Posts tagged science

ScienceDaily (July 6, 2012) — In a forthcoming issue of Topics in Cognitive Science researchers from the University of Amsterdam (UvA) argue that at least two, seemingly trivial musical skills can be considered fundamental to the evolution of music: relative pitch — the skill to recognise a melody independent of its pitch level — and beat induction — the skill to pick up regularity (the beat) from a varying rhythm. Both are considered cognitive mechanisms that are essential to perceive, make and appreciate music, and, as such, could be argued to be conditional to the origin of music.

While it recently became quite popular to address the study of the origins of music from an evolutionary perspective, there is still little agreement on the idea that music is in fact an adaptation, that it influenced our survival, or that it made us sexually more attractive. Music appears to be of little use. It doesn’t quell our hunger, nor do we live a day longer because of it. So why argue that music is an adaptation? There are even researchers who claim that studying the evolution of cognition is virtually impossible (Lewontin, 1998; Bolhuis & Wynne, 2009).

Distinguishing between music and musicality

The alternative that Henkjan Honing and Annemie Ploeger of the UvA propose is, first, to distinguish between the notion of ‘music’ and ‘musicality’, with musicality being defined as a natural, spontaneously developing trait based on and constrained by our cognitive system, and music as a social and cultural construct based on that very musicality. And secondly, to collect accumulative evidence from a variety of sources (e.g., psychological, physiological, genetic, phylogenetic, and cross-cultural evidence) to be able to show that a specific cognitive trait is indeed an adaptation.

Both relative pitch and beat induction are suggested as primary candidates for such cognitive traits, musical skills that are considered trivial by most humans, but that turn out to be quite special in the rest of the animal world.

Once these fundamental cognitive mechanisms are identified, it becomes possible to see how these might have evolved. In short: the study of the evolution of music cognition is conditional on a characterisation of the basic mechanisms that make up musicality.

Source: Science Daily

ScienceDaily (July 6, 2012) — If you’re concerned about losing your hearing because of noise exposure (earbud deafness syndrome), a new discovery published online in the FASEB Journal offers some hope. That’s because scientists from Germany and Canada show that the protein, AMPK, which protects cells during a lack of energy, also activates a channel protein in the cell membrane that allows potassium to leave the cell. This activity is important because this mechanism helps protect sensory cells in the inner ear from permanent damage following acoustic noise exposure.

This information could lead to new strategies and therapies to prevent and treat trauma resulting from extreme noise, especially in people with AMPK gene variants that may make them more vulnerable to hearing loss.

"Future research on the basis of the present study may lead to the development of novel strategies preventing noise-induced hearing loss or accelerating recovery from acoustic trauma," said Florian Lang, Ph.D., a researcher involved in the work from the Department of Physiology at the University of Tübingen, in Tübingen, Germany.

To make this discovery, Lang and colleagues compared two groups of mice. The first group was normal and the second lacked the AMPK protein. Hearing of the mice was tested by measuring sound-induced brain activity. All mice were exposed to well-defined noise causing an acoustic trauma and leading to hearing impairment. Prior to noise exposure, the hearing ability was similar in normal mice and mice lacking AMPK. After exposure, the hearing of the normal mice mostly recovered after two weeks, but the recovery of hearing in AMPK-deficient mice remained significantly impaired.

"When it comes to preventing hearing loss, keeping the volume down is still the best strategy, and this discovery doesn’t prevent loud music from beating on our ear drums," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “This discovery does help explain why some people seem more likely to lose their hearing than others. At the same time, it also provides a target for new preventive strategies — and perhaps even a treatment — for earbud deafness syndrome.”

Source: Science Daily

July 6, 2012

(Medical Xpress) — Scientists at the University of Liverpool have found that a protein produced by a gene identified in fruitflies, is responsible for communication between nerve cells in the brain.

Dr Stephen Royle: “This research is another step towards fully understanding the complexities of the human brain.”

