a number of diseases."

The researchers analyzed the bacteria in fecal samples of 310 members of the Old Order Amish community, using a process that enables them to identify a marker gene that serves as a bar code for each type of bacteria. Participants in the study ranged from lean to overweight to obese; some of the obese participants also had features of the metabolic syndrome. "Our hypothesis was that we would see a different composition in the gut microbiota in lean vs. obese individuals and possibly in individuals who were obese but also had features of the metabolic syndrome."

They discovered that every individual possessed one of three different communities of interacting bacteria, each characterized by a dominant bacterial genus. Neither BMI nor any metabolic syndrome trait was specifically associated with any of these communities. Instead, differing levels of 26 less abundant bacterial species present in all individuals appeared to be linked to obesity and certain features of the metabolic syndrome.

Interestingly, researchers also analyzed people's gut bacteria by their occupation and found that those who had regular contact with livestock, such as farmers and their wives, had bacterial communities dominated by Prevotella, a type of bacteria that is also abundant in the gut microbiota of cattle and sheep. "These findings suggest that environmental exposure may play a role in determining the composition of the gut microbiota in humans," Dr. Fraser says.

University of Maryland Medical Center (2012, August 15). Gut bacteria linked to obesity and metabolic syndrome identified. ScienceDaily. Retrieved April 26, 2013, from http://www.sciencedaily.com/releases/2012/08/120815174902.htm?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+sciencedaily+%28ScienceDaily%3A+Latest+Science+News%29

Scientists Can Now Block Heroin, Morphine Addiction

noreply@blogger.com (Anonymous) — Wed, 24 Apr 2013 14:58:00 +0000

In a major breakthrough, an international team of scientists has proven that addiction to morphine and heroin can be blocked, while at the same time increasing pain relief.

Photp: Jens Langner at http://commons.wikimedia.org/wiki/File:PET-image.jpg

Laboratory studies have shown that the drug (+)-naloxone (pronounced: PLUS nal-OX-own) will selectively block the immune-addiction response.The team from the University of Adelaide and University of Colorado has discovered the key mechanism in the body's immune system that amplifies addiction to opioid drugs.

The results -- which could eventually lead to new co-formulated drugs that assist patients with severe pain, as well as helping heroin users to kick the habit -- will be published August 16 in the Journal of Neuroscience.

"Our studies have shown conclusively that we can block addiction via the immune system of the brain, without targeting the brain's wiring," says the lead author of the study, Dr Mark Hutchinson, ARC Research Fellow in the University of Adelaide's School of Medical Sciences.

"Both the central nervous system and the immune system play important roles in creating addiction, but our studies have shown we only need to block the immune response in the brain to prevent cravings for opioid drugs."

The team has focused its research efforts on the immune receptor known as Toll-Like receptor 4 (TLR4).

"Opioid drugs such as morphine and heroin bind to TLR4 in a similar way to the normal immune response to bacteria. The problem is that TLR4 then acts as an amplifier for addiction," Dr Hutchinson says.

"The drug (+)-naloxone automatically shuts down the addiction. It shuts down the need to take opioids, it cuts out behaviours associated with addiction, and the neurochemistry in the brain changes -- dopamine, which is the chemical important for providing that sense of 'reward' from the drug, is no longer produced."

Senior author Professor Linda Watkins, from the Center for Neuroscience at the University of Colorado Boulder, says: "This work fundamentally changes what we understand about opioids, reward and addiction. We've suspected for some years that TLR4 may be the key to blocking opioid addiction, but now we have the proof.

"The drug that we've used to block addiction, (+)-naloxone, is a non-opioid mirror image drug that was created by Dr Kenner Rice in the 1970s. We believe this will prove extremely useful as a co-formulated drug with morphine, so that patients who require relief for severe pain will not become addicted but still receive pain relief. This has the potential to lead to major advances in patient and palliative care," Professor Watkins says.

The researchers say clinical trials may be possible within the next 18 months.

This study has been funded by the National Institute on Drug Abuse (NIDA) in the United States and the Australian Research Council (ARC).

Source: University of Adelaide (2012, August 14). Scientists can now block heroin, morphine addiction. ScienceDaily. Retrieved April 24, 2013, from http://www.sciencedaily.com/releases/2012/08/120814213246.htm

An Artificial Retina With the Capacity to Restore Normal Vision

noreply@blogger.com (Anonymous) — Tue, 23 Apr 2013 06:41:00 +0000

Two researchers at Weill Cornell Medical College have deciphered a mouse's retina's neural code and coupled this information to a novel prosthetic device to restore sight to blind mice. The researchers say they have also cracked the code for a monkey retina -- which is essentially identical to that of a human -- and hope to quickly design and test a device that blind humans can use.

Source: http://commons.wikimedia.org/wiki/File:Amandine_Eyes.jpg

The lead researcher, Dr. Sheila Nirenberg, a computational neuroscientist at Weill Cornell, envisions a day when the blind can choose to wear a visor, similar to the one used on the television show Star Trek. The visor's camera will take in light and use a computer chip to turn it into a code that the brain can translate into an image.The breakthrough, reported in theProceedings of the National Academy of Sciences (PNAS), signals a remarkable advance in longstanding efforts to restore vision. Current prosthetics provide blind users with spots and edges of light to help them navigate. This novel device provides the code to restore normal vision. The code is so accurate that it can allow facial features to be discerned and allow animals to track moving images.

"It's an exciting time. We can make blind mouse retinas see, and we're moving as fast as we can to do the same in humans," says Dr. Nirenberg, a professor in the Department of Physiology and Biophysics and in the Institute for Computational Biomedicine at Weill Cornell. The study's co-author is Dr. Chethan Pandarinath, who was a graduate student with Dr. Nirenberg and is currently a postdoctoral researcher at Stanford University.

This new approach provides hope for the 25 million people worldwide who suffer from blindness due to diseases of the retina. Because drug therapies help only a small fraction of this population, prosthetic devices are their best option for future sight. "This is the first prosthetic that has the potential to provide normal or near-normal vision because it incorporates the code," Dr. Nirenberg explains.

Discovering the Code

Normal vision occurs when light falls on photoreceptors in the surface of the retina. The retinal circuitry then processes the signals from the photoreceptors and converts them into a code of neural impulses. These impulses are then sent up to the brain by the retina's output cells, called ganglion cells. The brain understands this code of neural pulses and can translate it into meaningful images.

Blindness is often caused by diseases of the retina that kill the photoreceptors and destroy the associated circuitry, but typically, in these diseases, the retina's output cells are spared.

Current prosthetics generally work by driving these surviving cells. Electrodes are implanted into a blind patient's eye, and they stimulate the ganglion cells with current. But this only produces rough visual fields.

