Posts tagged science
Articles and news from the latest research reports.
Is sexual addiction the real deal?
Controversy exists over what some mental health experts call “hypersexuality,” or sexual “addiction.” Namely, is it a mental disorder at all, or something else? It failed to make the cut in the recently updated Diagnostic and Statistical Manual of Mental Disorders, or DSM-5, considered the bible for diagnosing mental disorders. Yet sex addiction has been blamed for ruining relationships, lives and careers.
Now, for the first time, UCLA researchers have measured how the brain behaves in so-called hypersexual people who have problems regulating their viewing of sexual images. The study found that the brain response of these individuals to sexual images was not related in any way to the severity of their hypersexuality but was instead tied only to their level of sexual desire.
In other words, hypersexuality did not appear to explain brain differences in sexual response any more than simply having a high libido, said senior author Nicole Prause, a researcher in the department of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA.
"Potentially, this is an important finding," Prause said. "It is the first time scientists have studied the brain responses specifically of people who identify as having hypersexual problems."
The study appears in the current online edition of the journal Socioaffective Neuroscience and Psychology.
A diagnosis of hypersexuality or sexual addiction is typically associated with people who have sexual urges that feel out of control, who engage frequently in sexual behavior, who have suffered consequences such as divorce or economic ruin as a result of their behaviors, and who have a poor ability to reduce those behaviors.
But, said Prause and her colleagues, such symptoms are not necessarily representative of an addiction — in fact, non-pathological, high sexual desire could also explain this cluster of problems.
One way to tease out the difference is to measure the brain’s response to sexual-image stimuli in individuals who acknowledge having sexual problems. If they indeed suffer from hypersexuality, or sexual addiction, their brain response to visual sexual stimuli could be expected be higher, in much the same way that the brains of cocaine addicts have been shown to react to images of the drug in other studies.
The study involved 52 volunteers: 39 men and 13 women, ranging in age from 18 to 39, who reported having problems controlling their viewing of sexual images. They first filled out four questionnaires covering various topics, including sexual behaviors, sexual desire, sexual compulsions, and the possible negative cognitive and behavioral outcomes of sexual behavior. Participants had scores comparable to individuals seeking help for hypersexual problems.
While viewing the images, the volunteers were monitored using electroencephalography (EEG), a non-invasive technique that measures brain waves, the electrical activity generated by neurons when they communicate with each other. Specifically, the researchers measured event-related potentials, brain responses that are the direct result of a specific cognitive event.
"The volunteers were shown a set of photographs that were carefully chosen to evoke pleasant or unpleasant feelings," Prause said. "The pictures included images of dismembered bodies, people preparing food, people skiing — and, of course, sex. Some of the sexual images were romantic images, while others showed explicit intercourse between one man and one woman."
The researchers were most interested in the response of the brain about 300 milliseconds after each picture appeared, commonly called the “P300” response. This basic measure has been used in hundreds of neuroscience studies internationally, including studies of addiction and impulsivity, Prause said. The P300 response is higher when a person notices something new or especially interesting to them.
The researchers expected that P300 responses to the sexual images would correspond to a person’s sexual desire level, as shown in previous studies. But they further predicted that P300 responses would relate to measures of hypersexuality. That is, in those whose problem regulating their viewing of sexual images could be characterized as an “addiction,” the P300 reaction to sexual images could be expected to spike.
Instead, the researchers found that the P300 response was not related to hypersexual measurements at all; there were no spikes or decreases tied to the severity of participants’ hypersexuality. So while there has been much speculation about the effect of sexual addiction or hypersexuality in the brain, the study provided no evidence to support any difference, Prause said.
"The brain’s response to sexual pictures was not predicted by any of the three questionnaire measures of hypersexuality," she said. "Brain response was only related to the measure of sexual desire. In other words, hypersexuality does not appear to explain brain responses to sexual images any more than just having a high libido."
But debate continues over whether sex addiction is indeed an addiction. A study published in 2012 by Prause’s colleague Rory Reid, a UCLA assistant professor of psychiatry, supported the reliability of the proposed DSM-5 diagnostic criteria for hypersexual disorder. However, Prause notes, that study was not focused on the validity of sex addiction or impulsivity, and did not use any biophysiological data in the analysis.