The ‘stoned’ gene was discovered in fruitflies by scientists in the 1970s. When this gene was mutated, the flies had problems walking and flying, giving rise to the term ‘stoned’ gene. The same gene was found in mammals some years later, but until now scientists have not known precisely what this gene is responsible for and why it causes problems with physical functions when it mutates.

‘Packets of chemicals’

Scientists at Liverpool have found that the protein the gene expresses in mammals, called stonin2, is responsible for retrieving ‘packets’ of chemicals that nerve cells in the brain release in order to communicate with each other.  The inability of the gene to express this protein in the fruitfly study, suggests why the insect appeared not to be able to walk or fly normally.

The team used advanced techniques to inactivate stonin2 for short and long periods of time in animal cells grown in the laboratory. The cells used where from an area of the brain associated with learning and memory.  They showed that without stonin2 the nerve cells could not retrieve the ‘packets’ needed to transport the chemicals required for communications between nerve cells.

Dr Stephen Royle, from the University’s Institute of Translational Medicine, explains: “Nerve cells in the brain communicate by releasing ‘packets’ of chemicals.  These ‘packets’ must be retrieved and refilled with chemicals so that they can be used once again. This recycling programme is very important for nerve cells to keep communicating with each other. 

“We have shown that a protein called stonin 2 is needed for the packets to be retrieved. There is currently no evidence to suggest that the gene which expresses this protein is mutated in human disease, but any failure in its function would be disastrous.  The research is another step towards fully understanding the complexities of the human brain.”

The research is published in the journal, Current Biology.

Provided by University of Liverpool

Source: medicalxpress.com

ScienceDaily (July 6, 2012) — Yona Goldshmit, Ph.D., is a former physical therapist who worked in rehabilitation centers with spinal cord injury patients for many years before deciding to switch her focus to the underlying science.

"After a few years in the clinic, I realized that we don’t really know what’s going on," she said.

Now a scientist working with Peter Currie, Ph.D., at Monash University in Australia, Dr. Goldshmit is studying the mechanisms of spinal cord repair in zebrafish, which, unlike humans and other mammals, can regenerate their spinal cord following injury. On June 23 at the 2012 International Zebrafish Development and Genetics Conference in Madison, Wisconsin, she described a protein that may be a key difference between regeneration in fish and mammals.

One of the major barriers to spinal regeneration in mammals is a natural protective mechanism, which incongruously results in an unfortunate side effect. After a spinal injury, nervous system cells called glia are activated and flood the area to seal the wound to protect the brain and spinal cord. In doing so, however, the glia create scar tissue that acts as a physical and chemical barrier, which prevents new nerves from growing through the injury site.

One striking difference between the glial cells in mammals and fish is the resulting shape: mammalian glia take on highly branched, star-like arrangements that appear to intertwine into dense tissue. Fish glia cells, by contrast, adopt a simple elongated shape — called bipolar morphology — that bridges the injury site and appears to help new nerve cells grow through the damaged area to heal the spinal cord.

"Zebrafish don’t have so much inflammation and the injury is not so severe as in mammals, so we can actually see the pro-regenerative effects that can happen," Dr. Goldshmit explained.

Studies in mice have found that mammalian glia can take up the same elongated shape, but in response to the environment around the injury they instead mature into scar tissue that does not allow nerve regrowth.

Dr. Goldshmit and her colleagues have focused on a family of molecules called fibroblast growth factors (Fgf), which have shown some evidence of improving recovery in mice and humans with spinal cord damage. The Monash University group found that Fgf activity around the damage site promotes the bipolar glial shape and encourages nerve regeneration in zebrafish.

Preliminary results in mice show that Fgf injections near a spinal injury increase both the number of glia cells at the site and the elongated morphology. Their evidence suggests that Fgfs may work to create an environment more supportive of regeneration in mammals as well and could be a valuable therapeutic target.

Spinal injury patients usually have few options, Dr. Goldshmit emphasized, and development of new, biologically-based approaches will be critical.

