Posts tagged science

Posts tagged science

EEG Identifies Seizures in Hospital Patients
Electroencephalogram (EEG), which measures and records electrical activity in the brain, is a quick and efficient way of determining whether seizures are the cause of altered mental status (AMS) and spells, according to a study by scientists at the UC San Francisco.
The research, which focused on patients who had been given an EEG after being admitted to the hospital for symptoms such as AMS and spells, appears on March 27 in Mayo Clinic Proceedings.
“We have demonstrated a surprisingly high frequency of seizures – more than 7 percent – in a general inpatient population,” said senior investigator John Betjemann, MD, a UCSF assistant professor of neurology. “This tells us that EEG is an underutilized diagnostic tool, and that seizures may be an underappreciated cause of spells and AMS.”
The results are important, he said, because EEG can identify treatable causes of AMS or spells, and because “it can prompt the physician to look for an underlying reason for seizures in persons who did previously have them.”
Seizures are treatable with a number of FDA-approved anticonvulsants, he said, “so patients who are quickly diagnosed can be treated more rapidly and effectively. This may translate to shorter lengths of stay and improved patient outcomes.”
In one of the first studies of its kind, Betjemann and his team analyzed the medical records of 1,048 adults who were admitted to a regular inpatient unit of a tertiary care hospital and who underwent an EEG. They found that 7.4 percent of the patients had a seizure of some kind while being monitored.
“As I tell my patients, seizures come in all different flavors, from a dramatic convulsion to a subtle twitching of the face or hand or finger,” said Betjemann. “There might be no outward manifestation at all, other than that the person seems a little spacey. It’s easily missed by family members and physicians alike, but can be picked up by EEG.”
Another 13.4 percent of patients had epileptiform discharges, which are abnormal patterns that indicate patients are at an increased risk of seizures.
Almost 65 percent of patients had their first seizure within one hour of EEG recording, and 89 percent within six hours.
“This is good news for smaller hospitals that don’t have 24 hour EEG coverage, but that do have a technician on duty during the day,” Betjemann said.
He speculated that lack of 24-hour coverage is a major reason that EEG is not used as an inpatient diagnostic tool as often as it might be. “This paper shows that, fortunately, it’s not necessary. Almost two thirds of patients with seizures can be identified in the first hour, and almost 90 percent in the course of a shift.”
EEGs are easy to obtain, painless and noninvasive, said Betjemann. “The technician applies some paste and electrodes and hooks up the machine. All the patient has to do is rest in bed.”
Betjemann said that the next logical research step would be a prospective study. “We have to start at the beginning, see if patients are altered when they are admitted, and do an EEG in a formal standardized setting. Then we’d want to see how often EEG is changing the management of patients – either starting or stopping medications,” he said. “A patient may be having spells, and an EEG might tell you this is not a seizure, and that it’s important not to treat it with anti-epileptic medications.”
(Image: Rex Features)

Pesticide combination affects bees’ ability to learn
Two new studies have highlighted a negative impact on bees’ ability to learn following exposure to a combination of pesticides commonly used in agriculture. The researchers found that the pesticides, used in the research at levels shown to occur in the wild, could interfere with the learning circuits in the bee’s brain. They also found that bees exposed to combined pesticides were slower to learn or completely forgot important associations between floral scent and food rewards.
In the study published today (27 March 2013) in Nature Communications, the University of Dundee’s Dr Christopher Connolly and his team investigated the impact on bees’ brains of two common pesticides: pesticides used on crops called neonicotinoid pesticides, and another type of pesticide, coumaphos, that is used in honeybee hives to kill the Varroa mite, a parasitic mite that attacks the honey bee.
The intact bees’ brains were exposed to pesticides in the lab at levels predicted to occur following exposure in the wild and brain activity was recorded. They found that both types of pesticide target the same area of the bee brain involved in learning, causing a loss of function. If both pesticides were used in combination, the effect was greater.