"If our study can be replicated," she said, "these findings would represent a major challenge to existing theories of a sex ‘addiction.’ "
(Source: newsroom.ucla.edu)
Gene mutation in dogs offers clues for neural tube defects in humans
A gene related to neural tube defects in dogs has for the first time been identified by researchers at the University of California, Davis, and University of Iowa.
The researchers also found evidence that the gene may be an important risk factor for human neural tube defects, which affect more than 300,000 babies born each year around the world, according to the U.S. Centers for Disease Control and Prevention. Neural tube defects, including anencephaly and spina bifida, are caused by the incomplete closure or development of the spine and skull.
The new findings appear this week in the journal PLOS Genetics.
“The cause of neural tube defects is poorly understood but has long been thought to be associated with genetic, nutritional and environmental factors,” said Noa Safra, lead author on the study and a postdoctoral fellow in the laboratory of Professor Danika Bannasch in the UC Davis School of Veterinary Medicine.
She noted that dogs provide an excellent biomedical model because they receive medical care comparable to what humans receive, share in a home environment and develop naturally occurring diseases that are similar to those found in humans. More specifically, several conditions associated with neural-tube defects are known to occur naturally in dogs. All DNA samples used in the study were taken from household pets, rather than laboratory animals, Safra said.
She and colleagues carried out genome mapping in four Weimaraner dogs affected by spinal dysraphism, a naturally occurring spinal-cord disorder, and in 96 such dogs that had no neural tube defects. Spinal dysraphism, previously reported in the Weimaraner breed, causes symptoms that include impaired motor coordination or partial paralysis in the legs, abnormal gait, a crouched stance and abnormal leg or paw reflexes.
Analysis of a specific region on canine chromosome eight led the researchers to a mutation in a gene called NKX2-8, one of a group of genes known as “homeobox genes,” known to be involved with regulating patterns of anatomical development in the embryo.
The researchers determined that the NKX2-8 mutation occurred in the Weimaraner breed with a frequency of 1.4 percent — 14 mutations in every 1,000 dogs.
Additionally, they tested nearly 500 other dogs from six different breeds that had been reported to be clinically affected by neural tube defects, but did not find copies of the NKX2-8 gene mutation among the non-Weimaraner dogs.
“The data indicate that this mutation does not appear as a benign mutation in some breeds, while causing defects in other breeds,” Safra said. “Our results suggest that the NKX2-8 mutation is a ‘private’ mutation in Weimaraners that is not shared with other breeds.”
The researchers say that identification of such a breed-specific gene may help veterinarians diagnose spinal dysraphism in dogs and enable Weimaraner breeders to use DNA screening to select against the mutation when developing their breeding plans.
In an effort to investigate a potential role for the NKX2-8 mutation in cases of neural tube defects in people, the researchers also sequenced 149 unrelated samples from human patients with spina bifida. They found six cases in which the patients carried mutations of the NKX2-8 gene but stress that further studies are needed to confirm whether these mutations are responsible for the diagnosed neural tube defects.
(Source: news.ucdavis.edu)
Haste and waste on neuronal pathways
Researchers of the Department of Biosystems Science and Engineering of ETH Zurich were able to measure the speed of neuronal signal conduction along segments of single axons in neuronal cultures by using a high-resolution electrical method. The bioengineers are now searching for plausible explanations for the large conduction speed variations.
To write this little piece of text, the brain sends commands to arms and fingers to tap on the keyboard. Neuronal cells with their cable-like extensions, such as axons, transfer this information as electrical pulses that trigger muscles to move. The axonal signal speed can be to up to 100m/s in myelinated axons along the spinal cord. For a long time, scientists assumed that axonal signal conduction is by and large digital: either there is a signal, “1”, or there is no signal, “0”.
Strong propagation speed variations
Now, a team of researchers under Douglas Bakkum and Andreas Hierlemann at the Department BSSE of ETH Zurich in Basel presents evidence that there may be more to axons than only digital signal conduction. They could directly measure and demonstrate that the speed of an axonal signal varies considerably within different segments of the very same axon by placing hundreds of electrodes along the axon. Moreover, the velocity pattern changed from day to day or within hours as did the morphology and position of the axon.
The exact meaning of these speed variations and the origin cannot be explained yet, as there is too little information available about axonal conduction. This may, to a large part, be a consequence of the tiny diameter of the axons. The length of an axon can be more than a meter, e.g., in the spinal cord, but the average diameter is in between 80 nm and a few micrometers. This small diameter makes any measurement of axonal potentials difficult, which, of course, also renders establishing the mechanisms that may produce the large speed variations a difficult task.