"This is a nice example of how we can use the zebrafish model," she said. "When we learn from the zebrafish what to look at, we can find things that give us hope for finding therapeutic approaches for spinal cord injury in humans."

Source: Science Daily

July 6, 2012 by Nancy Owano

(Phys.org) — Talk about fMRI may not be entirely familiar to many people, but that could change with new events that are highlighting efforts to link up humans and machines. fMRI (Functional Magnetic Resonance Imaging) is a promising technology that can help human move beyond joysticks to control robots via brain scanners instead. Now a research project exploring ways to develop robot surrogates with whom humans can interact has turned a corner. A university student‘s ability to make his robot surrogate move around, using fMRI technology, was successful. The experiment linked up Israeli student Tirosh Shapira in a lab at Bar-Ilan University, Israel, with a small robot in another lab far away at Beziers Technology Institute in France.

Shapira merely had to think about moving his arms or legs and the robot, with a camera on its head with an image displayed in front of Shapira, successfully would do the same. If Shapira thought about moving forward or backward, the robot responded accordingly.

fmri monitors blood flowing through the brain and can spot when areas associated with certain actions, such as movement, are in use. The fMRI read the student’s thoughts, which were translated via computer into commands relayed across the Internet to the robot in France.

There is much more work to be done to advance this approach, however. The researchers seek to devise a different type of scanning. An fMRI scanner is an expensive piece of equipment but the scientists believe that improvements in software might allow for a head-mounted device. Another research goal is to see if they can get humans to speak via the robot. The size of the robot will need modification, closer to the size and movement of a human, and engineered with a wider range of movement that would include hand gestures. In sum, according to the researchers, this experiment is only one of many steps ahead.

Medical applications for this technology are seen as promising, especially as scientists explore how patients with paralysis can interface with robots so that the patients can reconnect to the world. Another suggested application has been in the military, where robot surrogates rather than soldiers would be sent into battle.

Source: PHYS.ORG

July 6, 2012

(Medical Xpress) — Researchers decode a molecular mechanism that sheds light on how trauma can become engraved in the brain

Scientists at the Universities of Bonn and Berlin have discovered a mechanism which stops the process of forgetting anxiety after a stress event. In experiments they showed that feelings of anxiety don’t subside if too little dynorphin is released into the brain. The results can help open up new paths in the treatment of trauma patients. The study has been published in the current edition of the Journal of Neuroscience.

Feelings of anxiety very effectively prevent people from getting into situations that are too dangerous. Those who have had a terrible experience initially tend to avoid the place of tragedy out of fear. If no other oppressive situation arises, normally the symptoms of fear gradually subside. “The memory of the terrible events is not just erased.” states first author, PD Dr. Andras Bilkei Gorzo, from the Institute for Molecular Psychiatry at the University of Bonn. “Those impacted learn rather via an active learning process that they no longer need to be afraid because the danger has passed.” But following extreme psychical stress resulting from wars, hostage-takings, accidents or catastrophes chronic anxiety disorders can develop which even after months don’t subside.

Body’s own dynorphin weakens fears

Why is it that in some people terrible events are deeply engraved in their memory, while after a while others seem to have completely put aside any anxiety related to the incident? Scientists in the fields of psychiatry, molecular psychiatry and radiology at the University of Bonn are all involved in probing this issue. “We were able to demonstrate by way of a series of experiments that dynorphin plays an important role in weakening anxiety,” says Prof. Dr. Andreas Zimmer, Director of the Institute for Molecular Psychiatry at the University of Bonn. The substance group in question is opiods which also includes, for instance, endorphins. The latter are released by the body of athletes and have an analgesic and euphoric effect. The reverse, however, is true of dynorphins: They are known for putting a damper on emotional moods.