The study is the first to show that these pesticides have a direct impact on pollinator brain physiology. It was prompted by the work of collaborators Dr Geraldine Wright and Dr Sally Williamson at Newcastle University who found that combinations of these same pesticides affected learning and memory in bees. Their studies established that when bees had been exposed to combinations of these pesticides for 4 days, as many as 30% of honeybees failed to learn or performed poorly in memory tests. Again, the experiments mimicked levels that could be seen in the wild, this time by feeding a sugar solution mixed with appropriate levels of pesticides.
Dr Geraldine Wright said: “Pollinators perform sophisticated behaviours while foraging that require them to learn and remember floral traits associated with food. Disruption in this important function has profound implications for honeybee colony survival, because bees that cannot learn will not be able to find food.”
Together the researchers expressed concerns about the use of pesticides that target the same area of the brain of insects and the potential risk of toxicity to non-target insects. Moreover, they said that exposure to different combinations of pesticides that act at this site may increase this risk.
Dr Christopher Connolly said: “Much discussion of the risks posed by the neonicotinoid insecticides has raised important questions of their suitability for use in our environment. However, little consideration has been given to the miticidal pesticides introduced directly into honeybee hives to protect the bees from the Varroa mite. We find that both have negative impact on honeybee brain function.
"Together, these studies highlight potential dangers to pollinators of continued exposure to pesticides that target the insect nervous system and the importance of identifying combinations of pesticides that could profoundly impact pollinator survival."

Transmission routes of spreading protein particles
Study on cell cultures gives insights into the mechanisms of
neurodegenerative diseases
Bonn, Germany, March 27th, 2013. In diseases like Alzheimer’s and Parkinson’s endogenous proteins accumulate in the brain, eventually leading to the death of nerve cells. These deposits, which consist of abnormally formed proteins, are supposed to migrate between interconnected areas of the brain, thereby contributing to the development of the illness. Now, a new laboratory study by scientists from Germany and the US shows that certain protein particles are indeed capable of multiplying and spreading from one cell to the next. The investigation was conducted by researchers of the German Center for Neurodegenerative Diseases (DZNE) in Bonn and Munich who cooperated with scientists from the US and from other German institutions. The results are now published in the “Proceedings of the National Academy of Sciences of the USA“ (PNAS).
Are particles consisting of deformed proteins capable of moving from one cell’s interior to the next, multiplying and spreading as in a chain reaction? The team of scientists headed by Ina Vorberg, who is a researcher at the DZNE site in Bonn and a professor at the University of Bonn, investigated this hypothesis. The scientists did so with the help of cell cultures, which allowed them to adapt experiments to specific questions.
The researchers used cultured brain cells that originated from mice. The genetic code of a model protein was transferred into these cells, enabling the scientists to control production of the protein.
A yeast particle
The blueprint of the molecule was extracted from yeast DNA. This protein does not exist in humans. Nevertheless, the scientists chose this particular protein because it had several properties that were relevant for the study: In its natural environment – the yeast cell – it is capable of forming replicating “aggregates” (i. e. large protein particles). The protein deforms during this process. Now, the question was, whether something similar would happen in mammalian cells.
“At first, our mouse cells produced the protein, but no particles formed,” Vorberg reports. “The situation changed when we exposed the cells to aggregates of the same protein. Suddenly, the proteins which had been in solution started building clumps.”
Diffusing aggregates
Once this reaction had been triggered the cells went on producing aggregates. The researchers noticed that these clumps spread into neighboring cells, where they initiated synthesis of further aggregates.
“We have experimentally shown that certain protein particles originating from the cytosol, i. e. from inside the cells, are able to spread between cells. This means that in mammalian cells there are mechanisms capable of triggering such a chain reaction. Accordingly, what we have shown in our model system may be applicable to neurodegenerative diseases,” Vorberg comments.
