Newswise — What if a map of the brain could help us decode people's inner thoughts? Scientists at the University of California, Berkeley, have taken a step in that direction by building a "semantic atlas" that shows in vivid colors and multiple dimensions how the human brain organizes language. The atlas identifies brain areas that respond to words that have similar meanings. The findings, to be published April 28, 2016 in the journalNature, are based on a brain imaging study that recorded neural activity while study volunteers listened to stories from the "Moth Radio Hour." They show that at least one-third of the brain's cerebral cortex, including areas dedicated to high-level cognition, is involved in language processing. Notably, the study found that different people share similar language maps: "The similarity in semantic topography across different subjects is really surprising," said study lead author Alex Huth, a postdoctoral researcher in neuroscience at UC Berkeley. Detailed maps showing how the brain organizes different words by their meanings could eventually help give voice to those who cannot speak, such as victims of stroke or brain damage, or motor neuron diseases such as ALS. While mind-reading technology remains far off on the horizon, charting how language is organized in the brain brings the decoding of inner dialogue a step closer to reality, the researchers said. For example, clinicians could track the brain activity of patients who have difficulty communicating and then match that data to semantic language maps to determine what their patients are trying to express. Another potential application is a decoder that translates what you say into another language as you speak. "To be able to map out semantic representations at this level of detail is a stunning accomplishment," said Kenneth Whang, a program director in the National Science Foundation's Information and Intelligent Systems division. "In addition, they are showing how data-driven computational methods can help us understand the brain at the level of richness and complexity that we associate with human cognitive processes." Huth and six other native English-speakers served as subjects for the experiment, which required volunteers to remain still inside the functional Magnetic Resonance Imaging scanner for hours at a time. Each study participant's brain blood flow was measured as they listened, with eyes closed and headphones on, to more than two hours of stories from the "Moth Radio Hour," a public radio show in which people recount humorous and/or poignant autobiographical experiences. Their brain imaging data were then matched against time-coded, phonemic transcriptions of the stories. Phonemes are units of sound that distinguish one word from another. That information was then fed into a word-embedding algorithm that scored words according to how closely they are related semantically. The results were converted into a thesaurus-like map where the words are arranged on the flattened cortices of the left and right hemispheres of the brain rather than on the pages of a book. Words were grouped under various headings: visual, tactile, numeric, locational, abstract, temporal, professional, violent, communal, mental, emotional and social. Not surprisingly, the maps show that many areas of the human brain represent language that describes people and social relations rather than abstract concepts. "Our semantic models are good at predicting responses to language in several big swaths of cortex," Huth said. "But we also get the fine-grained information that tells us what kind of information is represented in each brain area. That's why these maps are so exciting and hold so much potential." "Although the maps are broadly consistent across individuals, there are also substantial individual differences," said study senior author Jack Gallant, a UC Berkeley neuroscientist. "We will need to conduct further studies across a larger, more diverse sample of people before we will be able to map these individual differences in detail." ###