Mice with disabled gene exhibit persistent anxiety

The team working with Prof. Zimmer tested the exact impact of dynorphins on the brain using mice whose gene for the formation of this substance had been disabled. After being exposed to a brief and unpleasant electric shock, the animals exhibited persistent anxiety symptoms, even if they hadn’t been confronted with the negative stimulus over a longer time. Mice exhibiting a normal amount of released dynorphin were anxious to begin with as well, but the symptoms quickly subsided. “This behavior is the same in humans: If you burn your hand on the stove once, you don’t forget the incident that quickly,” explains Prof. Zimmer. “Learning vocabulary, on the other hand, typically tends to be more tedious because it’s not tied to emotions.”

Results are transferrable to people

Next the researchers showed that these results can be transferred to people. “We took advantage of the fact that people exhibit natural variations of the dynorphin gene that lead to different levels of this substance being released in the brain,” reports Prof. Dr. Henrik Walter, Director of the Research Area Mind and Brain at the Psychiatric University Clinic at the Charité in Berlin, who also used to perform research in this area at the University Clinic in Bonn. A total of 33 healthy probands were divided into two groups: One with the genetically stronger dynorphin release and the other which exhibits less gene activity.

Unpleasant stimulus leads to stress reactions in the probands

Equipped with computer glasses the probands observed blue and green squares which appeared and then disappeared again in a magnetic resonance tomograph (MRT). When the green square was visible the scientists repeatedly gave probands an unpleasant stimulus on the hand using a laser. Scientists were able to prove that these negative stimuli actually led to a stress reaction given the increased sweat on the skin. At the same time, researchers recorded the activities of various brain areas with the tomograph. After this conditioning stage came part two of the experiment: The researchers showed the colored squares without any unpleasant stimuli and recorded how long the stress reaction acquired earlier lasted. The next day the experiment was continued without the laser stimulus in an effort to monitor the longer-term development.

New paths in the treatment of trauma patients

It became apparent that, as in mice human, probands with lower gene activity for dynorphin exhibited stress reactions lasting considerably longer than those probands who released considerably more. Moreover, in brain scans it could be observed that the amygdala – a brain structure in the temporal lobes that processes emotional contents - was also active even if in later testing rounds a green square was shown without the subsequent laser stimulus.

“After the negative laser stimulus stopped this amygdala activity gradually became weaker. This means that the acquired anxiety reaction to the stimulus was forgotten,” reports Prof. Walter. This effect was not as pronounced in the group with less dynorphin activity and prolonged anxiety. “But the ‘forgetting’ of acquired anxiety reactions isn’t a fading, but, rather, an active process which involves the ventromedial prefrontal cortex,” emphasizes Prof. Walter. To corroborate this, researchers found that in the group with less dynorphin activity there was reduced coupling between the prefrontal cortex and the amygdala. “In all likelihood dynorphins affect fear forgetting in a crucial way through this structure,” says Prof. Walter. The scientists now hope that by using the results they will be able to develop long-term approaches for new strategies when it comes to the treatment of trauma patients.

Provided by University of Bonn

Source: medicalxpress.com

ScienceDaily (July 5, 2012) — A gene whose mutation results in malformed faces and skulls as well as mental retardation has been found by scientists.

They looked at patients with Potocki-Shaffer syndrome, a rare disorder that can result in significant abnormalities such as a small head and chin and intellectual disability, and found the gene PHF21A was mutated, said Dr. Hyung-Goo Kim, molecular geneticist at the Medical College of Georgia at Georgia Health Sciences University.

The scientists confirmed PHF21A’s role by suppressing it in zebrafish, which developed head and brain abnormalities similar to those in patients. “With less PHF21A, brain cells died, so this gene must play a big role in neuron survival,” said Kim, lead and corresponding author of the study published in The American Journal of Human Genetics. They reconfirmed the role by giving the gene back to the malformed fish — studied for their adeptness at regeneration — which then became essentially normal. They also documented the gene’s presence in the craniofacial area of normal mice.

While giving the normal gene unfortunately can’t cure patients as it does zebrafish, the scientists believe the finding will eventually enable genetic screening and possibly early intervention during fetal development, including therapy to increase PHF21A levels, Kim said. It also provides a compass for learning more about face, skull and brain formation.