Propagation of aggregates was most effective between adjacent cells. “At least in our model system, protein particles are not released efficiently into the medium and assimilated by neighboring cells. The most effective transmission happens by direct cell-to-cell contact. It is possible that cells form protrusions and that aggregates move from one cell to the next through this connection”, says the neuroscientist. What is happening here will be the focus of further research.
Basis for potential therapies
“It is important to know how protein particles disseminate”, Vorberg emphasizes. “Disease-related protein particles might propagate in a similar way to the model protein we investigated.”
Unraveling the mechanism for transmission between cells could lead to new methods for treatment. “If we find a way to prevent the spreading of disease-related protein particles, we might be able to interfere with the progression of the diseases,” Vorberg says.
Novel intercellular transportation system may have potential for delivering RNAi and other gene-based therapeutics
Important new research from UMass Medical School demonstrates how exosomes shuttle proteins from neurons to muscle cells where they take part in critical signaling mechanisms, an exciting discovery that means these tiny vehicles could one day be loaded with therapeutic agents, such as RNA interference (RNAi), and directly target disease-carrying cells. The study, published this month in the journal Neuron, is the first evidence that exosomes can transfer membrane proteins that play an important role in cell-to-cell signaling in the nervous system.

“There has been a long-held belief that certain cellular materials, such as integral membrane proteins, are unable to pass from one cell to another, essentially trapping them in the cell where they are made,” said Vivian Budnik, PhD, professor of neurobiology and lead author of the study. “What we’ve shown in this study is that these cellular materials can actually move between different cell types by riding in the membrane of exosomes.
“What is so exciting about this discovery is that these exosomes can deliver materials from one cell, over a distance, to a very specific and different cell,” said Dr. Budnik. “Once inside the recipient cell, the materials contained in the exosome can influence or perform processes in the new cell. This raises the enticing possibility that exosomes can be packed with gene therapies, such as RNAi, and delivered to diseased cells where they could have a therapeutic effect for people.”
Discovered in the mid-80s, exosomes have only recently attracted the attention of scientists at large, according to Budnik. Exosomes are small vesicles containing cellular materials such as microRNA, messenger RNAs (mRNAs) and proteins, packaged inside larger, membrane-bound bodies called multivesicular bodies (MVBs) inside cells. When MVBs containing exosomes fuse with the cell plasma membrane, they release these exosome vesicles into the extracellular space. Once outside the cell, exosomes can then travel to other cells, where they are taken up. The recipient cells can then use the materials contained within exosomes, influencing cellular function and allowing the recipient cell to carry out certain processes that it might not be able to complete otherwise.
Budnik and colleagues made this startling discovery while investigating how the synapses at the end of neurons and nearby muscle cells communicate in the developing Drosophila fruit fly to form the neuromuscular junction (NMJ). The NMJ is essential for transmitting electrical signals between neurons and muscles, allowing the organism to move and control important physiological processes. Alterations of the NMJ can lead to devastating diseases, such as muscular dystrophy and Amyotrophic lateral sclerosis (ALS). Understanding how the NMJ develops and is maintained is important for human health.
As organisms develop, the synapse and muscle cell need to grow in concert. If one or the other grows too quickly or not quickly enough, it could have dire consequences for the ability of the organism to move and survive. To coordinate development, signals are sent from the neuron to the muscle cell (anterograde signals) and from the muscle cell to the neuron (retrograde signals). However, the identity of these signals and how their release is coordinated is poorly understood.
Normally, the vesicle protein Synaptotagmin 4 (Syt4) is found in both the synapse and the muscle cells. Previous knockout experiments eliminating the Syt4 protein from Drosophila have resulted in stunted NMJs. Suspecting that Syt4 played an important role in retrograde signaling at the developing NMJ, Budnik and colleagues used knockdown experiments to decrease Syt4 protein levels in either the neurons or the muscle cells. Surprisingly, when RNAi was used to knockdown Syt4 in the neurons alone, Syt4 protein was eliminated in both neurons and muscles. The opposite was not the case. When Syt4 was knocked down in muscle cells only, there was no change in the levels of Syt4 in either muscles or neurons.