Unclear cause
Up to now, only hypotheses concerning these speed variations exist. The temporal characteristics of axonal conduction may form part of the overall information processing abilities of ensembles of neurons or contribute to how neurons adapt to new information. The research group plans on further investigating these effects in collaboration with researchers in other disciplines and research institutions that have complementary expertise and technologies. The related research work is also facilitated through Hierlemann’s 5-year ERC Advanced Grant and Bakkum’s SNF Ambizione Grant awarded in 2010/2011. However, the researchers do not expect a fast elucidation of the axonal speed variations. Considering the small dimensions of axons, it will probably take years to collect conclusive evidence.
Up to now, a detailed and long-term investigation of signals of ensembles of neurons and their axons was hardly possible. The BSSE research group, during the last 10 years, devoted a lot of time and efforts to develop the high-resolution microelectronic chips, hosting thousands of microelectrodes. The now published, detailed and precise axonal propagation speed measurements reward the scientists for their investment and validate the approach. “We hope to acquire important new evidence with our technology,” they state. Other technologies have not yet provided a high enough spatio-temporal resolution to characterize details of axonal signal conduction.
High-resolution chip developed
The microelectrode array chip of the BSSE research group has 11’000 electrodes within a very small area (3150 electrodes per square millimeter) that record from or stimulate neuronal cells or ensembles. Data from 126 arbitrarily selectable electrodes can be simultaneously recorded by means of custom-developed on-chip microelectronic circuits. The neuronal cells grow directly atop the circuitry units on the microelectronic chip, which is fabricated in industrial complementary-metal-oxide-semiconductor (CMOS) technology. Signals traveling along the axons of the neurons can be measured and localized at high spatial and temporal resolution, owing to the small electrode diameter and tight electrode spacing. Moreover, electrodes can be used to stimulate single axons with the aim to evoke action potentials that propagate back to the respective cell body or soma and elicit action potentials there.
In his opinion, the neuroscience community has underestimated the potential of microelectrodes arrays for quite some time, says Prof. Hierlemann. With the work published now in “Nature Communications”, he hopes to further establish this method. “These results show that the microelectrode array technology is enabling access to data that are currently not accessible through other technologies,” says the bioengineer.
Neurons, axons and signal propagation
Nerve cells or neurons communicate with other neurons via electrical and chemical signals. If an electrical signal within a cell body, close to the axon initial segment, is large enough, it enters the axon and propagates along its length at a high speed. This is achieved by alterations in the so-called resting potential of the axon membrane, which usually has a steady negative value. Sodium ion channels open, and because of a concentration gradient, positively charged sodium ions from outside the axon travel into the axon. As a consequence, the membrane potential is briefly reversed in polarity until potassium channels open and positively charged potassium ions are released into the external liquid. This brief change in membrane potential, a so-called action potential, can be detected with the microelectrode array chip. An action potential travels without attenuation to synapses, neuron-to-neuron junctions, where the electrical signal is translated into a chemical signal: neurotransmitters are released, diffuse through the small synaptic cleft and initiate electrical activity in the neighboring postsynaptic cell. After an action potential event, the original sodium and potassium ion concentrations outside and inside of the axonal membrane and the associated resting potential across the membrane are restored through membrane pumps. The overall duration of an action potential event is on the order of 2 milliseconds.
Reference
Bakkum DJ, Frey U, Radivojevic M, Russell TL, Müller J, Fiscella M, Takahashi H & Hierlemann A. Tracking axonal action potential propagation on a high-density microelectrode array across hundreds of sites. Nature Communications, first published online 19th July 2013. DOI: 10.1038/ncomms3181
Movement without muscles study in insects could inspire robot and prosthetic limb developments
Neurobiologists from the University of Leicester have shown that insect limbs can move without muscles – a finding that may provide engineers with new ways to improve the control of robotic and prosthetic limbs.
Their work helps to explain how insects control their movements using a close interplay of neuronal control and ‘clever biomechanical tricks,’ says lead researcher Dr Tom Matheson, a Reader in Neurobiology at the University of Leicester.
In a study published today in the journal Current Biology, the researchers show that the structure of some insect leg joints causes the legs to move even in the absence of muscles. So-called ‘passive joint forces’ serve to return the limb back towards a preferred resting position.
