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Tests on Hereditary Diseases

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


Gut bacteria linked to obesity

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/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

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.

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/releases/2012/08/120814213246.htm


An Artificial Retina With the Capacity to Restore Normal Vision

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.

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/releases/2012/08/120814213326.htm


Why are some people smarter than others?

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

Photp: Jens Langner at

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

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

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/releases/2012/07/120703161526.htm


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

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.
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 tractJournal 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/releases/2012/06/120627092016.htm

How stress can boost the immune system

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.
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/releases/2012/06/120621223525.htm


Daily Stress Takes a Toll on Long-Term Mental Health

"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
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


New research suggests animal-to-human transmission of MRSA

"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:; Tel: 01223 765542."

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