The scientists zeroed in on the gene by using a distinctive chromosomal break found in patients with Potocki-Shaffer syndrome as a starting point. Chromosomes — packages of DNA and protein — aren’t supposed to break, and when they do, it can damage genes in the vicinity.

"We call this breakpoint mapping and the breakpoint is where the trouble is," said Dr. Lawrence C. Layman, study co-author and Chief of the MCG Section of Reproductive Endocrinology, Infertility and Genetics. Damaged genes may no longer function optimally; in PHF21A’s case it’s about half the norm.

"When you see the chromosome translocation, you don’t know which gene is disrupted," Layman said. "You use the break as a focus then use a bunch of molecular techniques to zoom in on the gene." Causes of chromosomal breaks are essentially unknown but likely are environmental and/or genetic, Kim said.

Little was known about PHF21A other than its role in determining how tightly DNA is wound in a package with proteins called histones. How tightly DNA is wound determines whether proteins called transcription factors have the access needed to regulate gene expression, which is important, for example, when a gene needs to be expressed only at a specific time or tissue. PHF21A is believed to primarily work by suppressing other genes, for example, ensuring that genes that should be expressed only in brain cells don’t show up in other cell types, Kim said.

Next steps include using PHF21A as a sort of geographic positioning system to identify other “depressor” genes it regulates then screening patients to look for mutations in those genes as well. “We want to find other people with different genes causing the same problem,” Layman said, and they suspect the genes PHF21A interacts with or regulates are the most likely suspects. It’s too early to know what percentage of Potocki-Shaffer syndrome patients have the PHF21A mutation, Kim noted. “Now that we know the causative gene, we can sequence the gene in more patients and see if they have a mutation,” Layman said.

They also want to look at less-severe forms of mental deficiency, including autism, for potentially milder mutations of PHF21A. More than a dozen of the 25,000 human genes are known to cause craniofacial defects and mental retardation, which often occur together, Kim said.

Source: Science Daily

ScienceDaily (July 5, 2012) — Sensory substitution devices (SSDs) use sound or touch to help the visually impaired perceive the visual scene surrounding them. The ideal SSD would assist not only in sensing the environment but also in performing daily activities based on this input. For example, accurately reaching for a coffee cup, or shaking a friend’s hand. In a new study, scientists trained blindfolded sighted participants to perform fast and accurate movements using a new SSD, called EyeMusic. Their results are published in the July issue of Restorative Neurology and Neuroscience.

Left: An illustration of the EyeMusic SSD, showing a user with a camera mounted on the glasses, and scalp headphones, hearing musical notes that create a mental image of the visual scene in front of him. He is reaching for the red apple in a pile of green ones. Top right: close-up of the glasses-mounted camera and headphones; bottom right: hand-held camera pointed at the object of interest. (Credit: Maxim Dupliy, Amir Amedi and Shelly Levy-Tzedek)

The EyeMusic, developed by a team of researchers at the Hebrew University of Jerusalem, employs pleasant musical tones and scales to help the visually impaired “see” using music. This non-invasive SSD converts images into a combination of musical notes, or “soundscapes.”

The device was developed by the senior author Prof. Amir Amedi and his team at the Edmond and Lily Safra Center for Brain Sciences (ELSC) and the Institute for Medical Research Israel-Canada at the Hebrew University. The EyeMusic scans an image and represents pixels at high vertical locations as high-pitched musical notes and low vertical locations as low-pitched notes according to a musical scale that will sound pleasant in many possible combinations. The image is scanned continuously, from left to right, and an auditory cue is used to mark the start of the scan. The horizontal location of a pixel is indicated by the timing of the musical notes relative to the cue (the later it is sounded after the cue, the farther it is to the right), and the brightness is encoded by the loudness of the sound.