Many groups are working to improve performance by placing more stimulators into the patient's eye. The hope is that with more stimulators, more ganglion cells in the damaged tissue will be activated, and image quality will improve.

Other research teams are testing use of light-sensitive proteins as an alternate way to stimulate the cells. These proteins are introduced into the retina by gene therapy. Once in the eye, they can target many ganglion cells at once.

But Dr. Nirenberg points out that there's another critical factor. "Not only is it necessary to stimulate large numbers of cells, but they also have to be stimulated with the right code -- the code the retina normally uses to communicate with the brain."

This is what the authors discovered -- and what they incorporated into a novel prosthetic system.

Dr. Nirenberg reasoned that any pattern of light falling on to the retina had to be converted into a general code -- a set of equations -- that turns light patterns into patterns of electrical pulses. "People have been trying to find the code that does this for simple stimuli, but we knew it had to be generalizable, so that it could work for anything -- faces, landscapes, anything that a person sees," Dr. Nirenberg says.

Vision = Chip Plus Gene Therapy

In a eureka moment, while working on the code for a different reason, Dr. Nirenberg realized that what she was doing could be directly applied to a prosthetic. She and her student, Dr. Pandarinath, immediately went to work on it. They implemented the mathematical equations on a "chip" and combined it with a mini-projector. The chip, which she calls the "encoder" converts images that come into the eye into streams of electrical impulses, and the mini-projector then converts the electrical impulses into light impulses. These light pulses then drive the light-sensitive proteins, which have been put in the ganglion cells, to send the code on up to the brain.

The entire approach was tested on the mouse. The researchers built two prosthetic systems -- one with the code and one without. "Incorporating the code had a dramatic impact," Dr. Nirenberg says. "It jumped the system's performance up to near-normal levels -- that is, there was enough information in the system's output to reconstruct images of faces, animals -- basically anything we attempted."

In a rigorous series of experiments, the researchers found that the patterns produced by the blind retinas in mice closely matched those produced by normal mouse retinas.

"The reason this system works is two-fold," Dr. Nirenberg says. "The encoder -- the set of equations -- is able to mimic retinal transformations for a broad range of stimuli, including natural scenes, and thus produce normal patterns of electrical pulses, and the stimulator (the light sensitive protein) is able to send those pulses on up to the brain."

"What these findings show is that the critical ingredients for building a highly-effective retinal prosthetic -- the retina's code and a high resolution stimulating method -- are now, to a large extent, in place," reports Dr. Nirenberg.

Dr. Nirenberg says her retinal prosthetic will need to undergo human clinical trials, especially to test safety of the gene therapy component, which delivers the light-sensitive protein. But she anticipates it will be safe since similar gene therapy vectors have been successfully tested for other retinal diseases.

"This has all been thrilling," Dr. Nirenberg says. "I can't wait to get started on bringing this approach to patients."

The study was funded by grants from the National Institutes of Health and Cornell University's Institute for Computational Biomedicine.

Both Drs. Nirenberg and Pandarinath have a patent application for the prosthetic system filed through Cornell University.

Source: Weill Cornell Medical College (2012, August 14). An artificial retina with the capacity to restore normal vision. ScienceDaily. Retrieved April 23, 2013, from http://www.sciencedaily.com/releases/2012/08/120814213326.htm

Why are some people smarter than others?

noreply@blogger.com (Anonymous) — Mon, 22 Apr 2013 03:52:00 +0000

"When it comes to intelligence, what factors distinguish the brains of exceptionally smart humans from those of average humans?

Photp: Jens Langner at http://commons.wikimedia.org/wiki/File:PET-image.jpg

As science has long suspected, overall brain size matters somewhat, accounting for about 6.7 percent of individual variation in intelligence. More recent research has pinpointed the brain’s lateral prefrontal cortex, a region just behind the temple, as a critical hub for high-level mental processing, with activity levels there predicting another 5 percent of variation in individual intelligence.

Now, new research from Washington University in St. Louis suggests that another 10 percent of individual differences in intelligence can be explained by the strength of neural pathways connecting the left lateral prefrontal cortex to the rest of the brain.

Published in the Journal of Neuroscience, the findings establish “global brain connectivity” as a new approach for understanding human intelligence.

Michael W. Cole

“Our research shows that connectivity with a particular part of the prefrontal cortex can predict how intelligent someone is,” suggests lead author Michael W. Cole, PhD, a postdoctoral research fellow in cognitive neuroscience at Washington University.

The study is the first to provide compelling evidence that neural connections between the lateral prefrontal cortex and the rest of the brain make a unique and powerful contribution to the cognitive processing underlying human intelligence, says Cole, whose research focuses on discovering the cognitive and neural mechanisms that make human behavior uniquely flexible and intelligent.

“This study suggests that part of what it means to be intelligent is having a lateral prefrontal cortex that does its job well; and part of what that means is that it can effectively communicate with the rest of the brain,” says study co-author Todd Braver, PhD, professor of psychology in Arts & Sciences and of neuroscience and radiology in the School of Medicine. Braver is a co-director of the Cognitive Control and Psychopathology Lab at Washington University, in which the research was conducted.

Todd Braver

One possible explanation of the findings, the research team suggests, is that the lateral prefrontal region is a “flexible hub” that uses its extensive brain-wide connectivity to monitor and influence other brain regions in a goal-directed manner.

“There is evidence that the lateral prefrontal cortex is the brain region that ‘remembers’ (maintains) the goals and instructions that help you keep doing what is needed when you’re working on a task,” Cole says. “So it makes sense that having this region communicating effectively with other regions (the ‘perceivers’ and ‘doers’ of the brain) would help you to accomplish tasks intelligently.”

While other regions of the brain make their own special contribution to cognitive processing, it is the lateral prefrontal cortex that helps coordinate these processes and maintain focus on the task at hand, in much the same way that the conductor of a symphony monitors and tweaks the real-time performance of an orchestra.

“We’re suggesting that the lateral prefrontal cortex functions like a feedback control system that is used often in engineering, that it helps implement cognitive control (which supports fluid intelligence), and that it doesn’t do this alone,” Cole says.

The findings are based on an analysis of functional magnetic resonance brain images captured as study participants rested passively and also when they were engaged in a series of mentally challenging tasks associated with fluid intelligence, such as indicating whether a currently displayed image was the same as one displayed three images ago.

Previous findings relating lateral prefrontal cortex activity to challenging task performance were supported. Connectivity was then assessed while participants rested, and their performance on additional tests of fluid intelligence and cognitive control collected outside the brain scanner was associated with the estimated connectivity.

