ScnTO's Very Own Last Chance Thread

Discussion in 'News and Current Events' started by DeathHamster, May 15, 2011.

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  1. Anonymous Member

    Neurologists develop software application to help identify subtle epileptic lesions

    February 16, 2011

    Researchers from the Department of Neurology at NYU Langone Medical Center identified potential benefits of a new computer application that automatically detects subtle brain lesions in MRI scans in patients with epilepsy. In a study published in the February 2011 issue of PLoS ONE, the authors discuss the software's potential to assist radiologists in better identifying and locating visually undetectable, operable lesions.
    "Our method automatically identified abnormal areas in MRI scans in 92 percent of the patients sampled, which were previously identified by expert radiologists reviewing multiple images," said first-author Thomas Thesen, PhD, assistant professor, Department of Neurology, NYU Langone Medical Center. "Based on these findings, we will focus on the ability of our application to detect the more subtle epileptic malformations that are not easily detectable by the human eye. We believe this could lead to new tools to greatly help radiologists provide more accurate and faster results with objective measures for standardizing readings."
    The proof-of-concept study, entitled "Detection of epileptogenic cortical malformations with surface-based MRI morphometry," demonstrates that non-invasive and automated detection of known epileptogenic structural abnormalities in cortex is possible, and supports its potential use as a tool for diagnosis and planning of epilepsy surgery.
    The researchers are encouraged by the initial results and have already started evaluating the applications ability to determine undetected lesions in previously negative MRI scans, with findings to be published later this year.
    More information: The article on PLoS ONE can be found at http://www.plosone … pone.0016430
    Provided by New York University School of Medicine (news : web)
  2. Anonymous Member

    Artificial retina helps some blind people

    February 14, 2011 By MARIA CHENG , AP Medical Writer
    In this photo taken Saturday, Feb. 12, 2011, Eric Selby poses for a photograph with a "sight" camera fitted in a pair of glasses, as well as its associated computer and transmitter, which work in conjunction with an artificial retina implant called the Argus II fitted in his right eye, enabling him to detect light, in Coventry, England. For two decades, Eric Selby, 68, had been completely blind and dependent on a guide dog to get around. But after having an artificial retina put into his right eye, he can detect ordinary things like the curb and pavement when he's walking outside. (AP Photo/Martin Cleaver)
    For two decades, Eric Selby had been completely blind and dependent on a guide dog to get around. But after having an artificial retina put into his right eye, he can detect ordinary things like the curb and pavement when he's walking outside.
    "It's basically flashes of light that you have to translate in your brain, but it's amazing I can see anything at all," said Selby, a retired engineer in Coventry, central England.
    More than a year ago, the 68-year-old had an artificial implant called the Argus II, made by U.S.-based company Second Sight, surgically inserted into his right eye. Dutch regulators are expected to decide within weeks on the company's request to market the device in the EU. If greenlighted, it would be the first artificial retina available for sale.
    The implant works with a tiny video camera and transmitter in a pair of glasses and a small wireless computer.
    The computer processes scenes captured by the camera and converts them into visual information in the form of an electronic signal that's sent to the implant. The device stimulates the retina's remaining healthy cells, causing them to relay the data to the optic nerve.
    The visual information then moves to the brain, where it's translated into patterns of light that can take the shape of an object's outline. Patients need to learn how to interpret the flashes of light; for instance, they might decode three bright dots as the three points of a triangle.
    The implant is intended only for people with a specific type of inherited retina problem, who still have some functional cells. They must have previously been able to see and their optic nerve must be working. About one in 3,000 people are blind due to one of this group of hereditary diseases, called retinitis pigmentosa, and might potentially benefit from the artificial retina.
    The device comes with a hefty price tag - about $100,000. In Britain, the national health service sometimes pays for expensive new technologies for a small number of patients, said Lyndon da Cruz, one of the doctors who tested the artificial retina at Moorfields Eye Hospital in London.
    He said if the artificial retina allows patients to be more self-sufficient, the implant could turn out to be cheaper than governments paying for higher levels of health care or in-home care for patients.
    So far, about 40 people have gotten the artificial retina since 2002 and some patients have seen well enough to identify objects, shapes, or even read large print during their participation in trials.
    The implant's maker has applied to the Netherlands' medical devices regulator for marketing permission. The company is also in talks with the U.S. Food and Drug Administration about the kind of tests needed to secure the retinal implant's approval in the United States.
    "The device is currently very crude, but it's impressive that some patients have been able to read large fonts," said Daniel Palanker, who works in opthalmology and experimental physics at Stanford University, and is not connected to the Argus II.
    He and colleagues are developing another artificial retina implant that delivers images to the eye via pulses of infrared light, though they are years away from having a commercial product.
    "It's just remarkable that we've gone from having no cure to blindness to a situation where we can restore sight to some extent," Palanker said.
    There are a handful of competing retinal implant projects worldwide. Last year, Eberhart Zrenner at the Centre for Opthalmology in Tuebingen, Germany and colleagues published research about their implant, which also depends on patients' remaining working retinal cells. Only 11 people have received the device so far, but one reported being able to see his girlfriend's face while another reported seeing a duck in a meadow. Zrenner hopes the device will be available in two years.
    Gregoire Cosendai, senior director of European Operations at Second Sight, said the Argus II implant's success depends largely on how adept patients are at decoding the flashing lights the device produces. He said the implant isn't meant to replace guide dogs or canes at the moment, but may improve patients' coordination and help them with daily tasks like cooking.
    Cosendai compared the retinal implant to the first cochlear implants for deaf people, which had mixed success when they were introduced more than 20 years ago. Modern cochlear implants are now good enough to allow some deaf people to talk on the telephone.
    Experts said future retinal implants might restore enough sight to make some patients self-sufficient. Still, most doubt the devices will ever come close to normal human vision.
    "The way these implants work is they plug into what's left of the retina, so that limits just how much you can reproduce," said da Cruz. He predicted the device would improve dramatically in the next decade.
    "The big breakthroughs - making a device you can sit on the retina which doesn't kill it and proving it works for years - have already been made," he said. He said it would be much easier to refine the implant and improve the quality of what patients see. Second Sight is already developing a new version of its retinal implant that will soon be tested.
    Selby says his artificial retina allows him to see certain shapes and shades of black, white and gray. He mostly uses it to help navigate his walking route when he goes outside.
    "I'm only seeing a fraction of things but it does still help," he said. Selby lost his sight nearly 20 years ago due to an inherited eye condition and hopes his grandchildren and future generations might benefit from his experience with the implant.
    "It's like when people were first trying to fly to the moon," he said. "Nowadays they're sending people to the moon and into space, but they had to start off with a propeller engine ... For artificial eye implants, it could be a whole different ballgame in a few years."
    ©2010 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
  3. Anonymous Member

