Chuck Bednar for redOrbit.com – @BednarChuck
Three men suffering from severe nerve damage volunteered to have their hands amputated and replaced with mind-controlled bionic prostheses, according to research published Tuesday in the medical journal The Lancet.
The process is known as “bionic reconstruction,” and according to Gizmodo, the procedures were performed by Dr. Oskar Aszmann at the Medical University of Vienna, Austria. Each of the volunteers had suffered damage to a bundle of nerves between the hand and the spine known as the brachial plexus that caused paralysis in their hands.
Teaching old dogs new tricks
All of the patients had reportedly undergone surgical procedures to attempt to repair the damage, but none of those operations were successful, leading them to volunteer for bionic reconstruction as an alternative, the website added.
Prior to surgery, their bodies and brains had to undergo a training procedure, as a section of leg muscle was transplanted into their arms to boost the signals of the few functioning nerves which remained. Nerves were allowed to grow into the muscle for a period of three months.
[VIDEO: Bionic eye helps man see wife for first time in 10 years]
Afterwards, the started practicing activating the muscle using an armband of sensors that could detect the electrical activity, New Scientist explained. Next, they moved on to using the signal to control a virtual arm, and finally, Dr. Aszmann amputated their hands and replaced them with a standard prosthesis under the control of the muscle and sensors.
Prosthetic works better than the real thing
The new hand is independently powered and requires only a small amount of input from the nerves of the grafted muscle to operate. The transplant was successful, as each of the patients can now pick up a ball, pour liquids from a jug and do up buttons and clothes fasteners. The simple and functional prosthetic hand outperformed their damaged biological on in all three cases.
“I was impressed and first struck with the surgical innovation,” Dustin Tyler of the Louis Stokes Veterans Affairs Medical Center in Cleveland, Ohio, told New Scientist. “There’s something very personal about having a hand; most people will go to great lengths to recover one, even if it’s not very functional. It’s interesting that people are opting for this.”

The patients went through a series of limb function tests, including one called the Southampton Hand Assessment Procedure, following the surgery. On this test, which is graded on a scale of 100 (with 100 being a normally functioning hand), the patients saw their scores improve from a nine to a 65. However, while the transplant restores functionality, it cannot restore touch.
“There are about 70,000 nerve fibres to a normal hand, and the majority of these are sensory fibres carrying hand-to-brain information. Only 10 per cent are motor fibers,” Dr. Aszmann said. Tyler, on the other hand, told New Scientist that he is working on a prototype prosthetic arm that will provide hand-to-brain information transmission, not just motor control.
[STORY: Child given 3D-printed Storm Trooper prosthetic arm]
The current version of Tyler’s device uses wires to deliver electronic stimulation to nerves in the arm, but he claims that his team will have a fully implantable wireless version in as little as three years. Even then, the website added, “our technological alternatives to the hand will remain crude compared with fully functional human hands.”
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Provided by Julie Cohen, University of California, Santa Barbara

Like the shape-shifting robots of Transformers fame, a unique class of proteins in the human body also has the ability to alter their configuration. These so-named intrinsically disordered proteins (IDPs) lack a fixed or ordered three-dimensional structure, which can be influenced by exposure to various chemicals and cellular modifications.

A new study by a team of UC Santa Barbara scientists looked at a particular IDP called tau, which plays a critical role in human physiology. Abundant in neurons located in the nervous system, tau stabilizes microtubules, the cytoskeletal elements essential for neuronal functions such as intracellular transport. Lacking a fixed 3D structure, tau can change shape so that it forms clumps or aggregates, which are associated with Alzheimer’s disease and related dementias. The researchers’ findings appear online in the Proceedings of the National Academy of Sciences.

“In the brain, these proteins need to change shape very rapidly to adapt to different conditions,” said co-author Joan-Emma Shea, a professor in UCSB’s Department of Chemistry and Biochemistry. “It’s important to understand the relationship between protein shape and function and how can you change the shape. So we used these external agents, small molecules called osmolytes, to affect the shape or conformations of these proteins.”

[STORY: Protein inactivates virtually all strains of HIV]

The researchers not only conducted biological experiments but also ran computer simulations to understand how these small molecules change the shape of tau and, when they do so, how it affects the protein’s ability to aggregate. They found that tau’s structure — whether extended or compact — was associated with how easily it bound to other tau proteins to promote the aggregation process.