Newswise — An international team of including the Lomonosov Moscow State University researchers discovered which enzyme enables Escherichia colibacterium (E. coli) to breathe. The study is published in theScientific Reports. Scientists discovered how the E. coli bacterium can survive in the human gut - earlier the question how they breathe was a mystery to experts. Vitaliy Borisov, Senior Researcher, Doctor of Biological Sciences, Professor of the Russian Academy of Sciences, A.N. Belozersky Research Institute physical and chemical biology employee, the Lomonosov Moscow State University and one of the authors, explains that breathing E. coli uses special enzymes, which are absent in the human body. This means that the discovery of the scientists can contribute to the creation of new drugs, which will be detrimental to the bacteria without harming a human. The energy for the vital activity of any organism comes from food, and is generated by the means of redox processes in the body. The food is converted into energy not directly but through intermediaries. First, the complex molecules are decomposed into simpler: proteins are decomposed into amino acids, fats - to fatty acids, carbohydrates - to monosaccharides. Oxidation of simpler molecules releases energy, which all is contained in the electrons. The electrons passes to the respiratory chain with the so-called reducing equivalents (electron-carrying compound). They are NADH (nicotinamide adenine dinucleotide) and ubiquinol, also known as coenzyme Q. These two basic reducing equivalents fully cope with the processing of food: NADH is a water-soluble compound and ubiquinol is fat-soluble. Membranous enzymes accept electrons from reducing equivalents and transfer them to molecular oxygen. The terminal cytochrome oxidase is the main membrane enzyme responsible for the human mitochondrial respiration and was thought to be used for the breath of E. coli as well. The scheme of oxidases action is simple: transferring electrons to molecular oxygen, reducing equivalents are oxidized again, and as a result "the energy currency" of the cell - the proton-moving force is generated. 'If you stop breathing, you die just because oxygen does not flow to the oxidase, and it does not produce energy,' says Vitaly Borisov. The Escherichia coli bacterium lives in the gastrointestinal tract, where a lot of hydrogen sulfide is produced, which attenuates mitochondrial respiration. Free hydrogen sulfide inhibits cytochrome oxidase work. Its concentration exceeds several hundred times the minimum concentration required for substantial blocking of this enzyme. Hence, it seems that the E. coli bacterium cannot "breathe", but despite that the bacteria somehow survive in the intestine. The researchers assumed that the breath in the presence of hydrogen sulfide is still possible, but due to other oxidase. The fact is that the breath in people and bacteria occur in different ways. Each cell in our body "breathes" due to the work of only the cytochrome-c oxidase, others we have not. However, the E. coli bacteria has two types of oxidase: bo-type cytochrome oxidase (analogue of "human" cytochrome-c oxidase) and completely different bd-type cytochromes. 'Our hypothesis was that the bd-type oxidase (bd-I and bd-II) are more resistant to the hydrogen sulfide inhibition than the bo-type cytochrome oxidase,' commented Vitaly Borisov. To test this hypothesis scientists needed to learn how the sulfide presence in the environment affects the growth of the E. coli bacteria cells, which have only one terminal oxidase (bd-I, bd-II or bo) in the respiratory chain. a variety of biochemical, biophysical and microbiological methods and approaches were applied, as well as the method of the intended mutagenesis. The hypothesis was fully confirmed. 'Bo-oxidase's activity is completely inhibited by the hydrogen sulfide, while the work of the bd-oxidases remains untouched by the H2S. Thus, in order to successfully produce the main types of "the energy currency" under a high concentration of hydrogen sulfide, the intestinal microflora inhabitants should use a unique type of terminal oxidases, which is missing in the cells of humans and animals,' says Vitaly Borisov. The discovery could be used in the future to develop medicines that regulate the intestinal microflora and relieving it from harmful bacteria. As human cells do not contain the bd-type oxidase, the question of the ability to combat disease-causing bacteria without causing harm to the human body becomes relevant. For example, the bacterium causing tuberculosis, which's primarily membrane enzyme is also a bd-type oxidase, quickly gaining resistance to classical antibiotics. Through this study there is a prospect of a new type of antibiotics "turning off" the oxygen only to the harmful bacteria cells, not to human cells.