Results indicate that levels of global brain connectivity with a part of the left lateral prefrontal cortex serve as a strong predictor of both fluid intelligence and cognitive control abilities.

Although much remains to be learned about how these neural connections contribute to fluid intelligence, new models of brain function suggested by this research could have important implications for the future understanding — and perhaps augmentation — of human intelligence.

The findings also may offer new avenues for understanding how breakdowns in global brain connectivity contribute to the profound cognitive control deficits seen in schizophrenia and other mental illnesses, Cole suggests.

Other co-authors include Tal Yarkoni, PhD, a postdoctoral fellow in the Department of Psychology and Neuroscience at the University of Colorado at Boulder; Grega Repovs, PhD, professor of psychology at the University of Ljubljana, Slovenia; and Alan Anticevic, an associate research scientist in psychiatry at Yale University School of Medicine.

Funding from the National Institute of Mental Health supported the study (National Institutes of Health grants MH66088, NR012081, MH66078, MH66078-06A1W1, and 1K99MH096801)."

Source: by Gerry Everding, Washington University in St. Louis

Cell's pressure matters

noreply@blogger.com (Anonymous) — Mon, 22 Apr 2013 03:40:00 +0000

"A model that describes dividing cells within human tissues from the perspective of physicists could help further the understanding of cancer growth.

Photo from: https://commons.wikimedia.org/wiki/File:South_African_Giraffes,_fighting.jpg

Jonas Ranft and team created a two-component mathematical model accounting for both the cells and the fluid caught in between. On the one hand, cells are modeled as behaving like a dividing fluid subject to expansion. On the other hand, the interstitial fluid is akin to an ideal fluid that cannot be compressed. This model is designed to elucidate the nature of mechanical pressure exerted upon dividing cells by their surrounding tissues, referred to as homeostatic pressure.Physicists from the Curie Institute, France, explored the relative impact of the mechanical pressure induced by dividing cells in biological tissues. This approach complements traditional studies on genetic and biochemical signalling mechanisms to explain experimental observations of how biological tissues evolve. This work, recently published inEuropean Physical Journal E, could have significant implications for the understanding of cancer growth.

It replaces a previous single-component model they developed last year. Its assumption: the homeostatic pressure is proportional to the fluid pressure within the tissue. If that were the case, very tall organisms such as giraffes could not exist, because the cells in their lower body would die under pressure.

Thanks to the two-component model, the authors found that it is the cells' pressure and not the interstitial fluid's pressure that influences the level of cell division. When there are as many new cells created from cell division as cells dying from programmed cell death, or apoptosis, the homeostatic pressure is balanced. This leads to a steady state of the biological tissue. Going one step further, the authors pinpointed the range of fluid pressure required to drive cell flow within the body.

Such models could help gain a greater understanding of the importance of the disruption of homeostatic pressure in biological tissues caused by cancer cells that are characterized by abnormal levels of cell proliferation."

Springer Science+Business Media (2012, July 3). Giraffes are living proof that cells' pressure
matters. ScienceDaily. Retrieved April 22, 2013, from http://www.sciencedaily.com/releases/2012/07/120703161526.htm

Half of Inhaled Soot Particles from Diesel Exhaust, Fires Gets Stuck in the Lungs

noreply@blogger.com (Anonymous) — Mon, 15 Apr 2013 16:15:00 +0000

The exhaust from diesel-fueled vehicles, wood fires and coal-driven power stations contains small particles of soot that flow out into the atmosphere. The soot is a scourge for the climate but also for human health. Now for the first time, researchers have studied in detail how diesel soot gets stuck in the lungs. The results show that more than half of all inhaled soot particles remain in the body. (Credit: © Imagenatural / Fotolia)

The figure is higher than for most other types of particles. For example "only" 20 per cent of another type of particle from wood smoke and other biomass combustion gets stuck in the lungs. One explanation is that diesel soot is made up of smaller particles and can therefore penetrate deeper into the lungs, where it is deposited. The study was made on diesel particles (which mainly consist of soot) and was recently published in the Journal of Aerosol Science. Ten healthy people volunteered for the the study.

"Findings of this kind can be extremely useful both for researchers to determine what doses of soot we get into our lungs out of the amount we are exposed to, and to enable public authorities to establish well-founded limits for soot particles in outdoor air," says Jenny Rissler, researcher in aerosol technology at Lund University's Faculty of Engineering and responsible for publishing the study.

In population studies, other researchers have been able to observe that people who live in areas with high concentrations of particulates are more affected by both respiratory and cardiovascular diseases. But since there is no conclusive evidence that it is precisely the soot that is to blame, the authorities have so far not taken any decisions on guidelines.

"Currently there is no specific limit for soot particles in the air, despite the fact that soot in the air is linked to both lung cancer and other diseases," says Jenny Rissler.

But Jenny Rissler thinks that in the future, limits on soot levels will also be set, with reference to the WHO's recent reclassification of diesel exhaust from "probably carcinogenic" to "carcinogenic."

Soot particles are not only connected to effects on health but may also contribute to a warmer climate. Paradoxically, other types of aerosol particles can partly be desirable, insofar as they have a cooling effect on the climate and thereby mitigate the warming effect of carbon dioxide.

"Soot particles are black and absorbs light, thus producing a warming effect. So it could be a double advantage to reduce it," she observes.

Jenny Rissler will next be studying individual variations in lung deposition and exposing cells to soot. She is also in the process of further developing methods to measure the surface area of the particles, as this has shown to be an important indicator of their harmfulness.

Background: Every time we breathe, we inhale tiny airborne particles, so-called aerosol particles. Some occur naturally, while others are the result of human activity. Soot mainly belongs in the latter category, as a by-product of combustion from power stations to small-scale wood fires and decorative candles. Another common source of soot is the exhaust from diesel engines, even though modern diesel cars have considerably reduced emissions thanks to efficient filters.

The EU will be tightening rules on emissions for heavy duty diesel vehicles in 2014.

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The above story is reprinted from materials provided byLund University.

Jenny Rissler, Erik Swietlicki, Agneta Bengtsson, Christoffer Boman, Joakim Pagels, Thomas Sandström, Anders Blomberg, Jakob Löndahl. Experimental determination of deposition of diesel exhaust particles in the human respiratory tract. Journal of Aerosol Science, 2012; 48: 18 DOI: 10.1016/j.jaerosci.2012.01.005

Lund University (2012, June 27). Half of inhaled soot particles from diesel exhaust, fires gets stuck in the lungs. ScienceDaily. Retrieved April 15, 2013, from http://www.sciencedaily.com/releases/2012/06/120627092016.htm

How stress can boost the immune system

noreply@blogger.com (Anonymous) — Mon, 15 Apr 2013 15:43:00 +0000

The study's findings provide a thorough overview of how a triad of stress hormones affects the main cell subpopulations of the immune system. They also offer the prospect of, someday, being able to manipulate stress-hormone levels to improve patients' recovery from surgery or wounds or their responses to vaccines.