“Continual aggregation of tau can, over time, result in an accumulation of pathological aggregates known as neurofibrillary tangles,” said lead author Zachary Levine, a postdoctoral scholar in UCSB’s Department of Chemistry and Biochemistry and Department of Physics. These tangles have long been known to be associated with Alzheimer’s disease and related dementias.

“In our computer simulations, we looked at certain chemical interactions called hydrogen bonds,” Levine explained. “We found that IDPs containing a large number of hydrogen bonds tended to take on smaller, more compact structures, but when we chemically removed them, we could create more extended protein structures. This allowed us to fine-tune what conformations tau could adopt. That’s really attractive if, say, you wanted to design a drug that intervenes in the pathological folding of IDPs.”

[STORY: Going against all we know: This protein doesn’t need DNA to build other proteins]

In order for aggregates of tau to develop, extended forms of the protein must stick together in a long sheet. The researchers exposed tau fragments to the osmolyte urea, which binds to the extended structures and prevents two of them from coming together. They were able to show that urea stopped aggregation, but the reason it did so wasn’t clear. However, subsequent computer simulations were able to reveal the interaction of urea with the tau protein, exposing underlying chemical interactions that decreased the likelihood of protein aggregation.

“The chemical structure of urea is quite similar to the backbone of tau,” Levine said. “Urea mimics the protein structure and binds to the surface, stopping other pieces of tau from binding to one another because the binding sites are already occupied by urea.”

The scientists also experimented with another osmolyte, trimethylamine N-oxide (TMAO), which had the exact opposite effect. They found that TMAO-exposed tau formed helical structures, which have been shown in other studies to accelerate aggregation.

[STORY: New protein ‘detonates’ antibiotic-resistant bacteria]

“With TMAO, you can see fibrils form, but with urea you don’t,” said co-author Nichole LaPointe, a researcher in UCSB’s Department of Molecular, Cellular and Developmental Biology (MCDB) and Neuroscience Research Institute (NRI) who conducted the experiments described in the paper. Fibrils are the beginning stages of harmful clumps or aggregates of tau. “So the predictions from the simulations are actually carrying forward into something pathologically relevant, which is the formation of these big aggregates.”

Only in recent years has technology advanced to the point where it can shed light on such microcellular functions. One of the interesting things to come out of this paper, according to co-author Stuart Feinstein, an MCDB professor and a co-director of the NRI, is the idea that various normal and pathological regulatory mechanisms alter the percentage of time proteins are spending in any one of these structures.

“The other great thing that comes out of this sort of collaborative research is the training of young students,” said Feinstein. “In bioengineering, physics or physical chemistry, you have a lot of established people who are trying to learn biology; on the other hand, there are a lot of established biologists who are trying to learn the more physical sciences, but in both cases, it is a retrofit. The people who intuitively understand both worlds are those trained in both disciplines in their 20s and 30s. And that — along with good science — is what comes out of a collaboration like this.”

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Chuck Bednar for redOrbit.com – @BednarChuck

Scientists from the UK and Israel have demonstrated for the first time that it is possible to make human egg and sperm cells using skin from two adults of the same sex – a breakthrough that may make it possible for same-sex couples to have children with shared DNA.

The research, which was funded by the Wellcome Trust, was completed at Cambridge University with the assistance of experts from the Weizmann Institute of Science, Cambridge News reported on Monday. They were able to use stem cell lines from embryos and from five different adults (a total of 10 different donor sources) to successfully create germ-cell lines.

According to CBS Atlanta, the experiment had previously been successful in creating live baby mice, but this new study marks the first time in which engineered human cells were found to be an identical match to aborted fetuses. It also marks the first time that human stem and skin cells were combined to form entirely new germ-cell lines.

[STORY: FDA reconsidering ban on homosexual, bisexual blood donors]

“We have succeeded in the first and most important step of this process, which is to show we can make these very early human stem cells in a dish,” Azim Surani, project leader at the Wellcome Trust and a professor of physiology and reproduction at Cambridge, told The Sunday Times.

Hope for those who can’t conceive

The key to the process was SOX17, a master gene which typically works to direct stem cells to form whatever type of tissue or organ is required. Their new process works by manipulating this gene so that it becomes part of a primordial germ cell specification (causing it to create cells that will form an entire person), making it possible to create primordial germ cells in the lab.

The study authors said that their work has already caught the attention of gay couples, advocacy groups, and heterosexual couples who are unable to conceive. They also told the media that they recognize the serious ethical issues that are raised by their research, but believe that many people will be able to benefit from the technique, which they have been testing on humans since first creating the artificial human eggs and sperm for the first time late last year.