The passive movements differ in limbs that have different behavioural roles and different musculature, suggesting that the joint structures are specifically adapted to complement muscle forces. The researchers propose a motor control scheme for insect limb joints in which not all movements are driven by muscles.
The study was funded by the Biotechnology and Biological Sciences Research Council (BBSRC), The Royal Society, and the Heinrich Hertz-Foundation of the German State of North Rhine-Westphalia.
Dr Matheson, of the Department of Biology, said:
“It is well known that some animals store energy in elastic muscle tendons and other structures. Such energy storage permits forces to be applied explosively to generate movements that are much more rapid than those which may be generated by muscle contractions alone. This is, for example, crucial when grasshoppers or fleas jump.
“This University of Leicester study provides a new insight into the ways that energy storage mechanisms can operate in a much wider range of movements.
“Our work set out to identify how the biomechanical properties of the limbs of a range of insects influence relatively slow movements such as those that occur during walking, scratching or climbing. The surprising result was that although some movements are influenced by properties of the muscles and tendons, other movements are generated by forces that arise from within the joints themselves.
“Even when we removed all of the muscles and associated tissues from a particular joint at the ‘knee’ of a locust, the lower part of the limb (the tibia) still moved back towards a midpoint from extended angles.”
Dr Matheson said that it was known from previous studies that some movements can be generated by spring-like properties of limbs, but the team was surprised to find passive forces that contribute to almost all movements made by the limbs that were studied - not just the highly specialised rapid movements needed to propel powerful jumps and kicks.
“We expected the forces to be generated within the muscles of the leg, but found that some continued to occur even when we detached both muscles – the extensor and the flexor tibiae – from the tibia.
“In the locust hind leg, which is specialised for jumping and kicking, the extensor muscle is much larger and stronger than the antagonist flexor muscle. This enables the animal to generate powerful kicks and jumps propelled by extensions of the tibia that are driven by contractions of the extensor muscle. When locusts prepare to jump, large amounts of energy generated by the extensor muscle are stored in the muscle’s tendon and in the hard exoskeleton of the leg.
“Surprisingly, we noticed that when the muscles were removed, the tibia naturally flexed back towards a midpoint, and we hypothesised that these passive return movements might be counterbalancing the strong extensor muscle.”
Jan M. Ache, a Masters student from the Department of Animal Physiology at the University of Cologne who worked in Matheson’s lab and is the first author on the paper, continues: “To test this idea we looked at the literature and examined other legs where the extensor and flexor muscles are more closely balanced in size or strength, or where the flexor is stronger than the extensor.
“We found that the passive joint forces really do counterbalance the stronger of the flexor or extensor muscle in the animals and legs we looked at. In the horsehead grasshopper, for example, passive joint forces even differ between the middle legs (which are primarily used for walking) and the hind legs (which are adapted for jumping), even in the same individual animal. In both pairs of legs, the passive joint forces support the weaker muscle.
“This could be very important for the generation of movements in insects because the passive forces enable a transfer of energy from the stronger to the weaker muscle.”
This work helps to explain how insects control their movements using a close interplay of neuronal control and clever biomechanical tricks. Using balanced passive forces may provide engineers with new ways to improve the control of robotic and prosthetic limbs, say the researchers.
Dr Matheson concluded: “We hope that our work on locusts and grasshoppers will spur a new understanding of how limbs work and can be controlled, by not just insects, but by other animals, people, and even by robots.”
No oxytocin benefit for autism
The so-called trust hormone, oxytocin, may not improve the symptoms of children with autism, a large study led by UNSW researchers has found.
Professor Mark Dadds, of the UNSW School of Psychology, says previous research suggested that oxytocin – a hormone with powerful effects on brain activity linked to the formation of social bonds – could have benefits for children with the disorder.
“Many parents of children with autism are already obtaining and using oxytocin nasal spray with their child, and clinical trials of the spray’s effects are underway all over the world. Oxytocin has been touted as a possible new treatment, but its effects may be limited,” Professor Dadds says.
Autism is a complex condition of unknown cause in which children exhibit reduced interest in other people, impaired social communication skills and repetitive behaviours.
To determine its suitability as a general treatment Professor Dadds’ team conducted a randomised controlled clinical trial of 38 boys aged between seven and 16 years of age with autism. Half were given a nasal spray of oxytocin on four consecutive days.
The study has been accepted for publication in the Journal of Autism and Developmental Disorders.