You've heard it a thousand times: Stress is bad for you. And it's certainly true that chronic stress, lasting weeks and months, has deleterious effects including, notably, suppression of the immune response. But short-term stress -- the fight-or-flight response, a mobilization of bodily resources lasting minutes or hours in response to immediate threats -- stimulates immune activity, said lead author Firdaus Dhabhar, PhD, an associate professor of psychiatry and behavioral sciences and member of the Stanford Institute for Immunity, Transplantation and Infection.

And that's a good thing. The immune system is crucial for wound healing and preventing or fighting infection, and both wounds and infections are common risks during chases, escapes and combat.

Working with colleagues at Stanford and two other universities in a study published online June 22 inPsychoneuroendocrinology, Dhabhar showed that subjecting laboratory rats to mild stress caused a massive mobilization of several key types of immune cells into the bloodstream and then onto destinations including the skin and other tissues. This large-scale migration of immune cells, which took place over a time course of two hours, was comparable to the mustering of troops in a crisis, Dhabhar said. He and colleagues had previously shown that a similar immune-cell redistribution in patients experiencing the short-term stress of surgery predicts enhanced postoperative recovery.

In the new study, the investigators were able to show that the massive redistribution of immune cells throughout the body was orchestrated by three hormones released by the adrenal glands, in different amounts and at different times, in response to the stress-inducing event. These hormones are the brain's call-to-arms to the rest of the body, Dhabhar said.

"Mother Nature gave us the fight-or-flight stress response to help us, not to kill us," said Dhabhar, who has been conducting experiments for well over a decade on the effects of the major stress hormones on the immune system. Last summer, Dhabhar received the International Society for Psychoneuroendocrinology's Curt. P. Richter Award for his work in this area, culminating in the new study.

The findings paint a clearer picture of exactly how the mind influences immune activity. "An impala's immune system has no way of knowing that a lion is lurking in the grass and is about to pounce, but its brain does," Dhabhar said. In such situations, it benefits lion and impala alike when pathogen-fighting immune cells are in positions of readiness in such places as the skin and mucous membranes, which are at high risk for damage and consequent infection.

So it makes perfect evolutionary sense that predator/prey activity and other situations in nature, such as dominance challenges and sexual approaches, trigger stress hormones. "You don't want to keep your immune system on high alert at all times," Dhabhar said. "So nature uses the brain, the organ most capable of detecting an approaching challenge, to signal that detection to the rest of the body by directing the release of stress hormones. Without them, a lion couldn't kill, and an impala couldn't escape." The stress hormones not only energize the animals' bodies -- they can run faster, jump higher, bite harder -- but, it turns out, also mobilize the immune troops to prepare for looming trouble.

The response occurs across the animal kingdom, he added. You see pretty much the same pattern of hormone release in a fish that has been picked up out of the water.

The experiments in this study were performed on rats, which Dhabhar subjected to mild stress by confining them (gently, and with full ventilation) in transparent Plexiglas enclosures to induce stress. He drew blood several times over a two-hour period and, for each time point, measured levels of three major hormones -- norepinephrine, epinephrine and corticosterone (the rat analog of cortisol in humans) -- as well as of several distinct immune-cell types in the blood.

What he saw was a pattern of carefully choreographed changes in blood levels of the three hormones along with the movement of many different subsets of immune cells from reservoirs such as the spleen and bone marrow into the blood and, finally, to various "front line" organs.

To show that specific hormones were responsible for movements of specific cell types, Dhabhar administered the three hormones, separately or in various combinations, to rats whose adrenal glands had been removed so they couldn't generate their own stress hormones. When the researchers mimicked the pattern of stress-hormone release previously observed in the confined rats, the same immune-cell migration patterns emerged in the rats without adrenal glands. Placebo treatment produced no such effect.

The general pattern, Dhabhar said, was that norepinephrine is released early and is primarily involved in mobilizing all major immune-cell types -- monocytes, neutrophils and lymphocytes -- into the blood. Epinephrine, also released early, mobilized monocytes and neutrophils into the blood, while nudging lymphocytes out into "battlefield" destinations such as skin. And corticosterone, released somewhat later, caused virtually all immune cell types to head out of circulation to the "battlefields."

The overall effect of these movements is to bolster immune readiness. A study published by Dhabhar and his colleagues in 2009 in the Journal of Bone and Joint Surgery assessed patients' recovery from surgery as a function of their immune-cell redistribution patterns during the stress of the operation. Those patients in whom the stress of surgery mobilized immune-cell redistributions similar to those seen in the confined rats in the new study did significantly better afterward than patients whose stress hormones less adequately guided immune cells to appropriate destinations.

The mechanisms Dhabhar has delineated could lead to medical applications, such as administering low doses of stress hormones or drugs that mimic or antagonize them in order to optimize patients' immune readiness for procedures such as surgery or vaccination. "More study will be required including in human subjects, which we hope to conduct, before these applications can be attempted," Dhabhar said. Closer at hand is the monitoring of patients' stress-hormone levels and immune-cell distribution patterns during surgery to assess their surgical prognosis, or during immunization to predict vaccine effectiveness.

The study was funded by the John D. & Catherine T. MacArthur Foundation, the Dana Foundation, the DeWitt Wallace Foundation, the Carl & Elizabeth Naumann Fund and the National Institutes of Health. The medical school's Department of Psychiatry and Behavioral Sciences also supported this work. Dhabhar's co-authors were statistician Eric Neri at Stanford, and neuroendocrinologists at Ohio State University and Rockefeller University.

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The above story is reprinted from materials provided byStanford University Medical Center. The original article was written by Bruce Goldman.

Stanford University Medical Center (2012, June 21). How stress can boost immune system.ScienceDaily. Retrieved April 15, 2013, from http://www.sciencedaily.com/releases/2012/06/120621223525.htm

Daily Stress Takes a Toll on Long-Term Mental Health

noreply@blogger.com (Anonymous) — Sat, 13 Apr 2013 15:26:00 +0000

"Our emotional responses to the stresses of daily life may predict our long-term mental health, according to a new study published inPsychological Science, a journal of the Association for Psychological Science.

Psychological scientist Susan Charles of the University of California, Irvine and colleagues conducted the study in order to answer a long-standing question: Do daily emotional experiences add up to make the straw that breaks the camel’s back, or do these experiences make us stronger and provide an inoculation against later distress?