To confirm this, Budnik and colleagues inserted a Syt4 gene into the neurons of a Drosophila mutant completely lacking the normal protein. This restored Syt4 in both neurons and muscle cells. Further experiments suggested that the only source of Syt4 is the neuron. These observations were consistent with the model that Syt4 is actually transferred from neurons to muscle cells. As a transmembrane protein, however, Syt4 was thought to be unable to move from one cell to another through traditional avenues. How the Syt4 protein was moving from neuron to muscle cell was unclear.
Knowing that exosomes had been observed to carry transmembrane proteins in other systems and from their own work on the Drosophila NMJ, Budnik and colleagues began testing to see if exosomes could be the vehicle responsible for carrying Syt4 form neurons to muscles. “We had previously observed that it was possible to transfer transmembrane proteins across the NMJ through exosomes, a process also observed in the immune system,” said Budnik. “We suspect this was how Syt4 was making its way from the neuron to the muscle.”
When exosomes were purified from cultured cells containing Syt4, they found that exosomes indeed contained Syt4. In addition, when these purified exosomes were applied to cultured muscle cells from fly embryos, these cells were able to take up the purified Syt4 exosomes. Taken together, these findings indicate that Syt4 plays a critical role in the signaling process between synapse and muscle cell that allows for coordinated development of the NMJ. While Syt4 is required to release a retrograde signal from muscle to neuron, a component of this retrograde signal must be supplied from the neuron to the muscle. This establishes a positive feedback loop that ensures coordinated growth of the NMJ. Equally important is the finding that this feedback mechanism is enabled by the use of exosomes, which can shuttle transmembrane proteins across cells.
“While this discovery greatly enhances our understanding of how the neural muscular junction develops and works, it also has tremendous promise as a potential vector for targeted genetic therapies,” said Budnik. “More work needs to be done, but this study significantly supports the possibility that exosomes could be loaded with therapeutic agents and delivered to specific cells in patients.”
(Source: umassmed.edu)
Neurobiologists at the Friedrich Miescher Institute have been able to dissect a mechanism in the retina that facilitates our ability to see both in the dark and in the light. They identified a cellular switch that activates distinct neuronal circuits at a defined light level. The switch cells of the retina act quickly and reliably to turn on and off computations suited specifically for vision in low and high light levels thus facilitating the transition from night to day vision. The scientists have published their results online in Neuron.

"It was fascinating to see how modern neurobiological methods allowed us to answer a question about vision that has been controversially discussed for the last 50 years", said Karl Farrow, postdoctoral fellow in Botond Roska’s group at the Friedrich Miescher Institute for Biomedical Research. Since the late 1950 scientists debated how the retina handles the different visual processes at low and high light intensities, at starlight and at daylight. Farrow and his colleagues have now identified a cellular switch in the retina that controls perception during these two settings.
At first glance, everything seems clear. The interplay of two photoreceptor types in the retina, the rods and the cones, allow us to see across a wide range of light intensities. The rods are highly sensitive and spring into action in the dark; the cones are activated during the day and in humans come in three diversities allowing us to see color. The rods help us detect objects during the night; while the cones allow us to discriminate the fine details of those objects during the day. The plethora of initial signals originating from the photoreceptors is computed in a system of only approximately 20 neuronal channels that transport information to the brain. The relay stations are the roughly 20 types of ganglion cells in the retina. How they manage the transition from light to dark and enable vision at the different light regimes has remained unclear.