“We found that, compared to a placebo, oxytocin did not significantly improve emotion recognition, social interaction skills, repetitive behaviours, or general behavioural adjustment,” says Professor Dadds.
“This is in contrast to a handful of previous smaller studies which have shown some positive effects on repetitive behaviours, social memory and emotion processing.
“These studies, however, were limited by having small numbers of participants and/or by looking at the effects of single doses of oxytocin on specific behaviours or cognitive effects while the participants had the oxytocin in their system.
“The results of our much larger study suggest caution should be exercised in recommending nasal oxytocin as a general treatment for young people with autism.”
The boys in the new study were assessed twice before treatment, three times during the treatment week, immediately afterwards and three months later, with a parent present. Factors such as eye contact with the parent, responsiveness, warmth, speech, positive body language, repetitive behaviours, and recognition of facial emotions were observed.
Research in people who are healthy shows oxytocin can increase levels of trust and eye-gazing and improve their identification of emotions in others.
One likely possibility is that many children with autism have impaired oxytocin receptor systems that do not respond properly, Professor Dadds says. But there may be a subgroup of children for whom oxytocin could be beneficial, and research is needed to determine who responds to it and how best to deliver it.
(Source: newsroom.unsw.edu.au)
Ultrasensitive Calcium Sensors Shine New Light on Neuron Activity
A new protein engineered by scientists at the Janelia Farm Research Campus fluoresces brightly each time it senses calcium, giving the scientists a way to visualize neuronal activity. The new protein is the most sensitive calcium sensor ever developed and the first to allow the detection of every neural impulse.
Every time you say a word, take a step, or read a sentence, a collection of neurons sends a speedy relay of messages throughout your brain to process the information. Now, researchers have a new way of watching those messages in action, by watching each cell in the chain light up when it fires.
When a neuron receives a signal from one of its neighbors, the impulse sets off a sudden series of electrochemical events geared toward passing the message along. Among the first events: calcium ions rush into the neurons when a set of channels opens. Scientists at the Howard Hughes Medical Institute’s Janelia Farm Research Campus have engineered a new protein that brightly fluoresces each time it senses these calcium waves, giving the scientists a way to visualize the activity of every neuron throughout the brain. The new protein is the most sensitive calcium sensor ever developed and the first to allow the detection of every neural impulse, rather than just a portion. The results are reported in the July 18, 2013 issue of the journal Nature.
“You can think of the brain as an orchestra with each different neuron type playing a different part,” says Janelia lab head Karel Svoboda, a neurobiologist and member of the team that developed the new sensor. “Previous methods only let us hear a tiny fraction of the melodies. Now we can hear more of the symphony at once. Improving the molecule and imaging methods in the future could allow us to hear the entire symphony.”
Detecting which neurons in the brain are firing, and when, is a key step in learning which areas of the brain are linked to particular activities or disorders, how memories are formed, how behaviors are learned, and basic questions about how the brain organizes neurons and stores information in this organization.
Two decades ago, scientists who wanted to use calcium to pinpoint neural activity relied on synthetic calcium-indicator dyes, first developed by HHMI Investigator Roger Tsien. The dyes lit up when neurons fired, but were difficult to inject and highly toxic—an animal’s brain could only be imaged once using the dyes.
In 1997, researchers led by Tsien developed the first genetically encoded calcium indicator (GECI). GECIs were made by combining a gene for a calcium sensor with the gene for a fluorescent protein in a way that made the calcium sensor fluoresce when it bound calcium. The GECI genes could be integrated into the genomes of model organisms like mice or flies so that no dye injection was necessary. The animals’ own brain cells would produce the proteins throughout their lives, and brain activity could be studied again and again in any one animal, allowing long-term studies of processes like learning and development. But GECIs weren’t as accurate as the cumbersome dyes had been, and improving them was a slow process.
“New versions were developed in a very piecemeal way,” says Svoboda, explaining that after chemists developed the sensors, it might be years before biologists had an opportunity to test them in the brains of living animals. “It was a very slow process of getting feedback.”
Svoboda, along with Janelia lab heads Loren Looger, Vivek Jayaraman and Rex Kerr formed the Genetically Encoded Neural Indicator and Effector (GENIE) project at Janelia to speed up the innovation. The GENIE project, led by Douglas Kim, an HHMI program scientist, is one of several collaborative team projects online at Janelia. The project developed a higher-throughput and more accurate way of testing new variants of the best-working GECI, called GCaMP. Steps included simple tests that could easily be performed on many proteins at once, like measuring how much fluorescence the protein gave off when exposed to calcium in a cuvette, as well as early tests of function in different types of neurons and final experiments in genetically engineered mice, flies, and zebrafish.