Using data from two national surveys, the researchers examined the relationship between daily negative emotions and mental health outcomes ten years later.

Participants’ overall levels of negative emotions predicted psychological distress (e.g., feeling worthless, hopeless, nervous, and/or restless) and diagnosis of an emotional disorder like anxiety or depression a full decade after the emotions were initially measured.

Participants’ negative emotional responses to daily stressors — such as argument or a problem at work or home — predicted psychological distress and self-reported emotional disorder ten years later.

The researchers argue that a key strength of the study was their ability to tap a large, national community sample of participants who spanned a wide age range. The results were based on data from 711 participants, both men and women, who ranged in age from 25 to 74. They were all participants in two national, longitudinal survey studies: Midlife Development in the United States (MIDUS) and National Study of Daily Experiences (NSDE).

According to Charles and her colleagues, these findings show that mental health outcomes aren’t only affected by major life events — they also bear the impact of seemingly minor emotional experiences. The study suggests that chronic nature of these negative emotions in response to daily stressors can take a toll on long-term mental health.

In addition to Charles, co-authors on the study include Jennifer Piazza of California State University, Fullerton; and Jacqueline Mogle, Martin Sliwinski, and David Almeida of Pennsylvania State University."

###

For more information about this study, please contact: Susan T. Charles at scharles@uci.edu.

The APS journal Psychological Science is the highest ranked empirical journal in psychology. For a copy of the article "The Wear and Tear of Daily Stressors on Mental Health" and access to other Psychological Science research findings, please contact Anna Mikulak at 202-293-9300 oramikulak@psychologicalscience.org.

Source: Association for Psychological Science

New research suggests animal-to-human transmission of MRSA

noreply@blogger.com (Anonymous) — Thu, 11 Apr 2013 14:17:00 +0000

"Using whole genome sequencing, scientists have found two independent human cases of infection have been linked to livestock.

Having found this new MRSA in both people and animals on the same farm it was likely that it is being transmitted between animals and people.
Mark Holmes

Cambridge scientists have linked two human cases of infection with the antibiotic- resistant superbug MRSA to farms in Denmark. The results of the study, published today in the journal EMBO Molecular Medicine, suggest the methicillin-resistantStaphylococcus aureus (MRSA) bacteria was transmitted from the livestock to the farmers.

The type of MRSA which was found in both of the human cases was only discovered two years ago by Dr Mark Holmes and his colleagues from the University of Cambridge. The new strain’s genetic makeup differs greatly from previous strains, which means that the ‘gold standard’ molecular tests currently used to identify MRSA - a polymerase chain reaction technique (PCR) and slide agglutination testing - do not detect it.

For this study, the scientists used whole genome sequencing to investigate two cases of the new MRSA where the patients lived on farms to see if the same strain could be found in the animals on the farm.

Dr Holmes, from Cambridge’s Department of Veterinary Medicine and the senior author on the paper, said: “Having found this new MRSA in both people and animals on the same farm it was likely that it is being transmitted between animals and people.

“By looking at the single differences in nucleotides, or SNPs, in the DNA sequences of each isolate, it became obvious that in both farms we looked at the human and animal MRSA were almost identical. In one case, the results also clearly showed that the most likely direction of transmission was from animal to human.”

The study raises questions about whether cows could be a reservoir for new strains of MRSA. It was previously not clear whether MRSA was transmitted to cows from humans or to humans from cows, but the new research indicates that the livestock is the likely source of these new strains.

“Our findings demonstrate that the MRSA strains we studied are capable of transmission between animals and humans, which highlights the role of livestock as a potential reservoir of antibiotic resistant bacteria,” remarked Dr Ewan Harrison, a post-doctoral research associate at the University of Cambridge’s Department of Veterinary Medicine and co-author of the paper.

For more information about this story, please contact: Genevieve Maul, Office of Communications, University of Cambridge. Email: Genevieve.Maul@admin.cam.ac.uk; Tel: 01223 765542."

Source: University of Cambridge

Avian Flu Viruses Which Are Transmissible Between Humans Could Evolve in Nature

noreply@blogger.com (Unknown) — Thu, 21 Jun 2012 08:00:00 +0000

It might be possible for human-to-human airborne transmissible avian H5N1 influenza viruses to evolve in nature, new research has found.

Colorized transmission electron micrograph of Avian influenza A H5N1 viruses (seen in gold) grown in MDCK cells (seen in green) [Credit: CDC/Courtesy of Cynthia Goldsmith; Jacqueline Katz; Sherif R. Zaki]

The findings, from research led by Professor Derek Smith and Dr Colin Russell at the University of Cambridge, were published June 22 in the journal Science.

Currently, avian H5N1 influenza, also known as bird flu, can be transmitted from birds to humans, but not (or only very rarely) from human to human. However, two recent papers by Herfst, Fouchier and colleagues in Science and Imai, Kawaoka and colleagues in Nature reveal that potentially with as few as five mutations (amino acid substitutions), or four mutations plus reassortment, avian H5N1 can become airborne transmissible between mammals, and thus potentially among humans. However, until now, it was not known whether these mutations might evolve in nature.

The Cambridge researchers first analysed all of the surveillance data available on avian H5N1 influenza viruses from the last 15 years, focusing on birds and humans. They discovered that two of the five mutations seen in the experimental viruses (from the Fouchier and Kawaoka labs) had occurred in numerous existing avian flu strains. Additionally, they found that a number of the viruses had both of the mutations.

Colin Russell, Royal Society University Research Fellow at the University of Cambridge, said: "Viruses that have two of these mutations are already common in birds, meaning that there are viruses that might have to acquire only three additional mutations in a human to become airborne transmissible. The next key question is 'is three a lot, or a little?' "

The scientists explored this key question using a mathematical model of how viruses replicate and evolve within a mammalian host and assessed the influence of various factors on whether the remaining three mutations could evolve in a single host or in a short chain of transmission between hosts

The factors that increased the likelihood of mutations evolving are:

1. Random mutation. The replication mechanisms of influenza viruses don't make perfect copies. On average, every time an influenza virus replicates itself it makes approximately one mutation somewhere in the genome of each new virus. In each infected human there will be billions of viruses, and thus with many viruses replicating, multiple mutations can accumulate within a single host.

2. Positive selection. If some of the remaining mutations help the avian virus to adapt to mammals, then those mutations will make the viruses more fit and thus will be positively selected and preferentially accumulate.

3. Long infection. The longer someone is infected and producing new viruses, the more time there is for mutations to accumulate.