In the retina several cell layers are stacked on top of each other. The photoreceptors are the first to be activated by light; they relay the information to bipolar cells, which in turn activate ganglion cells. The different types of ganglion cells take on distinct tasks during vision. These ganglion cells are embedded in a mesh of amacrine cells that modulate their activity. “Here is where our new genetic tools proofed very helpful,” said Farrow, “because they allowed us to look at individual ganglion cell types and to specifically measure their activities at different light intensities.” Farrow and colleagues could thus show that the activity of one particular type of ganglion cells, called PV1, is modulated like a switch by amacrine cells. The amacrine cells inhibit the ganglion cell strongly at high light intensities and weakly at low ambient light levels. This switch is abrupt and reversible and it occurs at the light intensities where cones are starting to be activated. “We were surprised to see how fast this switch occurs and how reliable we were able to switch between the two states at defined light intensities”, comments Farrow.
While the above experiments were done in a mouse model, the FMI neurobiologists could show that a similar switch operates in human vision. Their volunteers had to look at narrow and broader stripes at different light levels. They could show that there again a switch operates. While the general ability to see all striped patterns improved with increasing light intensity, suddenly, at a certain light level, the volunteers were much better able to detect thinner patterns as compared to the broader ones. Interestingly enough this switch happened at precisely the light level where the volunteers were also able to discriminate between red and blue, hence where the cones spring into action. “We think we have found a regulatory principle that could apply to several processes in the brain”, said Roska, “This principle could explain some situations when gradual changes in the sensory environment leads to abrupt changes in brain computations and perception”
(Source: medicalxpress.com)
Rats’ brains are more like ours than scientists previously thought
Neuroscientists face a multitude of challenges in their efforts to better understand the human brain. If not for model organisms such as the rat, they might never know what really goes on inside our heads.
The brain is a phenomenal processor that in a year’s time can generate roughly 300,000 petabytes of data — 30,000 times the amount generated by the Large Hadron Collider. Trying to decipher its signals is a daunting prospect.
But particularly for individuals who have lost a limb or been partially or fully paralyzed, such research has potentially life-changing results because it can enable such biotechnological advances as the development of a brain-computer interface for controlling prosthetic limbs.
Such devices require a detailed understanding of the motor cortex, a part of the brain that is crucial in issuing the neural commands that execute behavioral movements. A recent paper published in the journal Frontiers in Neural Circuits by Jared Smith and Kevin Alloway, researchers at the Penn State Center for Neural Engineering and affiliates of the Huck Institutes of the Life Sciences, details their discovery of a parallel between the motor cortices of rats and humans that signifies a greater relevance of the rat model to studies of the human brain than scientists had previously known.
"The motor cortex in primates is subdivided into multiple regions, each of which receives unique inputs that allow it to perform a specific motor function," said Alloway, professor of neural and behavioral sciences. "In the rat brain, the motor cortex is small and it appeared that all of it received the same type of input. We know now that sensory inputs to the rat motor cortex terminate in a small region of the motor cortex that is distinct from the larger region that issues the motor commands. Our work demonstrates that the rat motor cortex is parcellated into distinct subregions that perform specific functions, and this result appears to be similar to what is seen in the primate brain."
"You have to take into account the animal’s natural behaviors to best understand how its brain is structured for sensory and motor processing," said Jared Smith, graduate student in the Huck Institutes’ neuroscience program and the first author of the paper. "For primates like us, that means a strong reliance on visual information from the eyes, but for rats it’s more about the somatosensory inputs from their whiskers."
In fact, nearly a third of the rat’s sensorimotor cortex is devoted to processing whisker-related information, even though the whiskers’ occupy only one-third of one percent of the rat’s total body surface. In humans, nearly 40 percent of the entire cortex is devoted to processing visual information even though the eyes occupy a very tiny portion of our body’s surface.
To understand the structure and function of the rat motor cortex, Smith and Alloway conducted a series of experiments focused on the medial agranular region, which responds to whisker stimulation and elicits whisker movements when stimulated.
"Our research," said Smith, "was conducted in two stages to investigate the functional organization of the brain: first tracing the neuronal connectivity, and then measuring how the circuits behave in terms of their electrophysiology. Just like in any electrical circuit, the first thing you need to do is trace the wires to see how the different components are connected. Then you can use this information to make sense of the activity going on at any particular node. In the end, you can step back and see how all the circuits work together to achieve something more complex, such as motor control."