[STORY: LGBT teens who come out in high school have better self-esteem]

Robin Lovell-Badge, the head of stem-cell biology and developmental genetics at the National Institute for Medical Research, added that the breakthrough “will be important for understanding the causes of infertility and for the treatment of it. It is probably a long way off, but it would be a way for people who have had treatment for conditions such as childhood leukemia, which has left them infertile, to have children of their own.”

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Chuck Bednar for redOrbit.com – @BednarChuck

If you find yourself binging on pizza, chocolate, or French fries, there’s a good reason for that, according to a new University of Michigan study that confirmed what experts have suspected for years– highly processed foods are the most addictive kinds.

In research published Wednesday by the journal PLOS One, UM assistant psychology professor Ashley Gearhardt and her colleagues investigated which types of foods are most likely to be involved in “food addiction,” a phenomenon often linked to obesity.

That pizza is too tempting

Binge eaters often prefer highly processed foods such as pizza or French fries, but these foods haven’t previously been evaluated for generating an addiction-like response.

“We propose that highly processed foods share pharmacokinetic properties (e.g. concentrated dose, rapid rate of absorption) with drugs of abuse, due to the addition of fat and/or refined carbohydrates and the rapid rate the refined carbohydrates are absorbed into the system,” the authors wrote in their study. “The current study provides preliminary evidence for the foods and food attributes implicated in addictive-like eating.”

[STORY: Are artificial food additives really that bad?]

Gearhardt and her colleagues conducted a pair of studies to examine the potential link. In the first, they recruited 120 undergraduate students and had each of them complete the Yale Food Addiction Scale (YFAS). The participants then looked through a nutritionally-diverse group of foods and chose which ones were associated with addictive-like behavior.

In the second study, they recruited 384 participants recruited through Amazon Mechanical Turk and, using the same 35 foods, used hierarchical linear modeling to investigate which food attributes (grams of fat, protein content, etc.) were related to addictive-like eating behavior. Afterwards, the study authors examined how individual differences influenced this association.

[STORY: Food marketing often creates a false sense of health]

They ultimately found that unprocessed foods such as brown rice and salmon that have no added fat or refined carbohydrates were not associated with addictive eating behavior. Rather, men and women experiencing symptoms of food addiction or with higher body mass indexes reported having more problems resisting highly-processed foods that had added

Not all foods are created equal

“The current study provides preliminary evidence that not all foods are equally implicated in addictive-like eating behavior, and highly processed foods, which may share characteristics with drugs of abuse… appear to be particularly associated with ‘food addiction,’” the authors wrote.

Lead author Erica Schulte, a doctoral student in psychology at UM, noted that some individuals could be particularly sensitive to what they view as the “rewarding” properties of those types of food. “If properties of some foods are associated with addictive eating for some people, this may impact nutrition guidelines, as well as public policy initiatives,” Schulte added.

[STUDY: Fast food diets are affecting children’s school grades]

Among the issues the study’s findings could impact are the marketing of these types of foods to children, the researchers noted. Future studies could also examine if these potentially addictive foods could trigger changes in brain circuitry in a similar way as other known addictive substances.

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Brett Smith for redOrbit.com – Your Universe Online
Stuttering has typically been treated as a psychological or emotional condition, but a new study based on brain scans found that the speech disorder may be linked to irregular white matter in the brain.
Maybe just a crossed wire
Published in the Journal of Speech, Language, and Hearing Research, the new study applied a technique called diffusion spectrum imaging (DSI) in an MRI scanner to analyze the white matter of eight adult stutterers. Researchers uncovered abnormalities of the arcuate fasciculus, one of the pathways that link up the language regions of the brain.
[STORY: Do brain training programs actually make you smarter?]
The arcuate fasciculus attaches at the front end of the brain to the part of the cerebral cortex associated with speech creation. At the rear of the brain, it branches off into three parts.
“What’s interesting is the back half,” said study author Scott Grafton, a brain scientist at the University of California, Santa Barbara. “In the vast majority of the stutterers we scanned, there seems to be a large portion of the connection projecting into the temporal cortex, an area of the brain also critical for speech perception. Seven of eight subjects are missing this third branch of the arcuate fasciculus bundle.”
The study demanded both sensitive imaging, and totally new investigation processes to look at each path in the brain individually and at the individual subject level.
“Big advances have allowed us to reconstruct pathways with greater detail than we were able to do before,” said lead author Matt Cieslak, a graduate student in Grafton’s lab.
“In terms of data, each subject produces what looks like a bowl of spaghetti or a ball of yarn and we had to figure out how to put that data into an analytical framework,” Cieslak explained. “About 40,000 lines of code later we now have a platform for analyzing white matter data, which can be expanded to a large set of subjects.”
Goals for the future
The scientists said their future work would analyze the brains of recovered stutterers to see if white matter actually shifts with a treatment program.
“Is there something special in the wiring of people who recover?” Grafton asked. “Maybe they are missing part of the arcuate fasciculus pathway but they’ve got another one that’s strong enough to pick up the slack. We’d like to be able to investigate that possibility using DSI.”
[STORY: What causes brain farts?]
“I’m really excited about this work because it’s transforming how we do research in patient groups with very common and challenging developmental disorders that have a great impact on people’s lives but are otherwise largely ignored in neuroscience and by funding agencies,” Grafton continued. “They get diagnosed or described and we throw therapies at them but we don’t really understand the pathophysiologic basis or the biology of these problems.”
“The fact that we can now see big changes in scans of individuals who stutter is huge,” Grafton concluded. “It opens up a lot of opportunities, not just for stutterers but for all kinds of developmental problem like dyslexia, childhood speech apraxia and disorders of coordination.”
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Chuck Bednar for redOrbit.com – @BednarChuck