“When people developed previous GECIs, they would test somewhere between ten and twenty variants very carefully. We were able to screen a thousand in a highly quantitative neuronal assay,” Looger says. “And when you can look at that many constructs, you’re going to make better and more interesting observations on what makes the ideal sensor.”
The team made successive rounds of tweaks to the structure of the GCaMP so that it accurately sensed calcium, shone brightly in response, and worked in model organisms. After that work they settled upon a version of the sensor that performed better in all aspects than previous GECIs. Their new sensor, dubbed GCaMP6, produced signals seven times stronger than past versions. Surprisingly, its sensitivity even outperformed synthetic dyes.
“People had assumed that the synthetic dyes were letting us see every event in neurons,” says Looger. “But we’ve now shown that not only are these dyes hard to load and quite toxic, but they weren’t even recording every event.”
GCaMP6 will be a boon to researchers at Janelia, and around the world, who want to get a full picture of the activity of every neuron in the brain. Meanwhile, the team plans to continue to continue to improve it, developing entirely new versions for specific uses. For example, they hope to make a GECI that gives off red fluorescence rather than green, because red is easier to see in deeper tissues.
“One of the stated goals of Janelia Farm is to develop an atlas of every neuron in the Drosophila brain,” says Looger. “The most practical way I can think of to assign functions to such an atlas is with calcium sensors. With this new sensor, I think people will feel much more comfortable that they’re really getting all the information they can.”
Scientists Develop New Way to Measure Cumulative Effect of Head Hits in Football
Scientists at Wake Forest Baptist Medical Center have developed a new way to measure the cumulative effect of impacts to the head incurred by football players.
The metric, called Risk Weighted Cumulative Exposure (RWE), can capture players’ exposure to the risk of concussion over the course of a football season by measuring the frequency and magnitude of all impacts, said senior author of the study Joel Stitzel, Ph.D., chair of biomedical engineering at Wake Forest Baptist and associate head of the Virginia Tech - Wake Forest University School of Biomedical Engineering and Sciences.
The study is published in the current online edition of the Annals of Biomedical Engineering.
Based on data gathered throughout a season of high school football games and practices, the researchers used RWE to measure the cumulative risk of injury due to linear and rotational acceleration separately, as well as the combined probability of injury associated with both.
“This metric gives us a way to look at a large number of players and the hits they’ve incurred while playing football,” Stitzel said. “We know that young players are constantly experiencing low-level hits that don’t cause visible injury, but there hasn’t been a good way to measure the associated risk of concussion.”
Concussion is the most common sports-related head injury, with football players having the highest rate among high school athletes, according to the study. It is estimated that nearly 1.1 million students play high school football in the United States. However, research on the biomechanics of football-related head impacts traditionally has concentrated on the collegiate level rather than on the high school level.
With such a large number of players in the sport, it is critical to understand the risk associated with different levels of impact and accurately estimate cumulative concussion risk over the course of a practice, game, season or lifetime, Stitzel said.
In the Wake Forest Baptist study, the researchers measured the head impact exposure in 40 high school football players by using sensors placed in their helmets to record linear and rotational acceleration. A total of 16,502 impacts were collected over the course of one football season and the data were analyzed as a group and as individual players.
Impacts were weighted according to the associated risk from linear acceleration and rotational acceleration alone, as well as to the combined probability of injury associated with both. This is an improved method of capturing the cumulative effects from each impact because it accounts for nonlinear relationships between impact magnitude and the associated risk of injury, Stitzel said.
“All hits involve both linear and rotational acceleration, but rotation coveys the idea that your head is pivoting about the neck whereas linear acceleration is experienced from a direct blow in more of a straight line through the center of mass of the head,” Stitzel said.
The median impact for each player ranged from 15.2 to 27.0 g, with an average value of 21.7 g, which shows the wide variability in the force of impacts.
The study found that impact frequency was greater during games (15.5) than during practices (9.4). However, overall exposure over the course of the season was greater during practices.
This information may help teams reduce exposure to head impacts during practices by teaching proper tackling techniques that could reduce exposure to impacts that may result in a higher concussion rate, the researchers reported.