"We discovered different sensory input regions that were distinct from the region that issued the motor commands to move the whiskers," said Alloway. "In this respect, we were fortunate to have Patrick Drew [assistant professor of engineering science and mechanics and neurosurgery at Penn State] help us analyze the EMG signals produced by microstimulation because this showed that the sensory input region was significantly less effective in evoking whisker movements."
As a result of Smith and Alloway’s discovery, previously published data on the rat motor cortex can be revisited with a new degree of specificity, and more similarities between the brains and neural processes of rats and humans may eventually come to light, perhaps even informing studies of other model organisms. This discovery is also likely to advance the study of the human brain.
"This study opens up avenues for studying some very complex neural processes in rodents that are more like our own than we had previously thought," said Smith. "The tools now available for studying activity in the rodent brain are improving at a remarkable pace, and the findings are even more interesting as we discover just how similar these mammalian relatives are to us. This is a very exciting time in neuroscience."

The memories of near death experiences (NDE): more real than reality?
University of Liège researchers have demonstrated that the physiological mechanisms triggered during NDE lead to a more vivid perception not only of imagined events in the history of an individual but also of real events which have taken place in their lives! These surprising results – obtained using an original method which now requires further investigation – are published in PLOS ONE.
Seeing a bright light, going through a tunnel, having the feeling of ending up in another ‘reality’ or leaving one’s own body are very well known features of the complex phenomena known as ‘Near-Death Experiences ‘ (NDE), which people who are close to death can experience in particular. Products of the mind? Psychological defence mechanisms? Hallucinations? These phenomena have been widely documented in the media and have generated numerous beliefs and theories of every kind. From a scientific point of view, these experiences are all the more difficult to understand in that they come into being in chaotic conditions, which make studying them in real time almost impossible. The University of Liège’s researchers have thus tried a different approach.
Working together, researchers at the Coma Science Group (Directed by Steven Laureys) and the University of Liège’s Cognitive Psychology Research (Professor Serge Brédart and Hedwige Dehon), have looked into the memories of NDE with the hypothesis that if the memories of NDE were pure products of the imagination, their phenomenological characteristics (e.g., sensorial, self referential, emotional, etc. details) should be closer to those of imagined memories. Conversely, if the NDE are experienced in a way similar to that of reality, their characteristics would be closer to the memories of real events.
The researchers compared the responses provided by three groups of patients, each of which had survived (in a different manner) a coma, and a group of healthy volunteers. They studied the memories of NDE and the memories of real events and imagined events with the help of a questionnaire which evaluated the phenomenological characteristics of the memories. The results were surprising. From the perspective being studied, not only were the NDEs not similar to the memories of imagined events, but the phenomenological characteristics inherent to the memories of real events (e.g. memories of sensorial details) are even more numerous in the memories of NDE than in the memories of real events.
The brain, in conditions conducive to such phenomena occurring, is prey to chaos. Physiological and pharmacological mechanisms are completely disturbed, exacerbated or, conversely, diminished. Certain studies have put forward a physiological explanation for certain components of NDE, such as Out-of-Body Experiences, which could be explained by dysfunctions of the temporo-parietal lobe. In this context the study published in PLOS ONE suggests that these same mechanisms could also ‘create’ a perception – which would thus be processed by the individual as coming from the exterior – of reality. In a kind of way their brain is lying to them, like in a hallucination. These events being particularly surprising and especially important from an emotional and personal perspective, the conditions are ripe for the memory of this event being extremely detailed, precise and durable.
Numerous studies have looked into the physiological mechanisms of NDE, the production of these phenomena by the brain, but, taken separately, these two theories are incapable of explaining these experiences in their entirety. The study published in PLOS ONE does not claim to offer a unique explanation for NDE, but it contributes to study pathways which take into account psychological phenomena as factors associated with, and not contradictory to, physiological phenomena.