A new skin patch could help protect people suffering from potentially life-threatening peanut allergies by significantly increasing the amount of exposure needed to elicit a reaction.

According to The Seattle Times, use of the Viaskin Peanut patch upped the amount of peanut protein required to trigger an allergic reaction by at least 10-fold in an early stage clinical trial.

The patch, which was developed by French biotech firm DBV Technologies, was most effective for children under the age of 12, the researchers revealed at the annual meeting of the American Academy of Allergy, Asthma and Immunology in Houston, Texas on Sunday.

Desensitizing the immune system

The trial examined if the immunotherapy patch could essentially desensitize people to allergic reactions by administering relatively small amounts of peanut proteins into the outer layers of their skin. The goal was to trigger an immune response without releasing antigens into the blood, where they would trigger allergic shock, the newspaper explained.

Participants wearing the highest doses of the patches were able to consume the equivalent of four peanuts without triggering severe reactions, Today.com noted. As a result, those individuals should no longer have to worry about “traces of peanut in a package” from a factory which uses peanuts, or “minor contamination of food in a restaurant,” said lead author Dr. Hugh Sampson.

[STORY: Probiotics may help children with peanut allergies]

Dr. Sampson, a professor of pediatrics at the Icahn School of Medicine and director of the Jaffe Food Allergy Institute at Mount Sinai, and his colleagues conducted recruited 221 participants between the ages of six and 55 for a double-blind trial at various locations in the US, Canada, France, Poland and the Netherlands.

Each participant was tested to see how much peanut protein it took to trigger a reaction, and were then asked to wear the adhesive patches, which were infused with doses of between 50 and 250 micrograms of peanut protein. One year later, they were tested a second time to determine if their reaction thresholds had increased over that period.

[STORY: Peanut allergies may be from dry roasting process]

The 250-microgram patch was found to be the most effective, Dr. Sampson said, and more than 53 percent of children between the ages of six and 11 responded to the patch (compared to under 20 percent for a placebo). None of the patients required epinephrine injections to stop allergic reactions associated with the path itself, indicating that it is safe, the Times added.

We’re the allergic kids in America, woah-oh

Approximately 15 million people in the US have food allergies, and statistics from the Centers for Disease Control and Prevention indicate that the rate of peanut allergies in children tripled between 1997 and 2008, the newspaper said. In light of those figures, the results of the new trial are encouraging, according to Food Allergy Research & Education’s Dr. James Baker.

“The goal for most practicing allergists and for most parents is to get a child to the point where if there is an accidental ingestion of peanut it would not be as risky or life-threatening,” Dr. Amy Stallings, an assistant professor of pediatrics in the division of allergy and immunology at the Duke University Medical Center who is not affiliated with the new study, told Today. “And the patch may be a way of doing this that is safer.”

[STORY: Peanut butter may help prevent breast cancer]

The next step will be for the patch to undergo a Phase III clinical trial, and if the results from that are positive, it will be submitted to the Food and Drug Administration (FDA) for evaluation. However, Dr. Sampson cautioned that, even in a best-case scenario, it will likely be several more years before it becomes available to the general public.