The EyeMusic’s algorithm uses different musical instruments for each of the five colors: white (vocals), blue (trumpet), red (reggae organ), green (synthesized reed), yellow (violin); Black is represented by silence. Prof. Amedi mentions that “The notes played span five octaves and were carefully chosen by musicians to create a pleasant experience for the users.” Sample sound recordings are available at http://brain.huji.ac.il/em/.

"We demonstrated in this study that the EyeMusic, which employs pleasant musical scales to convey visual information, can be used after a short training period (in some cases, less than half an hour) to guide movements, similar to movements guided visually," explain lead investigators Drs. Shelly Levy-Tzedek, an ELSC researcher at the Faculty of Medicine, Hebrew University, Jerusalem, and Prof. Amir Amedi. "The level of accuracy reached in our study indicates that performing daily tasks with an SSD is feasible, and indicates a potential for rehabilitative use."

The study tested the ability of 18 blindfolded sighted individuals to perform movements guided by the EyeMusic, and compared those movements to those performed with visual guidance. At first, the blindfolded participants underwent a short familiarization session, where they learned to identify the location of a single object (a white square) or of two adjacent objects (a white and a blue square).

In the test sessions, participants used a stylus on a digitizing tablet to point to a white square located either in the north, the south, the east or the west. In one block of trials they were blindfolded (SSD block), and in the other block (VIS block) the arm was placed under an opaque cover, so they could see the screen but did not have direct visual feedback from the hand. The endpoint location of their hand was marked by a blue square. In the SSD block, they received feedback via the EyeMusic. In the VIS block, the feedback was visual.

"Participants were able to use auditory information to create a relatively precise spatial representation," notes Dr. Levy-Tzedek.

The study lends support to the hypothesis that representation of space in the brain may not be dependent on the modality with which the spatial information is received, and that very little training is required to create a representation of space without vision, using sounds to guide fast and accurate movements. “SSDs may have great potential to provide detailed spatial information for the visually impaired, allowing them to interact with their external environment and successfully make movements based on this information, but further research is now required to evaluate the use of our device in the blind ” concludes Dr. Levy-Tzedek. These results demonstrate the potential application of the EyeMusic in performing everyday tasks — from accurately reaching for the red (but not the green!) apples in the produce aisle, to, perhaps one day, playing a Kinect / Xbox game.

Source: Science Daily

July 5, 2012

Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal Cell have now mapped out the signals that travel between your gut and your brain to generate the feeling of satiety after eating a protein-rich meal. Understanding this back and forth loop between the brain and gut may pave the way for future approaches in the treatment and/or prevention of obesity.

Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal Cell have now mapped out the signals that travel between your gut and your brain to generate the feeling of satiety after eating a protein-rich meal. Understanding this back and forth loop between the brain and gut may pave the way for future approaches in the treatment and/or prevention of obesity. Credit: Duraffourd et al., Cell

Food intake can be modulated through mu-opioid receptors (MORs, which also bind morphine) on nerves found in the walls of the portal vein, the major blood vessel that drains blood from the gut. Specifically, stimulating the receptors enhances food intake, while blocking them suppresses intake. Investigators have now found that peptides, the products of digested dietary proteins, block MORs, curbing appetite. The peptides send signals to the brain that are then transmitted back to the gut to stimulate the intestine to release glucose, suppressing the desire to eat.

Mice that were genetically engineered to lack MORs did not carry out this release of glucose, nor did they show signs of ‘feeling full’, after eating high-protein foods. Giving them MOR stimulators or inhibitors did not affect their food intake, unlike normal mice.

Because MORs are also present in the neurons lining the walls of the portal vein in humans, the mechanisms uncovered here may also take place in people.

"These findings explain the satiety effect of dietary protein, which is a long-known but unexplained phenomenon,” says senior author Dr. Gilles Mithieux of the Université de Lyon, in France. “They provide a novel understanding of the control of food intake and of hunger sensations, which may offer novel approaches to treat obesity in the future,” he adds.

Provided by Cell Press

Source: medicalxpress.com