Additionally, the study found a wide variation in player exposure within the team, with a 22-fold variation in the exposure per impact for practices and a 47-fold variation in the exposure for impact for games.
Studies like this are vital to understanding the biomechanical basis of head injuries related to football, Stitzel said. The metric fully captures a player’s exposure over the course of the season and will be used in conjunction with other pre- and post-season evaluations, including MRI and neurological tests conducted as part of this study.
The research team hopes that this work may ultimately improve helmet safety and design to make football a safer sport.
(Image: Getty Images)
Biochemical mapping helps explain who will respond to antidepressants
Duke Medicine researchers have identified biochemical changes in people taking antidepressants – but only in those whose depression improves. These changes occur in a neurotransmitter pathway that is connected to the pineal gland, the part of the endocrine system that controls the sleep cycle, suggesting an added link between sleep, depression and treatment outcomes. The study, published on July 17, 2013, in the journal PLOS ONE, uses an emerging science called pharmacometabolomics to measure and map hundreds of chemicals in the blood in order to define the mechanisms underlying disease and to develop new treatment strategies based on a patient’s metabolic profile.
"Metabolomics is teaching us about the differences in metabolic profiles of patients who respond to medication, and those who do not," said Rima Kaddurah-Daouk, PhD, associate professor of psychiatry and behavioral sciences at Duke Medicine and leader of the Pharmacometabolomics Research Network.
"This could help us to better target the right therapies for patients suffering from depression who can benefit from treatment with certain antidepressants, and identify, early on, patients who are resistant to treatment and should be placed on different therapies."
Major depressive disorder – a form of depression characterized by a severely depressed mood that persists two weeks or more – is one of the most prevalent mental disorders in the United States, affecting 6.7% of the adult population in a given year.
Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants for major depressive disorder, but only some patients benefit from SSRI treatment. Others may respond to placebo, while some may not find relief from either. This variability in response creates dilemmas for treating physicians where the only choice they have is to test one drug at a time and wait for several weeks to determine if a patient is going to respond to the specific SSRI.
Recent studies by the Duke team have used metabolomics tools to map biochemical pathways implicated in depression and have begun to distinguish which patients respond to treatment with an SSRI or placebo based on their metabolic profiles. These studies have pointed to several metabolites on the tryptophan metabolic pathway as potential contributing factors to whether patients respond to antidepressants.
Tryptophan is metabolized in different ways. One pathway leads to serotonin and subsequently to melatonin and an array of melatonin-like chemicals called methoxyindoles produced in the pineal gland. In the current study, the researchers analyzed levels of metabolites within branches of the tryptophan pathway and correlated changes with treatment outcomes.
Seventy-five patients with major depressive disorder were randomized to take sertraline (Zoloft) or placebo in the double-blind trial. After one week and four weeks of taking the SSRI or placebo, the researchers measured improvement in symptoms of depression to determine response to treatment, and blood samples were taken and analyzed using a metabolomics platform build to measure neurotransmitters.
The researchers observed that 60 percent of patients taking the SSRI responded to the treatment, and 50 percent of those taking placebo also responded. Several metabolic changes in the tryptophan pathway leading to melatonin and methoxyindoles were seen in patients taking the SSRI who responded to the treatment; these changes were not found in those who did not respond to the antidepressant.
The results suggest that serotonin metabolism in the pineal gland may play a role in the underlying cause of depression and its treatment outcomes, based on the biochemical changes that were seen to be associated with improvements in depression.
"This study revealed that the pineal gland is involved in mechanisms of recovery from a depressed state," said Kaddurah-Daouk. "We have started to map serotonin which is believed to be implicated in depression, but now realize that it may not be serotonin itself that is important in depression recovery. It could be metabolites of serotonin that are produced in the pineal gland that are implicated in sleep cycles.
"Shifting utilization of tryptophan metabolism from kynurenine to production of melatonin and other methoxyindoles seems important for treatment response but some patients do not have this regulation mechanism. We can now start to think about ways to correct this."
The identification of a metabolic signature for patients who have a milder form of depression and who can improve with use of placebo is critically important for streamlining clinical trials with antidepressants. The Duke team is the first to start to define in depth early biochemical effects of treatment with SSRI and placebo, and a molecular basis for why antidepressants take several weeks to start showing benefit.