Newswise — Research from Ann & Robert H. Lurie Children’s Hospital of Chicago conducted in mice shows the drug hydrocortisone — a steroid commonly used to treat a variety of inflammatory and allergic conditions — can also prevent lung damage that often develops in premature babies treated with oxygen. If affirmed in human studies, the results could help pave the way to a much-needed therapy for a bronchopulmonary dysplasia (BPD), a condition that affects 10,000 newborns in the United States each year and can lead to chronic lung disease and, ultimately, heart failure. In a set of experiments, to be published in the May print issue of the journal Pediatric Research, a team of Lurie Children’s scientists showed the drug reduced damage to the delicate blood vessels inside the lungs of newborn mice and reversed some of BPD’s harmful downstream effects on the heart. “Bronchopulmonary dysplasia is a devastating, often unavoidable side effect of a standard lifesaving therapy with oxygen used to treat newborn babies, so our findings are a promising indicator that a well-known drug that’s been around for a long time may help stave off some of this condition’s worst after-effects,” says study lead investigator and Lurie Children’s neonatologist Marta Perez, M.D., who is also assistant professor of Pediatrics at Northwestern University Feinberg School of Medicine. BPD often develops in preemies as a result of oxygen treatment — a lifesaving therapy given to premature babies to ensure their brains, hearts and lungs get enough of this vital gas so they can develop and function properly. However, high levels of oxygen can also damage the delicate air sacs inside the lungs, the tiny filters that exchange carbon dioxide for oxygen. Damaged by high levels of oxygen, these immature sacs, called alveoli, can become misshapen and reduce the lungs’ capacity to filter. Over time, the damage spreads further, as the blood vessels inside the lungs harden and develop abnormally high pressure. Persistently elevated pressure inside the lungs, a disease known as pulmonary hypertension can, over time, lead to heart failure. Oxygen supplementation is vital for premature newborns, yet because it can have such serious side effects, scientists have long sought therapies that can avert oxygen-induced damage in premature lungs. The new study findings show that hydrocortisone prevented the development of pulmonary hypertension and enlarged heart muscle, the two common consequences of BPD. In a set of experiments, researchers placed a group of newborn mice in chambers with high levels of oxygen, while another group was allowed to breathe room air. Animals living in high-oxygen chambers quickly developed the mouse version of BPD, mimicking human disease. Mice with BPD were given either low or high doses of hydrocortisone or placebo. As expected, mice treated with placebo developed pulmonary hypertension and enlarged right side of the heart. However, mice treated with hydrocortisone showed near normal right heart ventricles, despite having BPD. Mice with BPD treated with placebo went on to develop abnormally thickened lung vessels, a cardinal sign of pulmonary hypertension, while mice with BPD treated with hydrocortisone had near-normal blood vessels in their lungs, the researchers found. Next, researchers set out to find out how hydrocortisone protected the lungs of premature mice. Building on an earlier observation, the scientists focused on an enzyme called PDE-5, known to break down a signaling molecule that shields and strengthens blood vessels. In a previous study, the Lurie Children’s team found that too much oxygen can interfere with the activity of PDE-5 and thus speed up the breakdown of this vessel-shielding signaling molecule. Hydrocortisone, the new study found, protected the lung by preventing PDE-5 from going haywire despite high levels of oxygen. Comparing lung cells from mice exposed to high levels of oxygen, the researchers noticed that animals treated with steroids had far lower levels of PDE-5 than mice that didn’t get the treatment. That finding, the team says, points to the underlying mechanism behind the drug’s protective effect. In a final observation, the team discovered that higher doses of hydrocortisone could have the opposite effect and damage lung tissue. Indeed, when researchers examined lung tissue under a microscope, they noticed that animals treated with 10 mg of cortisone per kilogram of body weight had abnormal lung tissue. By contrast, animals given half that dose or a tenth of that dose had normal lung tissue. “Supplemental oxygen has been our standard treatment for critically ill preemies, and while needed, it’s not without risk,” says senior author Kathryn Farrow, M.D., Ph.D., a neonatologist at Lurie Children’s and associate professor of pediatrics at Northwestern University Feinberg School of Medicine. “Our findings provide new insights and new possible pathways to mitigate or completely eliminate the damaging side effects of an otherwise lifesaving therapy.” The work was funded by the National Institutes of Health under grant HL 109478 and the Lurie Children’s Department of Pediatrics Physician Scientist Research Award. Co-investigators included Kamila Wisniewska, Keng Jin Lee, Herminio Cardona, and Joann Taylor, from Northwestern University Feinberg School of Medicine. Research at Ann & Robert H. Lurie Children’s Hospital of Chicago is conducted through the Stanley Manne Children’s Research Institute. The Manne Research Institute is focused on improving child health, transforming pediatric medicine and ensuring healthier futures through the relentless pursuit of knowledge. In partnership with Northwestern University Feinberg School of Medicine, our scientists work in labs, in clinics, at the patient bedside and in the community to unravel the root causes of pediatric and adolescent disease, to understand childhood injury and to find factors that precipitate health problems in childhood and over a lifetime. Our researchers work every day to develop new therapies and prevention strategies.