    Hearing with your nose: How nasal stem cells could tackle childhood hearing problems

    February 10, 2011

    Stem Cell scientists in Australia have found that patients suffering from hearing problems which began during infancy and childhood could benefit from a transplant of stem cells from their nose. The research, published today in Stem Cells, reveals that mucosa-derived stem cells can help preserve hearing function during the early-onset of sensorineural hearing loss.
    Sensorineural hearing loss is caused by the loss of sensory cells or neurons in the cochlea, the sensory organ of the inner ear responsible for hearing. The condition can have genetic causes, often arising during infancy and childhood, hindering cognitive development and leading to speech and language problems.
    "One of the challenges in tackling this condition is that the regenerative ability of the human cochlea is severely limited", said lead author Dr. Sharon Oleskevich from the Hearing Research Group at The University of New South Wales. "It has been proposed that the transplantation of cells from other parts of the body could treat, prevent or even reverse hearing loss. The transplanted cells have the potential to repair tissue by replacing damaged cells and enhancing the survival of existing cells, preventing the condition from developing further."
    To investigate the effects of this treatment, nasal stem cells were injected into the cochlea of mice displaying symptoms of hearing loss. Mice were chosen for this treatment as they display a similar decline in hearing function following infancy.
    "The authors have used an interesting type of adult stem cell, related to mesenchymal stem cells, to reduce the extent of hearing loss. Since the cells did not integrate into the cochlea, it is likely that the effects from the adult stem cells were due to the release of factors to preserve function of the endogenous stem cells. Mesenchymal stem cells are known to provide factors to keep many types of cells healthy and functioning," said Jan Nolta, Associate Editor of Stem Cells.
    Patient hearing levels were examined using the auditory brainstem response assay, which determines the lowest sound level to which the brain responds, known as the hearing threshold.
    The mice which received the transplanted cells were compared to mice who had not received the treatment a month later, revealing that the hearing threshold level in stem cell-transplanted mice was significantly lower.
    "The results demonstrate a significant effect of nasal stem cell transplantations for sensorineural hearing loss," concluded Oleskevich. "These cells can be obtained easily from the nasal cavity making this transplantation a potential treatment for other human conditions including Parkinson's disease and cardiac infarction."
    Provided by Wiley (news : web)
  4. Anonymous Member