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Chuck Bednar for redOrbit.com – @BednarChuck

A new bionic eye implant has made it possible for a 68-year-old Minnesota native suffering from a degenerative eye condition to see his wife for the first time in more than a decade.

Go ahead, try to keep a dry eye.

Retinitis pigmentosa

According to Mashable, Allen Zderad was diagnosed with retinitis pigmentosa nearly 20 years ago, and since then he had lost nearly all of his eyesight to the disease, which causes damage to the tissue at the back of the inner eye that converts light images to nerve signals.

There is no cure or effective treatment for retinitis pigmentosa, but thanks to a clinical trial of a new device built by Second Sight, Zderad has regained the ability to see shapes, make out human forms and even see his own reflection in a window, the website added in its report.

[STORY: DARPA implant could give people Terminator-like vision]

“It’s crude, but it’s significant. It works,” he said after seeing his wife for the first time following the implant, which the Mayo Clinic described as a “tiny  wafer-like chip” that was embedded in his right eye and “sends light wave signals to the optic nerve, bypassing the damaged retina.”

Wires required for the bionic eye’s operation were implanted in January, and two weeks later, the rest of the prosthetic device was surgically implanted. Though the device works, it still needs to be adjusted, and Zderad will have to undergo several hours of instruction and physical therapy in order to make full use of the instrument, according to the man’s doctors.

Greatly improves quality of life

Zderad is the first man in Minnesota and just the 15th person in America to receive the device, but there are limitations to what he will be able to do with it. While he will be able to navigate a room full of people without needing to use a cane, he will not be able to make out detail in faces or images. Even so, the clinic said it will “greatly improves his quality of life.”

“The retinal prosthesis implant has taken over 25 years to develop. Hundreds of millions of dollars and hundreds of people to bring this forward to this point,” Dr. Raymond Iezzi, a retinal surgeon and clinical ophthalmologist at the Mayo Clinic, told KARE News in Minnesota.

It really is a bionic eye

The device, officially known as the Argus II Retinal Prosthesis System, was approved by the US Food and Drug Administration (FDA) in January 2014 and reportedly cost between $300 million and $500 million to develop. Second Sight explains that it provides electrical stimulation of the retina to induce visual perception in patients with severe to profound retinitis pigmentosa.

“It’s a bionic eye – in every sense of the word. It’s not a replacement for the eyeball, but it works with interacting with the eye,” Dr. Iezzi said. “Mankind has been seeking to cure blindness for 2,000 years or more, but only in the past quarter of a century have we had the electronics… all the other things come together to build a retinal prosthesis that could restore sight to the blind.”

[STORY: World of Warcraft adds color-blind support]

The device was first implanted in a pair of patients at the University of Michigan Kellogg Eye Center in January 2014, and earlier clinical studies indicated that most recipients of the Argus II were able to perform basic activities better with the prosthesis than without it. Many were able to follow lines in a cross walk, while some could even sort laundry or read very large letters.

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Provided by Verity Leatherdale, University of Sydney
Oxytocin, sometimes referred to as the “love” or “cuddle” hormone, has a legendary status in popular culture due to its vital role in social and sexual behaviour and long-term bonding.
Now researchers from the University of Sydney and the University of Regensburg have discovered it also has a remarkable influence on the intoxicating effect of alcohol, which they report in the scientific journal Proceedings of the National Academy of Sciences on 24 February.
When the researchers infused oxytocin into the brains of rats which were then given alcohol it prevented the drunken lack of coordination caused by the alcohol.
[STORY: Our ancestors were getting drunk 10 million years ago]
“In the rat equivalent of a sobriety test, the rats given alcohol and oxytocin passed with flying colors, while those given alcohol without oxytocin were seriously impaired,” Dr. Bowen said.
The researchers demonstrated that oxytocin prevents alcohol from accessing specific sites in the brain that cause alcohol’s intoxicating effects, sites known as delta-subunit GABA-A receptors.
“Alcohol impairs your coordination by inhibiting the activity of brain regions that provide fine motor control. Oxytocin prevents this effect to the point where we can’t tell from their behaviour that the rats are actually drunk. It’s a truly remarkable effect,” Dr. Bowen said.
[STORY: When science got drunk in 2014]
This “sobering-up” effect of oxytocin has yet to be shown in humans, but the researchers plan to conduct these studies in the near future.
“The first step will be to ensure we have a method of drug delivery for humans that allows sufficient amounts of oxytocin to reach the brain. If we can do that, we suspect that oxytocin could also leave speech and cognition much less impaired after relatively high levels of alcohol consumption,” Dr Bowen said.
It’s worth noting that oxytocin can’t save you from being arrested while driving home from the pub.
“While oxytocin might reduce your level of intoxication, it won’t actually change your blood alcohol level,” Dr. Bowen said. “This is because the oxytocin is preventing the alcohol from accessing the sites in the brain that make you intoxicated, it is not causing the alcohol to leave your system any faster.”
[STORY: Buzzed driving just as fatal as drunk driving, study says]
Some people might worry a drug which decreases your level of intoxication could encourage you to drink more. As it turns out, separate experiments conducted by the researchers and other groups have shown that taking oxytocin actually reduces alcohol consumption and craving in both rats and humans.
“We believe that the effects of oxytocin on alcohol consumption and craving act through a similar mechanism in the brain to the one identified in our research,” said Dr. Bowen.
Their findings could see the development of new oxytocin-based treatments for alcohol-use disorders that target this mechanism.
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Chuck Bednar for redOrbit.com – @BednarChuck