Newswise — Hearing socially meaningful sounds can change the ear and enable it to better detect those sounds, according to researchers at Georgia State University who studied the phenomenon in green treefrogs. The findings are published in the Journal of Experimental Biology. “The ear is modifiable,” said Walter Wilczynski, a professor in the Neuroscience Institute at Georgia State. “It’s plastic. It can change by getting better or worse at picking up signals, depending on particular types of experiences, such as listening to social signals. If frogs have a lot of experience hearing their vocal signals, the ones that are behaviorally meaningful to them, their ear changes to help them better cope with processing those signals.” Each species has its own calls that influence social behavior. For instance, dogs bark, cats meow, frogs croak and humans speak using language. In animals, when males hear the calls of other males, they can determine if these males are getting too close in proximity or competing with them for females. When females listen to these calls, they can select the mate of their choice. The findings could have important implications for elderly people in nursing homes or prisoners in solitary confinement, both of whom have little social interaction. Scientists already know a lack of social structure is a “huge risk factor for every neurological and psychiatric disease we know about,” but this study shows it could also have an effect on basic sensory function, Wilczynski said. The study explored a phenomenon called forward masking, which occurs when a sound immediately precedes another sound someone is trying to hear and interferes with the ability to understand it. Because of the closeness in time between the two noises, the ear hasn’t finished processing the first signal before the second one occurs. This phenomenon can be detected with electrophysiological hearing tests. Researchers used green treefrogs because they have a simple social system with only one or two vocal calls. The research team examined how animals detect socially meaningful sound after hearing their species’ calls for an extended period of time versus being in social isolation and only hearing random sounds. In the lab, the experimental group heard their species’ specific calls every night for 10 consecutive nights as they would in a normal social breeding chorus in the wild, while the control group heard random tones with no social meaning. Then the researchers placed electrodes on the skin near the frogs’ ears and measured the response of their ears to sound. “What we find is that if they’ve had a lot of social stimulation, through their socially meaningful calls, the forward masking is reduced,” Wilczynski said. In a previous study published in the journal Proceedings of the Royal Society B: Biological Sciences, the researchers found when green treefrogs heard social signals over several nights, not just random sounds, their ears were more sensitive to the amplitude (loudness) of sound and responded more robustly. “If you have a lot of social interactions, a lot of social stimulation in the form of vocal signals, it’s actually modifying your ear and making your ear more sensitive,” Wilczynski said. “It’s making it easier to pick out signals in acoustically cluttered environments. And these are things that are not only important to frogs, which have to do this in a chorus, but to us, too.” “My guess is people who have a lot of experience with our social vocal signal, which is our speech, this probably helps keep their sensory system in a healthy state that helps them pick out those signals,” Wilczynski said. The researchers are unsure, however, how this change in the ear occurs or what particular change has been made, although they believe the modification occurs in the inner ear based on electrophysiological tests. The study was led by Megan Gall, previously a post-doctoral researcher at Georgia State and now an assistant professor of biology at Vassar College.