Mindfulness Improves Reading Ability, Working Memory, and Task-Focus
If you think your inability to concentrate is a hopeless condition, think again –– and breathe, and focus. According to a study by researchers at the UC Santa Barbara, as little as two weeks of mindfulness training can significantly improve one’s reading comprehension, working memory capacity, and ability to focus.
Their findings were recently published online in the empirical psychology journal Psychological Science.
"What surprised me the most was actually the clarity of the results," said Michael Mrazek, graduate student researcher in psychology and the lead and corresponding author of the paper, "Mindfulness Training Improves Working Memory Capacity and GRE Performance While Reducing Mind Wandering." "Even with a rigorous design and effective training program, it wouldn’t be unusual to find mixed results. But we found reduced mind-wandering in every way we measured it."
Many psychologists define mindfulness as a state of non-distraction characterized by full engagement with our current task or situation. For much of our waking hours, however, we are anything but mindful. We tend to replay past events –– like the fight we just had or the person who just cut us off on the freeway –– or we think ahead to future circumstances, such as our plans for the weekend.
Mind-wandering may not be a serious issue in many circumstances, but in tasks requiring attention, the ability to stay focused is crucial.
To investigate whether mindfulness training can reduce mind-wandering and thereby improve performance, the scientists randomly assigned 48 undergraduate students to either a class that taught the practice of mindfulness or a class that covered fundamental topics in nutrition. Both classes were taught by professionals with extensive teaching experience in their fields. Within a week before the classes, the students were given two tests: a modified verbal reasoning test from the GRE (Graduate Record Examination) and a working memory capacity (WMC) test. Mind-wandering during both tests was also measured.
The mindfulness classes provided a conceptual introduction along with practical instruction on how to practice mindfulness in both targeted exercises and daily life. Meanwhile, the nutrition class taught nutrition science and strategies for healthy eating, and required students to log their daily food intake.
Within a week after the classes ended, the students were tested again. Their scores indicated that the mindfulness group significantly improved on both the verbal GRE test and the working memory capacity test. They also mind-wandered less during testing. None of these changes were true of the nutrition group.
"This is the most complete and rigorous demonstration that mindfulness can reduce mind-wandering, one of the clearest demonstrations that mindfulness can improve working memory and reading, and the first study to tie all this together to show that mind-wandering mediates the improvements in performance," said Mrazek. He added that the research establishes with greater certainty that some cognitive abilities often seen as immutable, such as working memory capacity, can be improved through mindfulness training.
Mrazek and the rest of the research team –– which includes Michael S. Franklin, project scientist; mindfulness teacher and research specialist Dawa Tarchin Phillips; graduate student Benjamin Baird; and senior investigator Jonathan Schooler, professor of psychological and brain sciences –– are extending their work by investigating whether similar results can be achieved with younger populations, or with web-based mindfulness interventions. They are also examining whether or not the benefits of mindfulness can be compounded by a program of personal development that also targets nutrition, exercise, sleep, and personal relationships.
(Image: fotopakismo)
A new study published in the March issue of Autism Research from the University of Tennessee Health Science Center and Le Bonheur researchers is making the genetic connections between autism and Chromosome 15q Duplication Syndrome (Dup15q).
The Memphis researchers determined that the maternally derived or inherited duplication of the region inclusive of the UBE3A gene (also known as the Angelman/Prader-Willi syndrome locus) are sufficient to produce a phenotype on the autism spectrum in all ten maternal duplication subjects. The number of subjects was too small to determine if parental duplications do not cause autism. The team assembled the largest single cohort of interstitial 15q duplication subjects for phenotype/genotype analysis of the autism component of the syndrome.
Chromosome 15q Duplication Syndrome (Dup15q) results from duplications of chromosome 15q11-q13. Duplications that are maternal in origin often result in developmental problems. The larger 15q duplication syndrome, which includes individuals with idic15, manifests itself in a wide range of developmental disabilities including autism spectrum disorders; motor, cognitive and speech/language delays; and seizure disorders among others. While there is no specific treatment plan, therapies are available to address or manage symptoms.