4. Functionally equivalent substitutions. The sets of substitutions identified by Fouchier and Kawaoka are unlikely to be the only combinations of substitutions capable of producing an aerosol transmissible virus. The probability of emergence increases with the number of combinations.

5. Diversity in the within-bird virus population. Given all of the mutations there are likely to be within a host due to random mutation, it is possible that the viruses from a bird that infect a human might have a mutation that would not be detected by routine surveillance. For example, if 100 virus particles from a bird infect a human and one of those particles had a key mutation, it would increase the probability of the mutation reaching high levels within a host even though routine sequencing would not detect it.

6. Transmission between mammals. If mammals are capable of transmitting viruses that have some but not all of the necessary substitutions it could increase the probability of an airborne transmissible virus evolving.

The factors that decreased the likelihood of mutations evolving are:

1. An effective immune response. An effective immune response would shorten the length of an infection and thus decrease the time available to accumulate mutations.

2. Deleterious substitutions. If any of the substitutions necessary for airborne transmission were harmful to the virus it would, on average, slow the accumulation of mutations.

3. Order of acquiring mutations. It is not currently known if the mutations for airborne transmissibility need to be acquired in a specific order. If they do, it would, on average, slow the accumulation of mutations.

"With the information we have, it is impossible to say what the exact risk is of the virus becoming airborne transmissible among humans. However, the results suggest that the remaining three mutations could evolve in a single human host, making a virus evolving in nature a potentially serious threat," said Derek Smith, Professor of Infectious Disease Informatics at the University of Cambridge. "We now know that it is in the realm of possibility that these viruses can evolve in nature, and what needs to be done to assess the risk more accurately of these mutations evolving in nature."

The scientists recommend the following activities be considered high priority for estimating and ameliorating the risk of emergence of aerosol transmissible H5N1 viruses.

First, additional surveillance in regions where viruses with airborne transmission enabling substitutions have been observed and in regions connected to those regions by bird migration and trade. Also, increased surveillance for mutations that might have the same function as those found by the Fouchier and Kawaoka labs.

Second, related to surveillance, some targeted sequencing of H5N1 viruses should be done by "deep sequencing" where the lab sequences many viruses from an individual host to look for viruses that might have accumulated the critical mutations, even if those viruses are just a small proportion of the viruses within an animal.

Third, further investigations are needed to determine which substitutions and combinations of substitutions that are not the same as, but have the same function as, the substitutions identified by the Fouchier and Kawaoka labs are capable of making viruses airborne transmissible between mammals.

Fourth, further studies are needed to elucidate the changes in within-host fitness and between-host transmissibility associated with each airborne transmission enabling substitution and combination of substitutions.

Professor Smith added: "The situation is similar to assessing the risk of an earthquake or tsunami. We don't know exactly when and where, but by increasing monitoring and research -- some of which is already underway -- scientists and public health officials will be able to increase the accuracy with which the risk can be assessed and to minimise those risks."

The research was funded by multiple sources including the European Commission through framework 7 grants EMPERIE and ANTIGONE, the Royal Society, the Human Frontiers Science Program, the Wellcome Trust, and the National Institutes of Health.

Source: University of Cambridge [June 21, 2012]

The Power of Suggestion: What We Expect Influences Our Behavior, for Better or Worse

noreply@blogger.com (Unknown) — Thu, 07 Jun 2012 09:00:00 +0000

A lucky rabbit foot. A glass of wine. A pill. What do these things all have in common? Their effects -- whether we do well on a test, whether we mingle at the cocktail party, whether we feel better -- all depend on the power of suggestion.

In a new article, psychological scientists Maryanne Garry and Robert Michael of Victoria University of Wellington, along with Irving Kirsch of Harvard Medical School and Plymouth University, delve into the phenomenon of suggestion, exploring the intriguing relationship between suggestion, cognition, and behavior. The article is published in the June issue of Current Directions in Psychological Science, a journal of the Association for Psychological Science.

Over their research careers, Garry and Kirsch have both studied the effects of suggestion on cognition and behavior. Kirsch focused mostly on suggestion in clinical psychology, while Garry, whose work is supported by the Marsden Fund of New Zealand, was interested in the effects of suggestion on human memory. When the two got to talking, "we realized that the effects of suggestion are wider and often more surprising than many people might otherwise think," says Garry.

Across many studies, research has shown that deliberate suggestion can influence how people perform on learning and memory tasks, which products they prefer, and how they respond to supplements and medicines, which accounts for the well-known placebo effect.

But what can explain the powerful and pervasive effect that suggestion has in our lives? The answer lies in our 'response expectancies,' or the ways in which we anticipate our responses in various situations. These expectancies set us up for automatic responses that actively influence how we get to the outcome we expect. Once we anticipate a specific outcome will occur, our subsequent thoughts and behaviors will actually help to bring that outcome to fruition.

So, if a normally shy person expects that a glass of wine or two will help him loosen up at a cocktail party, he will probably feel less inhibited, approach more people, and get involved in more conversations over the course of the party. Even though he may give credit to the wine, it is clear that his expectations of how the wine would make him feel played a major role.

But it's not just deliberate suggestion that influences our thoughts and behaviors -- suggestions that are not deliberate can have the very same effects. As the authors point out, "simply observing people or otherwise making them feel special can be suggestive," a phenomenon termed the Hawthorne effect. As a result, people might work harder, or stick to a task for longer. And this case is more worrying, says Garry, "because although we might then give credit to some new drug or treatment, we don't realize that we are the ones who are actually wielding the influence."

It is for precisely this reason that the issue of unintentional suggestion has important implications for academic researchers. "In the scientific community, we need to be aware of -- and control for -- the suggestions we communicate to subjects," says Garry. The authors note that some recent failures to replicate previous research findings may ultimately be explained by such unintentional suggestion. "Recent research suggests that some of psychological science's most intriguing findings may be driven, at least in part, by suggestion and expectancies," Garry observes. "For example, a scientist who knows what the hypothesis of an experiment is might unwittingly lead subjects to produce the hypothesized effect -- for reasons that have nothing to do with the experiment itself."

And the unintended effects of suggestion aren't just restricted to the laboratory -- they cut across many real world domains, including the fields of medicine, education, and criminal justice. For example, converging evidence on eyewitness identification procedures demonstrates that the rate of false identifications is significantly higher when lineups are conducted by people who know who the suspect is than when the lineups are conducted by people who don't.

While research has provided clear evidence for the phenomenon of suggestion, there is still much more to learn about the underlying relationship between suggestion, cognition, and behavior. As the authors point out, researchers still don't know where the boundaries and limitations of these effects lie. "And, if a 'real' treatment and a 'suggestion' lead to a similar outcome, what differentiates between the two?" says Garry. Understanding these issues has important real world implications. "If we can harness the power of suggestion, we can improve people's lives."