Newswise — FINDINGS Researchers from the David Geffen School of Medicine at UCLA found that cardiovascular disease patients who have high muscle mass and low fat mass have a lower mortality risk than those with other body compositions. The findings also suggest that regardless of a person’s level of fat mass, a higher level of muscle mass helps reduce the risk of death.This findings indicate the importance of assessing body composition as a way to help predict cardiovascular and total mortality in people with cardiovascular disease. BACKGROUND In previous studies on the relationship between body composition and mortality, the researchers used a simpler clinical measure of body composition called the bio electrical impedance scale. They noted a possible protective effect of muscle mass on both mortality and metabolism in healthy people. The new study extends the findings from the earlier research using dual X-ray absorptiometry, a more rigorous method of measuring body composition.The researchers examined data from the National Health and Nutrition Examination Survey, 1999 to 2004, of 6,451 participants who had prevalent cardiovascular disease. Each subject was categorized into one of four groups: low muscle/low fat mass low muscle/high fat mass high muscle/low fat mass high muscle/high fat mass Those with high muscle mass and low fat mass had the lowest risk of cardiovascular and total mortality. IMPACT Because people with higher muscle mass were more likely to have a high body mass index, the findings could explain the “obesity paradox,” which holds that people with a higher BMI have lower mortality levels. The findings also highlight the importance of maintaining muscle mass, rather than focusing on weight loss, in order to prolong life, even in people who have a higher cardiovascular risk. The authors suggest that clinicians encourage their patients to participate in resistance exercises as a part of healthy lifestyle changes, rather than focusing primarily on, and monitoring, weight loss. AUTHORS Dr. Preethi Srikanthan, associate clinical professor of medicine in the division of endocrinology at the David Geffen School of Medicine, is the study’s primary investigator. The study’s co-authors are Dr. Tamara Horwich, health sciences clinical professor of medicine, division of cardiology, and Dr. Chi-hong Tseng, adjunct associate professor of medicine in the division of general internal medicine and health services research. JOURNAL The study was published in the American Journal of Cardiology.
Newswise — Catherine Aaron and Gabrielle Beaudry were 17 when they knocked on the door of the laboratory of Alex Parker, a neuroscience researcher at the University of Montreal Hospital Research Centre (CRCHUM). While students at Collège Jean-de-Brébeuf in Montreal, they were looking for a mentor for an after-school research project. Two and half years later, the results of this scientific adventure were published today in the Journal of Agricultural and Food Chemistry. "We wanted to test the effect of a natural product on a neurodegenerative disease such as Alzheimer's. Professor Parker had already discovered that sugar prevents the occurrence of amyotrophic lateral sclerosis (ALS) in an animal model of the disease, the C. elegans worm. That’s how we got the idea of maple syrup, a natural sugar produced in Quebec,” said Beaudry. Supervised by PhD student Martine Therrien and Alex Parker, Aaron and Beaudry added maple syrup to the diet of these barely 1 mm-long nematodes. "We just gave them a supplement of maple syrup at various concentrations and compared with a control group that had a normal diet," said Aaron. “After twelve days, we counted under the microscope the worms that were moving and those that were paralyzed. The worms that had consumed the highest dose of syrup were much less likely to be paralyzed.” Alex Parker's C. elegans worms are genetically modified to express a protein involved in ALS in motor neurons – TDP-43. "When they are adults, around 12 days, their motor neurons break down. Normally, at two weeks of life, 50% of the worms are completely paralyzed. But among those that received a diet enriched with 4% maple syrup, only 17% were paralyzed. We can therefore conclude that maple syrup protects neurons and prevents the development of amyotrophic lateral sclerosis in C. elegans worms," said Parker, a researcher at the CRCHUM and professor at the Faculty of Medicine, University of Montreal. How can we explain this dramatic effect? "Sugar is good for the nervous system. Diseased neurons require more energy to combat toxic proteins. But maple syrup is rich in polyphenols, powerful antioxidants found in certain foods. We isolated phenols contained in the maple syrup, and we showed that two polyphenols in particular, gallic acid and catechol, have a neuroprotective effect. In pure maple syrup, these polyphenols are found in low concentrations. Probably a combination of sugar and polyphenols prevents the occurrence of the disease in worms," said Therrien, a PhD student at the CRCHUM. But don’t go ahead and gorge yourself on maple syrup thinking it'll protect you against neurological diseases! "The life expectancy of C. elegans worms is only three weeks. They are spared the long-term toxic effects of sugar. Humans who consume comparable amounts of sugar risk developing chronic diseases such Type 2 diabetes and obesity,” cautioned Parker. Amyotrophic lateral sclerosis is a rare neuromuscular disease that causes paralysis and death a few years after the onset of symptoms. So far, no cure is available for patients. This latest study on maple syrup and the C. elegans worm was conducted for educational purposes. Other studies by Alex Parker with C. elegans have led to the discovery of promising drugs, which will be tested in patients in a few years. Catherine Aaron and Gabrielle Beaudry won the Sanofi Biogenius Canada People’s Choice Award – Quebec section – for this project in April 2014. Aaron is now a first-year medical student at the University of Montreal, and Beaudry studies psychology at the University of Sherbrooke.