In future studies, researchers may collect blood samples from patients during both the day and night to define how the circadian cycle, changes in sleep patterns, neurotransmitters and hormonal systems are modified in those who respond and do not respond to SSRIs and placebo. This can lead to more effective treatment strategies.
(Source: dukehealth.org)
Brain imaging study reveals our brains ‘divide and conquer’
University of Queensland (UQ) researchers have found human brains ‘divide and conquer’ when people learn to navigate around new environments.
The research by UQ’s Queensland Brain Institute (QBI) could provide hope for people with spatial memory impairments.
The study found that the mental picture people create to help navigate to a new location is split into two sections.
The size of the environment is coded by one area of the brain and its complexity is coded in another.
QBI postdoctoral research fellow and lead researcher Dr Oliver Baumann said the work shed new light on how learning the layout of a new environment, and then accessing this information from memory, was represented in the brain.
“We’ve known for some time that a part of the brain called the hippocampus is important for building and maintaining cognitive maps,” he said.
“The results of our study have shown for the first time that different aspects of a learned environment – specifically its size and complexity – are represented by distinct areas within the hippocampus.”
QBI Cognitive Neuroscience Laboratory Head Professor Jason Mattingley said the findings could have important implications for people suffering from spatial memory impairments.
“This research is important for understanding how our brain normally stores and manages spatial information,” Professor Mattingley said.
“It also gives us clues as to why people with memory loss due to Alzheimer’s disease often become lost in new or previously familiar surroundings.”
Dr Baumann said 18 people navigated their way through three virtual mazes that differed either in the number of corridors through which they could travel or the length of the corridors.
After learning the task, the participants were asked to recall mental maps from each of the mazes while their brain activity was measured using functional magnetic resonance imaging.
“We found that one region in the hippocampus was more active when participants recalled a complex maze in which there were many corridors to choose from, irrespective of the overall size of the maze,” Dr Baumann said.
“Conversely, we found that a separate area of the hippocampus was more active when the overall size of the maze increased, regardless of the number of corridors.”
The study, “Dissociable representations of environmental size and complexity in the human hippocampus”, is published in The Journal of Neuroscience.
(Image: iStockphoto)
Uncovering a Healthier Remedy for Chronic Pain
Physicians and patients who are wary of addiction to pain medication and opioids may soon have a healthier and more natural alternative.
A Duke University study revealed that a derivative of DHA (docosahexaenoic acid), a main ingredient of over-the-counter fish oil supplements, can sooth and prevent neuropathic pain caused by injuries to the sensory system. The results appear online in the Annals of Neurology.
The research focused on a compound called neuroprotectin D1=protectin D1 (NPD1=PD1), a bioactive lipid produced by cells in response to external stimuli. NPD1=PD1 is present in human white blood cells, and was first identified based on its ability to resolve abdominal and brain inflammation.
"These compounds are derived from omega-3 fatty acids found in fish oil, but are 1,000 times more potent than their precursors in reducing inflammation," said Ru-Rong Ji, professor of anesthesiology and neurobiology at Duke University Medical Center and principal investigator of the study.
The team used laboratory mouse models of nerve injuries to simulate pain symptoms commonly associated with post-surgical nerve trauma. They treated these animals with chemically synthesized NPD1=PD1, either through local administration or injection, to investigate whether the lipid compound could relieve these symptoms.
Their findings revealed that NPD1=PD1 not only alleviated the pain, but also reduced nerve swelling following the injuries. Its analgesic effect stems from the compound’s ability to inhibit the production of cytokines and chemokines, which are small signaling molecules that attract inflammatory macrophages to the nerve cells. By preventing cytokine and chemokine production, the compound protected nerve cells from further damage. NPD1=PD1 also reduced neuron firing so the injured animals felt less pain.
Ji believes that the new discovery has clinical potential. “Chronic pain resulting from major medical procedures such as amputation, chest and breast surgery is a serious problem,” he said. Current treatment options for neuropathic pain include gabapentin and various opioids, which may lead to addiction and destruction of the sensory nerves.
On the other hand, NPD1=PD1 can relieve neuropathic pain at very low doses and, more importantly, mice receiving the treatment did not show signs of physical dependence or enhanced tolerance toward the lipid compound.
"We hope to test this compound in clinical trials," Ji said. The initial stages of the trial could involve DHA administration through diet and injection. "DHA is very inexpensive, and can be converted to NPD1 by an aspirin-triggered pathway," he said. The ultimate goal is to develop a safer approach to managing chronic pain.