    'Thinking cap' makes brain waves in Australia

    February 10, 2011
    Professor Allan Snyder displays a "thinking cap" (R) on a glass head at the University of Sydney. Australian scientists say they are encouraged by initial results of the "thinking cap" that aims to promote creativity by passing low levels of electricity through the brain.
    Scientists in Australia say they are encouraged by initial results of a revolutionary "thinking cap" that aims to promote creativity by passing low levels of electricity through the brain.
    The device, which consists of two conductors fastened to the head by a rubber strap, significantly boosted results in a simple arithmetic test, they said.
    Three times as many people who wore the "thinking cap" were able to complete the test, compared to those who did not use the equipment. Sixty people took part in total.
    Allan Snyder, director of the University of Sydney's Centre for the Mind, said the device worked by suppressing the left side of the brain, associated with knowledge, and stimulating the right side, linked to creativity.
    "You wouldn't use this to study or to help your memory," Snyder told AFP. "You would use this if you wanted to look at a problem anew.
    "If you wanted to look at the world, just briefly, with a child's view, if you wanted to look outside the box."
    He said goal was to suppress mental templates gathered through life experiences to help users see problems and situations as they really appear, rather than through the prism of earlier knowledge.
    Snyder added that the work was inspired by accident victims who experienced a sudden surge in creativity after damaging the left side of their brains.
    "We know that from certain types of brain damage and abnormalities or injuries, people who suddenly have damage to the left temporal lobe will burst out in the arts or other types of creative activities," he said.
    Snyder said the device had been in use by scientists for a decade, but this was the first study into how current passing through the brain could amplify insight.
    He said the "thinking cap" had potential applications in the arts and problem-solving, although the science remained in its infancy.
    "The dream is that one day we may be able to stimulate the brain in a particular way to give you, just momentarily, an unfiltered view of the world," Snyder said.
    (c) 2011 AFP
  5. Anonymous Member

    Researchers working on tiny, implantable computers to restore lost brain functions