Newswise — Researchers have shown that various types of intestinal bacteria might be factors in both causing and preventing obesity, and in other conditions and diseases. Now, a UCLA study suggests that it could also potentially be used to reduce the risk for some types of cancer. The research, published online April 13 in the peer-reviewed journal PLOS ONE, offers evidence that anti-inflammatory “health beneficial” gut bacteria can slow or stop the development of some types of cancer. Ultimately, doctors might be able to reduce a person’s risk for cancer by analyzing the levels and types of intestinal bacteria in the body, and then prescribing probiotics to replace or bolster the amount of bacteria with anti-inflammatory properties, said Robert Schiestl, professor of pathology, environmental health sciences and radiation oncology at UCLA and the study’s senior author. “It is not invasive and rather easy to do,” he said. Over millions of years, gut bacteria have evolved into both good and bad types: The good ones have anti-inflammatory properties and the bad ones promote inflammation. The human body typically contains about 10 trillion bacterial cells, compared with only 1 trillion human cells. Schiestl and his colleagues isolated a bacterium called Lactobacillus johnsonii 456, which is the most abundant of the beneficial bacteria, and which has some pretty useful applications outside of medicine. “Since it is a Lactobacillus strain, it makes excellent yogurt, kefir, kombucha and sauerkraut.” In the UCLA study the bacterium reduced gene damage and significantly reduced inflammation — a critical goal because inflammation plays a key role in many diseases, including cancer, neurodegenerative diseases, heart disease, arthritis and lupus, and in the aging process. Previous research led by Schiestl presented the first evidence of a relationship between intestinal microbiota and the onset of lymphoma, a cancer that originates in the immune system. The new study explains how this microbiota might delay the onset of cancer, and suggests that probiotic supplements could help keep cancer from forming. For both studies, Schiestl and his team used mice that had mutations in a gene called ATM, which made them susceptible to a neurologic disorder called ataxia telangiectasia. The disorder, which affects 1 in 100,000 people, is associated with a high incidence of leukemia, lymphomas and other cancers. The mice were divided into two groups — one that was given only anti-inflammatory bacteria and the other that received a mix of inflammatory and anti-inflammatory microbes that typically co-exist in the intestines. In the Cancer Research paper, Schiestl and his team showed that in the mice with more of the beneficial bacteria, the lymphoma took significantly longer to form. In the new study, the researchers analyzed the metabolites — molecules produced by the gut’s natural metabolic action — in the mice’s urine and feces. The scientists were surprised to find that the mice that were receiving only the beneficial microbiota produced metabolites that are known to prevent cancer. Those mice also had more efficient fat and oxidative metabolism, which the researchers believe might also lower the risk for cancer. Among the other results, in the mice receiving only the good bacteria, lymphoma formed only half as quickly as it did in the other mice. In addition, mice with the good bacteria lived four times longer and had less DNA damage and inflammation. “Together, these findings lend credence to the notion that manipulating microbial composition could be used as an effective strategy to prevent or alleviate cancer susceptibility,” the researchers write. “Remarkably, our findings suggest that composition of the gut microbiota influence and alter central carbon metabolism in a genotype independent manner. In the future, it is our hope that the use of probiotics-containing [supplements] would be a potential chemopreventive for normal humans, while the same type of microbiota would decrease tumor incidence in cancer susceptible populations.”