The development of new neurons in adults appears to help the hippocampus better prepare for a variety of environmental factors, and the process is influenced in different ways by positive and negative experiences, researchers from Princeton University have discovered.

In research published Saturday in the journal Trends in Cognitive Sciences, Maya Opendak and Elizabeth Gould of the Princeton Neuroscience Institute explained that the birth of new neurons in the hippocampus (a region of the brain involved in memory and learning) can help people and animals adapt to their current circumstances in a complex, constantly changing world.

Fine-tuning the hippocampus

Opendak and Gould reviewed previous studies and other literature addressing the topic, and they reported that aversive experiences decrease neurogenesis, while rewarding ones tend to increase the production of new neurons. They added that those new neurons appear to be involved in most functions of the hippocampus, and may help optimize it anticipated circumstances.

As Opendak explained in a statement, “New neurons may serve as a means to fine-tune the hippocampus to the predicted environment. In particular, seeking out rewarding experiences or avoiding stressful experiences may help each individual optimize his or her own brain. However, more naturalistic experimental conditions may be a necessary step toward understanding the adaptive significance of neurons born in the adult brain.”

[STORY: The brain effects of a good novel]

It has become increasingly clear over the past few years that environmental factors have a profound influence on the adult brain in humans and several other types of mammals, the study authors explained. Stressful experiences such as social defeat, sleep deprivation and exposure to predator odors have been shown to decrease the number of new neurons in the hippocampus, while pleasant experiences such as mating and exercise increased neurogenesis.

The birth of new neurons during adulthood may come with important cognitive and behavioral consequences, they added. Stress-induced suppression of adult neurogenesis has been linked to impaired performance on spatial navigation learning, object memory and other cognitive tasks that depend on the hippocampus.

[STORY: Brain of Carl Friedrich Gauss was apparently switched with another]

Likewise, stressful experiences have been shown to increase the anxiety-type behaviors that are associated with the hippocampus. On the other hand, rewarding experiences have been linked to a reduction in anxiety-like behavior and improved performance on cognitive tasks involving the hippocampus, Opendak and Gould noted.

Improving the odds of survival

While most scientists agree that their daily actions change a person’s brain even in adulthood, there is no consensus on the adaptive significance of the development of new neurons. In their new study, the authors propose that stress-induced decreases in neurogenesis could improve the odds of survival by increasing anxiety and prioritizing safety and avoidant behavior by limiting the desire to explore and sacrificing some degree of cognitive performance.

“Because the past is often the best predictor of the future, a stress-modeled brain may facilitate adaptive responses to life in a stressful environment, whereas a reward-modeled brain may do the same but for life in a low-stress, high-reward environment,” explained Gould, a professor of psychology and neuroscience at Princeton University.

[STORY: This is your brain on poetry]

When aversive experiences drastically outnumber rewarding ones in terms of quantity and intensity, however, a person’s system could reach a breaking point and produce maladaptive outcomes, she and Opendak added. For instance, repeated stress causes a prolonged reduction in neurogenesis, ultimately causing extreme anxiety and depression-like symptoms to emerge.

“Such a scenario could represent processes that are engaged under pathological conditions and may be somewhat akin to what humans experience when exposed to repeated traumatic stress,” said Opendak.

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Chuck Bednar for redOrbit.com – @BednarChuck

New research from the Medical College of Wisconsin (MCW) and the Children’s Hospital of Wisconsin Research Institute has linked a specific type of protein to the development of viral-induced asthma – a discovery that could help treat the condition in young children.