    February 8, 2011
    Dr. Eberhard Fetz at the University of Washington in Seattle is principal investigator on a W.M. Keck Foundation grant to develop tiny, implantable computers to restore brain functions lost to injury or disease. Credit: Leila Gray
    Tiny, implantable computers that would restore brain function lost to disease or injury is the goal of University of Washington research recently funded by a $1 million, three-year grant from the W.M. Keck Foundation.
    The UW has made significant progress in neural engineering – the study of communication and control between biological and machine systems. The Keck project is the next step in advancing the technology of miniature devices developed at the UW to record from and stimulate the brain, spinal cord and muscles.
    The principal investigator on the Keck Foundation grant is Dr. Eberhard E. Fetz, UW professor of physiology and biophysics and a core staff researcher at the Washington National Primate Research Center. He and his colleagues have successfully deployed tiny, battery-powered implantable brain-computer interfaces called neurochips in animals.
    The neurochip can record nerve cell activity in one part of the brain, process this activity and then stimulate cells in another brain region. The battery-powered device operates continuously during free behavior. When primates carry out their usual daily activities – socializing, climbing, eating, and exploring – their brains can learn to exploit these new resources under normal behavioral conditions.
    One potential clinical application is to bridge lost biological connections. For example, the researchers have shown that monkeys can learn to bypass an anesthetic block in the nerves of the arm and to activate temporarily paralyzed muscles with activity of cortical neurons. In some ways the device acts as a volition processor, tapping into signals representing the will to move and using them to stimulate the paralyzed muscles to reach targets.
    "Using an implantable computer interface to implement novel interactions between brain sites opens many fundamentally new research directions," Fetz said, "depending on the site of recording and stimulation, and how these signals are processed and transformed."
    He explained that a second application is to promote neural plasticity, which could strengthen connections and allow some of the brain's functions to be rescued when impaired. This happens naturally when people recover the ability to move or speak again after a stroke or brain injury. The bidirectional brain computer interface could facilitate this recovery and exploit the brain's innate talent for re-organizing itself as it heals.
    "We expect that the recurrent type of brain computer interface we are trying to develop," he added, "will eventually have numerous clinical applications for bridging damaged biological pathways and strengthening weak neural connections." For example, signals from the motor-control regions of the brain can be used to stimulate parts of the spinal cord to evoke coordinated movements. This would create connections that could replace lost pathways between the brain and spinal cord, a loss that occurs with strokes and spinal cord injuries.
    Many labs around the world are working on brain-computer interfaces that convert neural activity to control of external devices such as prosthetic limbs or computer cursors. What makes the recently funded project unusual is that its scientists are developing a recurrent implantable device that would interact bidirectionally with the brain. By operating autonomously and continuously, without the need for connection to external instrumentation, it would facilitate long-term behavioral adaptation and plasticity.
    The proposed research plans to develop this new paradigm to promote restoration of brain, spine, and muscle function. The work could eventually lead to miniaturized electrical and biological interfaces that operate around the clock on a small amount of power while the wearer goes about his or her usual activities, according to Fetz. He added that, if successful, this implantable technology would advance the ability of subjects to effectively control a brain computer interface by allowing long-term adaptation to consistent contingencies, and would open opportunities for the brain to exploit bidirectional interactions with miniature computers. This implementation of continuous reciprocal interaction goes beyond the existing paradigm of using brain signals to control external devices through tethered connections.
    As part of the project the team also plans to create a powerful multichannel "Keck Active Electrode Array" with integrated electronics to record and stimulate large numbers of brain sites. This array would operate with electrodes on the surface of the brain and be less invasive than penetrating intracortical electrodes.
    To overcome the many technical problems in creating safe, effective devices of this nature and realizing their clinical potential, the project depends on a team of UW experts in different fields.
    Dr. Brian Otis, UW assistant professor of electrical engineering, has extensive experience in wireless sensors and in designing extremely small radios that can be incorporated into other devices. He is also an expert in bioelectronics and the processing of signals with minimal power. His group will design and miniaturize the low power circuitry for the computer and the signal amplifiers, and will work toward harvesting energy to operate the device, perhaps from the body's own heat or muscle activity.
    Dr. Babak Parviz, the UW McMorrow Innovation Associate Professor of Electrical Engineering, has skill in the fabrication of micro- and nano-scale tools, self-assembled biocompatible machinery, and sensors for detecting very faint signals. His group will create the specialized electrode arrays for recording and stimulation, and will help integrate the miniature electronic systems used in the project.
    Dr. Jeffrey Ojemann, UW professor of neurological surgery, has expanded his father's original studies on mapping of the human brain to identify critical areas for movement, language, memory and other functions prior to epilepsy surgery. He will bring his extensive knowledge of functional brain mapping and clinical recording of signals from the human brain to the project. He will help design and test the custom computer-enabled electrode arrays for potential applications to patient care.
    Among the engineering and health issues the team will be addressing are integrating the electronics with the electrode array and making it small enough, finding a reliable source of the low power necessary to operate the system, evaluating any hazards the device might pose or serious long-term side effects, and developing biomaterials that won't cause irritation or be rejected, as well as meeting other safety, performance, and acceptability criteria.
    "We are extremely grateful to the Keck Foundation for supporting this highly ambitious endeavor," Fetz said. "Looking ahead, we can anticipate that future innovations in nanotechnology, computers and brain science will advance this effort beyond the current state of the art. The grant allows us to be poised to incorporate these advances into the development of more powerful recurrent brain computer interfaces. We expect that these devices will have numerous applications in basic neuroscience research and as well as in clinical care."
    Provided by University of Washington (news : web)
  6. Anonymous Member

    A second pathway for antidepressants: New fluorescent assay reveals TREK1 mechanism