Newswise — Have you had the experience of being just on the verge of saying something when the phone rang? Did you then forget what it is you were going to say? A study of the brain’s electrical activity offers a new explanation of how that happens. Published in Nature Communications, the study comes from the lab of neuroscientist Adam Aron at the University of California San Diego, together with collaborators at Oxford University in the UK, and was led by first author Jan Wessel, while a post-doctoral scholar in the Aron Lab. The researchers suggest that the same brain system that is involved in interrupting, or stopping, movement in our bodies also interrupts cognition – which, in the example of the phone ringing, derails your train of thought. The findings may give insights into Parkinson’s disease, said Aron, a professor of psychology in the UC San Diego Division of Social Sciences, and Wessel, now an assistant professor of psychology and neurology at the University of Iowa. The disease can cause muscle tremors as well as slowed-down movement and facial expression. Parkinson’s patients may also present as the “opposite of distractible,” often with a thought stream so stable that it can seem hard to interrupt. The same brain system that is implicated in “over-stopping” motor activity in these patients, Aron said, might also be keeping them over-focused. The current study focuses particularly on one part of the brain’s stopping system – the subthalamic nucleus (STN). This is a small lens-shaped cluster of densely packed neurons in the midbrain and is part of the basal ganglia system. Earlier research by Aron and colleagues had shown that the STN is engaged when action stopping is required. Specifically, it may be important, Aron said, for a “broad stop.” A broad stop is the sort of whole-body jolt we experience when, for example, we’re just about to exit an elevator and suddenly see that there’s another person standing right there on the other side of the doors. The study analyzes signals from the scalp in 20 healthy subjects as well as signals from electrode implants in the STN of seven people with Parkinson’s disease. (The STN is the main target for therapeutic deep brain stimulation in Parkinson’s disease.) All the volunteers were given a working memory task. On each trial, they were asked to hold in mind a string of letters, and then tested for recall. Most of the time, while they were maintaining the letters in mind, and before the recall test, they were played a simple, single-frequency tone. On a minority of trials, this sound was replaced by a birdsong segment – which is not startling like a “bang!” but is unexpected and surprising, like a cell phone chirping suddenly. The volunteers’ brain activity was recorded, as well as their accuracy in recalling the letters they’d been shown. The results show, the researchers write, that unexpected events manifest the same brain signature as outright stopping of the body. They also recruit the STN. And the more the STN was engaged – or the more that part of the brain responded to the unexpected sound – the more it affected the subjects’ working memory and the more they lost hold of what they were trying to keep in mind. “For now,” said Wessel, “we’ve shown that unexpected, or surprising, events recruit the same brain system we use to actively stop our actions, which, in turn, appears to influence the degree to which such surprising events affect our ongoing trains of thought.” A role for the STN in stopping the body and interrupting working memory does fit anatomical models of how the nucleus is situated within circuitry in the brain. Yet more research is needed, the researchers write, to determine if there’s a causal link between the activity observed in the STN and the loss in working memory. “An unexpected event appears to clear out what you were thinking,” Aron said. “The radically new idea is that just as the brain’s stopping mechanism is involved in stopping what we’re doing with our bodies it might also be responsible for interrupting and flushing out our thoughts.” A possible future line of investigation, Aron said, is to see if the STN and associated circuitry plays a role in conditions characterized by distractibility, like Attention Deficit Hyperactivity Disorder. “This is highly speculative,” he said, “but it could be fruitful to explore if the STN is more readily triggered in ADHD.” Wessel added: “It might also be potentially interesting to see if this system could be engaged deliberately – and actively used to interrupt intrusive thoughts or unwanted memories.” If further research bears out the connection suggested by the current study, between the STN and losing your train of thought following an unexpected event, the researchers say it might be that it is an adaptive feature of the brain, something we evolved long ago as a way to clear our cognition and re-focus on something new. Aron suggests this example: You’re walking along one morning on the African Savannah, going to gather firewood. You’re daydreaming about the meal you’re going to prepare when you hear a rustle in the grass. You make a sudden stop – and all thoughts of dinner are gone as you shift your focus to figure out what might be in the grass. In this case, it’s a good thing to forget what you had been thinking about.