In the study, MCW biochemistry professor Dr. Brian F. Volkman, Dr. Mitchell H. Grayson of the CHW Research Institute and their colleagues report that CCL28, a human chemokine that is expressed by columnar epithelial cells and which has been shown to attract various types of immune cells, is associated with the pathogenesis of acute post-viral asthma.

[STORY: Surgery for sleep apnea improves asthma control]

“Elevated levels of CCL28 have been found in the airways of individuals with asthma, and previous studies have indicated that CCL28 plays a vital role in the acute development of post-viral asthma,” they wrote in a recent edition of the Journal of Biological Chemistry. “Our study builds on this, demonstrating that CCL28 is also important in the chronic post-viral asthma phenotype… [and] is both necessary and sufficient for induction of asthma pathology.”

Looking for preventative measures

Asthma, a chronic condition of the respiratory system affecting more than 300 million people worldwide, is the primary cause of illness-related school absences in children, the study authors explained. It also accounts for more than 1.8 million emergency room visits annually, and since there is no cure, the focus is on treating symptoms and preventing severe attacks.

Dr. Grayson and Dr. Volkman had previously found evidence linking CCL28 to the development of chronic asthma, but this new study is the first to analyze the structural features of the human chemokine and its impact on the development of the disease. They found that its structure is vital to its role in pathogenesis, and that inhibiting the protein could help prevent post-viral asthma.

[STUDY: Energy efficient homes may be linked to increased asthma risk]

“Understanding the molecular mechanisms by which asthma develops and establishes itself as a chronic disease is key to elucidating alternative and potentially curative therapies,” explained Dr. Grayson, who is also the director of Fight Asthma Milwaukee (FAM) Allies and a member of the board of directors of the national Asthma and Allergy Foundation of America.

“Even in the absence of a viral infection, CCL28 can play a role in the induction of asthma pathology – when the protein is natively folded. If unfolded, it does not,” added Dr. Volkman, calling it “the first step in generating a novel type of asthma therapy that may have the power to prevent development of post-viral asthma in young children.”

[STORY: Childhood asthma linked to poor ventilation of gas stoves]

By exploiting the unique structural features of the protein, the study authors said, powerful and specific CCL28 inhibitors could be developed. Because of the “intimate relationship” between the chemokine and asthma pathology, CCL28 could well be “a novel target for the development of alternative asthma theraputics,” they added.

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Provided by David Kohn, University of Maryland School of Medicine

Baltimore, Md., February 20, 2015 – The average heart beats 35 million times a year – 2.5 billion times over a lifetime. Those beats must be precisely calibrated; even a small divergence from the metronomic rhythm can cause sudden death. For decades, scientists have wondered exactly how the heart stays so precisely on rhythm even though it contains so many moving parts.

Now, researchers at the University of Maryland School of Medicine (UM SOM) have helped identify how a particular protein plays a central role in this astonishing consistency. This is the first time the mechanism has been described; the discovery could eventually help scientists treat heart problems that kill millions of people every year.

W. Jonathan Lederer, MD, PhD, professor of physiology at the UM SOM, as well as director of the Center for Biomedical Engineering and Technology, and David Warshaw, PhD, professor of molecular physiology and biophysics at University of Vermont (UVM) and the Cardiovascular Research Institute of Vermont, describe how myosin-binding protein C (“C protein”) allows the muscle fibers in the heart to work in perfect synchrony. The results appear today in the latest issue of the journal Science Advances.

“This protein turns out to be really important to this process,” said Dr. Lederer. “This is a really exciting finding. We envision a lot of research that we can do with this new knowledge. We will continue to investigate this in all kinds of ways.”

For years, researchers have known that calcium acts as a trigger for the heartbeat, activating proteins that cause the sarcomeres – the fibrous proteins that make up heart muscle cells – to contract. Dr. Lederer found that the calcium molecules are not distributed evenly across the length of each sarcomere; the molecules are released from the ends. Despite this, the sarcomeres contract uniformly. But exactly how has remained a thorny mystery.

Drs. Lederer, Warshaw and their colleagues found the answer: C protein. This protein was known to exist in all heart muscle cells, but until now, its function was unknown. Using an animal model, the researchers studied the physiology of sarcomeres, measuring calcium release and the muscle fibers’ mechanical reaction. It turns out that C protein sensitizes certain parts of the sarcomere to calcium. As a result, the middle of the sarcomere contracts just as much as the ends, despite having much less calcium. In other words, C protein enables the sarcomeres to contract synchronously.