Previous research suggests that as many as 1,000 genes may contribute to autism phenotypes, but as much as 1-3 percent of all autism spectrum disorder cases may be a result of 15q11-q13 duplication alone.
The researchers also found through EEG evaluations a pattern that looks like the type of signal you see when individuals take GABA promoting drugs (benzodiazepines). The lead researcher on this study, Lawrence T. Reiter, PhD, says this signal gives clinicians a clue about what types of anti-seizure medication may be most useful in children with 15q duplications.
Reiter says genetic testing can help families connect to resources, like the Dup15q Alliance. Reiter is an associate professor in Department of Neurology with an adjunct appointment in Pediatrics at UTHSC.
“If a pediatrician suspects autism due to hypotonia and developmental delay, I highly recommend they order an arrayCGH test. Duplication 15q is the second most common duplication in autism. The test will help families in future treatments specific to this sub-type of autism,” he said.
(Source: lebonheur.org)

NSF-funded Superhero Supercomputer Helps Battle Autism
'Gordon,' a supercomputer with unique flash memory, helps identify gene-related paths to treating mental disorders
When it officially came online at the San Diego Supercomputer Center (SDSC) in early January 2012, Gordon was instantly impressive. In one demonstration, it sustained more than 35 million input/output operations per second—then, a world record.
Input/output operations are an important measure for data intensive computing, indicating the ability of a storage system to quickly communicate between an information processing system, such as a computer, and the outside world. Input/output operations specify how fast a system can retrieve randomly organized data common in large datasets and process it through data mining applications.
The supercomputer’s record-breaking feat wasn’t a surprise; after all, Gordon is named after a comic strip superhero, Flash Gordon.
Gordon’s new and unique architecture employs massive amounts of the type of flash memory common in cell phones and laptops—hence its name. The system is used by scientists whose research requires the mining, searching and/or creating of large databases for immediate or later use, including mapping genomes for applications in personalized medicine and examining computer automation of stock trading by investment firms on Wall Street.
Commissioned by the National Science Foundation (NSF) in 2009 for $20 million, Gordon is part of NSF’s Extreme Science and Engineering Discovery Environment, or XSEDE program, a nationwide partnership comprising 16 high-performance computers and high-end visualization and data analysis resources.
"Gordon is a unique machine in NSF’s Advanced Cyberinfrastructure/XSEDE portfolio," said Barry Schneider, NSF program director for advanced cyberinfrastructure. “It was designed to handle scientific problems involving the manipulation of very large data. It is differentiated from most other resources we support in having a large solid-state memory, 4 GB per core, and the capability of simulating a very large shared memory system with software.”
Last month, a team of researchers from SDSC, the United States and the Institute Pasteur in France reported in the journal Genes, Brain and Behavior that they used Gordon to devise a novel way to describe a time-dependent gene-expression process in the brain that can be used to guide the development of treatments for mental disorders such as autism-spectrum disorders and schizophrenia.
The researchers identified the hierarchical tree of coherent gene groups and transcription-factor networks that determine the patterns of genes expressed during brain development. They found that some “master transcription factors” at the top level of the hierarchy regulated the expression of a significant number of gene groups.
The scientists’ findings can be used for selection of transcription factors that could be targeted in the treatment of specific mental disorders.
"We live in the unique time when huge amounts of data related to genes, DNA, RNA, proteins, and other biological objects have been extracted and stored," said lead author Igor Tsigelny, a research scientist with SDSC as well as with UC San Diego’s Moores Cancer Center and its Department of Neurosciences.
"I can compare this time to a situation when the iron ore would be extracted from the soil and stored as piles on the ground. All we need is to transform the data to knowledge, as ore to steel. Only the supercomputers and people who know what to do with them will make such a transformation possible," he said.