Newswise — Expert: Frank Leone, MD, chair of the Tobacco Action Committee of the American Thoracic Society and noted expert in tobacco use treatment and smoking cessation. The CDC’s latest report on tobacco use among teens between 2011 and 2015 showed decreased use of traditional tobacco products and significant increase in the use of e-cigarettes. Frank Leone, MD, chair of the ATS Tobacco Action Committee, believes the misconception that e-cigarettes are safer than traditional cigarettes is driving the trend to increased use, which puts children and other first-time users at risk for significant health problems. Key Messages:• There are risks associated with liquid nicotine, including addiction.• Studies have shown that the mechanical and chemical characteristics of e-cigarettes contribute to potentially hazardous health effects.• Chemicals in the liquid nicotine flavorings are particularly dangerous for children, and one study showed that flavorings altered lung function at the cellular level. The CDC report states that “if current smoking rates continue, 5.6 million Americans aged <18 years who are alive today are projected to die prematurely from smoking-related disease.” “That’s not only a cause for great concern,” said Dr. Leone. “It’s a call to action. President Obama and the FDA need to lead the charge now by regulating e-cigarettes and all tobacco products.
Newswise — The fates of immune cells can be decided at the initial division of a cell. Researchers at St. Jude Children’s Research Hospital have discovered that the production of daughter cells with different roles in the immune system is driven by the lopsided distribution of the signaling protein c-Myc. Nudging c-Myc in one direction or the other could make vaccines more effective or advance immunotherapies for cancer treatment. The research appears online today in the scientific journal Nature. Asymmetric cell division generates two types of cells with distinct properties. This type of cell division is essential for producing various cell types and plays an important role in development. Rather than producing two identical daughter cells, the cells undergoing asymmetric division produce daughter cells that are fated for vastly different roles. In the case of activated T cells, researchers knew that one daughter cell became the rapidly dividing effector T cells that launch the immediate attack on infectious agents and other threats. The other daughter cell became the slowly dividing memory T cells that function like sentries to provide long-term protection against recurring threats. Until now, the mechanism underlying the process was unknown. “Our study shows that the way in which the regulatory protein c-Myc distributes during asymmetric cell division directly influences the fate and roles of activated T cells,” said corresponding author Douglas Green, Ph.D., St. Jude Department of Immunology chair. “We also show how this asymmetry is established and sustained.” The researchers worked with cells growing in the laboratory and in mice. Scientists showed that during asymmetric cell division of activated T cells, high levels of c-Myc accumulated in one daughter cell. There, c-Myc functioned like a shot of caffeine to launch and sustain the rapid proliferation of effector T cells, including those in mice infected with the influenza virus. In contrast, the daughter cells with low levels of c-Myc functioned like memory T cells, proliferating to mount an immune response a month later when mice were again exposed to the virus. Researchers also identified the metabolic and signaling pathways that serve as a positive feedback loop to sustain the high levels of c-Myc that effector T-cells require to maintain their identities and function. The scientists showed that disrupting certain components of the system disturbed c-Myc production, which altered the fate of T cells and caused effector T cells to operate like memory T cells. “Our work suggests that it may be possible to manipulate the immune response by nudging production of c-Myc in one direction or the other,” Green said. “Potentially that could mean more effective vaccines or help to advance T-cell immune therapy for cancer treatment.” c-Myc is an important transcription factor that regulates expression of a variety of genes and plays a pivotal role in cell growth, differentiation and death via apoptosis (programmed cell death). Excessive or inappropriate production of c-Myc is a hallmark of a wide variety of cancers. Previous research from Green and his colleagues showed that c-Myc also drives metabolic changes following T cell activation. The metabolic reprogramming fuels proliferation of effector T cells. “Activated T cells divide every four to six hours. There is no other cell in adults that can divide that fast, not even cancer cells,” Green explained.In this study, the researchers observed several metabolic changes that arose from the way c-Myc partitioned in the cell. These metabolic changes help regulate the way the cells divide, proliferate and differentiate. In a series of experiments, researchers showed how manipulating that system could affect T cell fate following asymmetric cell division by modifying production of c-Myc. “While daughter cells of activated T cells seem to have very different fates, we showed their behavior could be altered by manipulating these metabolic and regulatory pathways to increase or decrease c-Myc levels.” Green said. Asymmetric cell division is an important driver of other fundamental processes in cells, including early embryonic development and the self-renewal of stem cells. “Similar control mechanisms exist in other cells that divide asymmetrically, including stem cells in the digestive and nervous systems,” he added.