“Calcium is like the sparkplugs in an automobile engine and C protein acts like the rings that increase the efficiency of the movement of the pistons,” says Michael J. Previs, PhD, an assistant professor in the Department of Molecular Physiology and Biophysics at UVM.

C protein appears to play a large part in many forms of heart disease. In the most severe cases, defects in C-protein lead to extremely serious arrhythmias, which cause sudden death when the heart loses the ability to pump blood. In the U.S., arrhythmias contribute to about 300,000 deaths a year, according to the American Heart Association. (Not all arrhythmias are fatal; some can be controlled with medicines and electrical stimulation.)

Lederer and his colleagues think that it may be possible to affect arrhythmias by modifying the activity of C protein through drugs. “I think this could be very big,” says Dr. Lederer. “This protein is definitely a drug target.”

Drs. Lederer and Warshaw also collaborated with scientists from the University of Pennsylvania, the University of Massachusetts Medical School, Cincinnati Children’s Hospital Medical Center, and Eulji University in South Korea.

“This work by Dr. Lederer and his colleagues is a great example of collaborative basic science research with potentially huge translational implications,” said Dean E. Albert Reece, MD, PhD, MBA, who is also the vice president for Medical Affairs, University of Maryland, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean of the School of Medicine. “Beyond the elegant findings of this work, there remain many challenges in unravelling how C protein mutations produce contractile and arrhythmic dysfunction in disease.”

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Chuck Bednar for redOrbit.com – @BednarChuck

While scientists have known for well over a century which part of the brain is responsible for producing speech, new research published Tuesday in the journal Proceedings of the National Academy of Sciences reveals the details of this process for the first time.

Researchers from the Johns Hopkins University School of Medicine examined the brain region known as Broca’s area, which was found to play a key role in speech production more than 150 years ago, to learn exactly what that key role was.

By studying recordings from the surface of the brain, made between surgical procedures to treat epileptic seizures, they found that it is active early in the process of sentence formation and ends its task before even a single word is spoken – far earlier than experts had predicted.

[STORY: Vibrating sex toys used to loosen up vocal chords]

Senior author Dr. Nathan E. Crone, an associate professor of neurology at Johns Hopkins, explained that Broca’s area (which is located in the frontal cortex, above and behind the left eye) “mediates a cascade of activation from sensory representations of words in temporal cortex to their corresponding articulatory gestures in motor cortex.”

However, it remains largely inactive during the actual process of articulation, and is not involved in the actual production of individual word. Rather, the authors said that Broca’s area coordinates the transformation of information processing across cortical networks involved in the production of spoken words. Their findings may help treat stroke or injury-related language issues.

“We were interested in studying how information flows through the brain during speech, and in this study, for the first time, we were able to record very precisely the timing of activation of different centers of the brain during different language tasks,” Crone said in a statement Tuesday.

[STORY: Trickiest tongue twisters provide insight into speech planning]

“Broca’s area has always been viewed as very important for the articulation of speech, but until now its precise role was unclear,” he added. “We found that rather than carrying out the articulation of speech, Broca’s area is developing a plan for articulation, and then monitoring what is said to correct errors and make adjustments in the flow of speech.”

Conducting the research

Crone’s team conducted their research with the help of seven patients receiving treatment for epilepsy seizures at Johns Hopkins. While those individual were undergoing brain mapping to locate the source of their seizures, doctors recorded the electrical activity from Broca’s area and other parts of the brain using electrodes placed directly on the frontal cortex.

Since patients are awake and alert during this process, the researchers asked each of them to read or listen to a one-syllable word and repeat it out loud. They found that Broca’s area was the most active part of the brain just before the words were spoken, but its activity levels declined as the patients started speaking. The study also found that the region of the brain was most active when the patients were presented with unfamiliar, nonsense words instead of actual ones.

Based on their observations, Crone and his colleagues believe that Broca’s area serves as a sort of intermediary between the temporal cortex (where incoming sensory information is organized) and the motor cortex (which triggers the movements of the mouth).

While the area shuts down during speech delivery, it may remain active during a conversation, helping to plan future words and full sentences, said lead author Adeen Flinker, a postdoctoral researcher at New York University.

Flinker explained that neuroscientists previously believed that the brain’s language center was divided into two main areas: one that perceived speech, and one that produced it. The new study, however, reveals that Broca’s area “is not simply a center for speech production but rather a critical area for integrating and coordinating information across brain regions.”

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