Source: Association for Psychological Science [June 06, 2012]

Statistical Model Attempting to Estimate Level of Alcohol Consumption That Is 'Optimal' for Health

noreply@blogger.com (Unknown) — Thu, 07 Jun 2012 08:00:00 +0000

Cutting the amount we drink to just over half a unit a day could save 4,600 lives a year in England, according to a modelling study by Oxford University researchers published in the journal BMJ Open.

Half a unit of alcohol is as little as a quarter of a glass of wine, or a quarter of a pint [Credit: © G.G. Lattek / Fotolia]

Scientists have carried out a complex analysis in an attempt to determine the "optimal" level of alcohol consumption that is associated with the lowest rates of chronic disease in the UK. They conclude that the intake of about one-half of a typical drink per day would result in the healthiest outcomes, and the authors conclude that the recommended alcohol intake for the UK should be reduced from the current advised level of drinking.

Half a unit of alcohol is as little as a quarter of a glass of wine, or a quarter of a pint. That's much lower than current government recommendations of between 3 to 4 units a day for men and 2-3 units for women.

The researchers set out to find the optimum daily amount of alcohol that would see fewest deaths across England from a whole range of diseases connected to drink. Previous studies have often looked at the separate effects of alcohol on heart disease, liver disease or cancers in isolation.

'Although there is good evidence that moderate alcohol consumption protects against heart disease, when all of the chronic disease risks are balanced against each other, the optimal consumption level is much lower than many people believe,' says lead author Dr Melanie Nichols of the BHF Health Promotion Research Group in the Department of Public Health at Oxford University.

The team used a mathematical model to assess what impact changing average alcohol consumption would have on deaths from 11 conditions known to be at least partially linked to drink.

These included coronary heart disease, stroke, high blood pressure, diabetes, cirrhosis of the liver, epilepsy, and five cancers. Over 170,000 people in England died from these 11 conditions in 2006, and ill health linked to alcohol is estimated to cost the NHS in England £3.3 billion every year.

The researchers used information from the 2006 General Household Survey on levels of alcohol consumption among adults in England. They combined this with the disease risks for differing levels of alcohol consumption as established in large analyses of published research.

They found that just over half a unit of alcohol a day was the optimal level of consumption among current drinkers.

They calculate this level of drinking would prevent around 4,579 premature deaths, or around 3% of all deaths from the 11 conditions.

The number of deaths from heart disease would increase by 843, but this would be more than offset by around 2,600 fewer cancer deaths and almost 3,000 fewer liver cirrhosis deaths.

'Moderating your alcohol consumption overall, and avoiding heavy-drinking episodes, is one of several things, alongside a healthy diet and regular physical activity, that you can do to reduce your risk of dying early of chronic diseases,' says Dr Nichols.

She adds: 'We are not telling people what to do, we are just giving them the best balanced information about the different health effects of alcohol consumption, so that they can make an informed decision about how much to drink.

'People who justify their drinking with the idea that it is good for heart disease should also consider how alcohol is increasing their risk of other chronic diseases. A couple of pints or a couple of glasses of wine per day is not a healthy option.'

Although this study in BMJ Open did not look at patterns of drinking, Dr Nichols says: 'Regardless of your average intake, if you want to have the best possible health, it is also very important to avoid episodes of heavy drinking ("binge drinking") as there is very clear evidence that this will increase your risks of many diseases, as well as your risk of injuries.'

Source: University of Oxford [June 06, 2012]

To Quit Smoking, Try Eating More Veggies and Fruits

noreply@blogger.com (Unknown) — Wed, 06 Jun 2012 12:00:00 +0000

If you're trying to quit smoking, eating more fruits and vegetables may help you quit and stay tobacco-free for longer, according to a new study published online by University at Buffalo public health researchers.

If you're trying to quit smoking, eating more fruits and vegetables may help you quit and stay tobacco-free for longer [Credit: © taviphoto / Fotolia]

The paper, in the journal Nicotine and Tobacco Research, is the first longitudinal study on the relationship between fruit and vegetable consumption and smoking cessation.

The authors, from UB's School of Public Health and Health Professions, surveyed 1,000 smokers aged 25 and older from around the country, using random-digit dialing telephone interviews. They followed up with the respondents fourteen months later, asking them if they had abstained from tobacco use during the previous month.

"Other studies have taken a snapshot approach, asking smokers and nonsmokers about their diets," says Gary A. Giovino, PhD, chair of the Department of Community Health and Health Behavior at UB. "We knew from our previous work that people who were abstinent from cigarettes for less than six months consumed more fruits and vegetables than those who still smoked. What we didn't know was whether recent quitters increased their fruit and vegetable consumption or if smokers who ate more fruits and vegetables were more likely to quit."

The UB study found that smokers who consumed the most fruit and vegetables were three times more likely to be tobacco-free for at least 30 days at follow-up 14 months later than those consuming the lowest amount of fruits and vegetables. These findings persisted even when adjustments were made to take into account age, gender, race/ethnicity, education, household income and health orientation.

They also found that smokers with higher fruit and vegetable consumption smoked fewer cigarettes per day, waited longer to smoke their first cigarette of the day and scored lower on a common test of nicotine dependence.

"We may have identified a new tool that can help people quit smoking," says Jeffrey P. Haibach, MPH, first author on the paper and graduate research assistant in the UB Department of Community Health and Health Behavior. "Granted, this is just an observational study, but improving one's diet may facilitate quitting."

Several explanations are possible, such as less nicotine dependence for people who consume a lot of fruits and vegetables or the fact that higher fiber consumption from fruits and vegetables make people feel fuller.

"It is also possible that fruits and vegetables give people more of a feeling of satiety or fullness so that they feel less of a need to smoke, since smokers sometimes confuse hunger with an urge to smoke," explains Haibach.

And unlike some foods which are known to enhance the taste of tobacco, such as meats, caffeinated beverages and alcohol, fruits and vegetables do not enhance the taste of tobacco.

"Foods like fruit and vegetables may actually worsen the taste of cigarettes," says Haibach.

While smoking rates in the U.S. continue to decline, Giovino notes, the rate of that decline has slowed during the past decade or so. "Nineteen percent of Americans still smoke cigarettes, but most of them want to quit," he says.

Haibach adds: "It's possible that an improved diet could be an important item to add to the list of measures to help smokers quit. We certainly need to continue efforts to encourage people to quit and help them succeed, including proven approaches like quitlines, policies such as tobacco tax increases and smoke-free laws, and effective media campaigns."

The UB researchers caution that more research is needed to determine if these findings replicate and if they do, to identify the mechanisms that explain how fruit and vegetable consumption may help smokers quit. They also see a need for research on other dietary components and smoking cessation.

Gregory G. Homish, PhD, assistant professor in the UB Department of Community Health and Health Behavior, also is a co-author.

Funding was provided by the Robert Wood Johnson Foundation and LegacyA®.

Source: University at Buffalo [June 06, 2012]

1 Million Billion Billion Billion Billion Billion Billion: Number of Undiscovered Drugs

noreply@blogger.com (Unknown) — Wed, 06 Jun 2012 10:00:00 +0000

A new voyage into "chemical space" -- occupied not by stars and planets but substances that could become useful in everyday life -- has concluded that scientists have synthesized barely one tenth of 1 percent of the potential medicines that could be made. The report, in the journal ACS Chemical Neuroscience, estimates that the actual number of these so-called "small molecules" could be 1 novemdecillion (that's 1 with 60 zeroes), 1 million billion billion billion billion billion billion, which is more than some estimates of the number of stars in the universe.

Jean-Louis Reymond and Mahendra Awale explain that small molecules, which are able to cross cell walls and interact with biological molecules in the body, are prime targets for scientists who develop new medicines. Most existing medications are small molecules. The authors focused on the "chemical space" inhabited by all of the small molecules that could possibly exist according to the laws of physics and chemistry.

Researchers have identified millions of these compounds -- the ACS' Chemical Abstracts Service database contains almost 67 million substances. Reymond and Awale estimate that the molecules synthesized and tested as potential drugs so far represent less than 0.1 percent of chemical space. To aid researchers looking for new ways to prevent and treat disease, they set out to find the best ways to search for new small molecules.

The authors discuss several ways of getting a handle on chemical space, including by the size, shape and makeup of molecules. They show how computers can help researchers efficiently narrow a search for a new drug candidate. Computer modeling of chemical interactions can help researchers find a handful of promising molecules to synthesize and test in the lab. "Small molecule drugs are essential to the success of modern medicine," the authors note, and suggest that their methods may be particularly useful for finding new pharmaceuticals that target the central nervous system.

Source: American Chemical Society [June 06, 2012]

Air Pollution Linked to Chronic Heart Disease

noreply@blogger.com (Unknown) — Tue, 05 Jun 2012 10:00:00 +0000

Air pollution, a serious danger to the environment, is also a major health risk, associated with respiratory infections, lung cancer and heart disease. Now a Tel Aviv University researcher has concluded that not only does air pollution impact cardiac events such as heart attack and stroke, but it also causes repeated episodes over the long term.

Cardiac patients living in high pollution areas were found to be over 40 percent more likely to have a second heart attack when compared to patients living in low pollution areas, according to Dr. Yariv Gerber of TAU's School of Public Health at the Sackler Faculty of Medicine. "We know that like smoking cigarettes, pollution itself provokes the inflammatory system. If you are talking about long-term exposure and an inflammatory system that is irritated chronically, pollution may well be involved in the progression of atrial sclerosis that manifests in cardiac events," explains Dr. Gerber.

Done in collaboration with Prof. Yaacov Drory and funded by the Environmental and Health Fund in Jerusalem, the research was presented at the San Diego Epidemiological Meeting of the American Heart Association in March and the Annual Meeting of the Israeli Heart Society in April.

Risking recurrence

Air pollution has previously been acknowledged as a factor in heart attack risk, as well as other health risks. The goal of this study, says Dr. Gerber, was to quantify that association and determine the long-term effects of air pollution on myocardial infarction (MI) patients. Their study followed 1,120 first-time MI patients who had been admitted to one of eight hospitals in central Israel between 1992 and 1993, all of whom were under the age of 65 at the time of admittance. The patients were followed up until 2011, a period of 19 years.

Air quality was measured at 21 monitoring stations inareas where the patients lived, and analyzed by a group of researchers at the Technion in Haifa. After adjusting for other factors such as socio-economic status and disease severity, the researchers identified an association between pollution and negative clinical outcomes, including mortality and recurrent vascular events such as heart attack, stroke and heart failure.

Compared to patients who lived in areas with the lowest recorded levels of pollution, those in the most polluted environment were 43 percent more likely to have a second heart attack or suffer congestive heart failure and 46 percent more likely to suffer a stroke. The study also found that patients exposed to air pollution were 35 percent more likely to die in the almost 20 year period following their first heart attack than those who were exposed to lower levels of pollution.

According to Dr. Gerber, the true impact of air pollution might be even stronger than this study shows. "Our method of assessing exposure does have limitations. Because we are using data from monitoring stations, it's a crude estimate of exposure, which most likely leads to an underestimation of the association," he warns. He estimates that air pollution could have double the negative impact with more precise measurement.

Identifying vulnerable groups

The results of the study not only indicate a health benefit for a public policy that curtails air pollution caused by industrial emissions and second hand smoke, but also call for heightened awareness by clinicians. Doctors should be making their patients aware of the risks of remaining in high pollution areas, suggesting that they work to limit their exposure, Dr. Gerber suggests.

Another purpose of this study was to begin identifying populations that are vulnerable to MI and re-occurring MI. Establishing the connection between air pollution and long-term risk for patients with cardiovascular diseases was an important step towards that goal.

Source: American Friends of Tel Aviv University [June 05, 2012]

Female Choice Key to Evolutionary Shift to Modern Family

noreply@blogger.com (Unknown) — Wed, 30 May 2012 10:00:00 +0000

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]

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

noreply@blogger.com (Unknown) — Tue, 29 May 2012 10:00:00 +0000

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]

Nanoparticles Seen as Artificial Atoms

noreply@blogger.com (Unknown) — Thu, 24 May 2012 10:00:00 +0000

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]

Drug Destroys Human Cancer Stem Cells but Not Healthy Ones

noreply@blogger.com (Unknown) — Thu, 24 May 2012 09:00:00 +0000

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]

Stressed Men Are More Social

noreply@blogger.com (Unknown) — Mon, 21 May 2012 09:00:00 +0000

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]

Genetic Discovery Will Revolutionize Understanding Of Gene Expression

noreply@blogger.com (Unknown) — Sat, 19 May 2012 08:00:00 +0000

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]

Emotionally Intelligent People Are Less Good at Spotting Liars

noreply@blogger.com (Unknown) — Fri, 18 May 2012 09:00:00 +0000

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]

How Exercise Affects the Brain

noreply@blogger.com (Unknown) — Fri, 18 May 2012 08:00:00 +0000

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]

Are character traits determined genetically?

noreply@blogger.com (Unknown) — Wed, 16 May 2012 09:00:00 +0000

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]