    February 7, 2011 by Lynn Yarris
    A Second Pathway for Antidepressants: Berkeley Lab Reports New Fluorescent Assay Reveals TREK1 Mechanism
    ( -- Using a unique and relatively simple cell-based fluorescent assay they developed, scientists with the U.S. Department of Energy (DOE)'s Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC), Berkeley have identified a means by which fluoxetine, the active ingredient in Prozac, suppresses the activity of the TREK1 potassium channel. TREK1 activity has been implicated in mood regulation and could be an important target for fluoxetine and other antidepressant drugs.
    "Whereas the inhibiting of serotonin re-uptake remains fluoxetine's primary antidepression mechanism, many pharmacological agents have more than one target," says Ehud Isacoff, a neurobiophysicist who holds joint appointments with Berkeley Lab's Physical Biosciences Division and UC Berkeley's Department of Molecular and Cell Biology. "Our study shows that the inhibition of TREK1 by fluoxetine, which was found in earlier studies, is accompanied by an unbinding of the protein's C-terminal domain from the membrane. This is the first observation of the mechanism by which TREK1 might be regulated by antidepressant drugs."
    Isacoff is the corresponding author on a paper reporting the results of this study that appears in the Proceedings of the National Academy of Sciences (PNAS). The paper is titled "Optical probing of a dynamic membrane interaction that regulates the TREK1 channel." Co-authoring this paper were Guillaume Sandoz, a TREK1 specialist with France's National Center for Scientific Research at the Institute for Molecular and Cellular Physiology, and PhD student Sarah Bell, both of whom were with Isacoff's research group at the time the work was done.
    Neurons in the human brain are like high-speed transistors, controlling the flow of electrical current through channels in their membranes by the opening and closing of molecular "gates" that control the flow of ions through selective pores. TREK1 is one of the most ubiquitous of these transmembrane proteins, gating the passage of potassium ions through neural membranes, which sets the excitability of the neuron. Earlier studies had shown that when the TREK1 gene is "knocked out" of mice, the mice display a depression-resistant phenotype that mimics the behavior of mice treated with fluoxetine and that the antidepressant inhibits the activity of the TREK1 channel. While these results pointed to a possible role for the TREK1 ion channel in the beneficial response to fluoxetine, the mechanism behind this activity was unclear.
    "Studying what the different protein parts of an ion channel do is a huge challenge," Isacoff says. "Over the years, my group has developed techniques by which the domains of channel proteins can be labeled with site-specific fluorescent dyes. Structural rearrangements of the labeled sites in the channel can then be detected through changes in the fluorescence."
    The TREK1 ion channel (blue) controls the passage of potassium ions (pink) through the plasma membrane (grey) of neurons, which sets neuron excitability. (Image from Isacoff group)
    Isacoff and his group separated the C-terminal domain from the rest of the protein and tagged it with a green fluorescent protein (GFP) - a fluorescent protein from jellyfish commonly used to paint cells green for biological studies. Whereas the pore of the TREK1 ion channel is embedded in the plasma membrane of a neuron, the C-terminal is a short tail that protrudes out into the surrounding cytoplasm.
    Using voltage clamps to measure electrical currents through the channel and fluorescence to monitor the disposition of the C-terminal domain, Isacoff and his group found that when the C-terminal tail is fully bound to the plasma membrane, the TREK1 potassium channel opens more; when the tail is unbound from the plasma membrane, the ion channel tends to close.
    "We found that fluoxetine causes the isolated C-terminal domain to unbind from the membrane and also causes an inhibition of current from the full TREK1 channel," Isacoff says.
    The next step will be to see how the C-terminal tail is affected by the presence of fluoxetine when the tail is still attached to the rest of the TREK1 protein. In the meantime, Isacoff and his team feel they now have a valuable assay that can be used to monitor the reversible plasma membrane association of protein domains without the need for scanning, optical slicing or imaging.
    "Pharmaceutical companies screening for potential new drugs, such as improved antidepressants, prefer assays that are fast and simple," Isacoff says. "Our technique can be used to follow changes in lipid composition that result from membrane signaling events, or to study the binding to membranes by cytoplasmic regulatory domains of ion channels. This could be very useful for pharmaceutical research."
    Provided by Lawrence Berkeley National Laboratory (news : web)
  7. Anonymous Member

    2nd member in Alzheimer's toxic duo identified

    February 4, 2011

    Like two unruly boys who need to be split up in class, a pair of protein molecules work together to speed up the toxic events of Alzheimer's disease. Researchers at the UT Health Science Center San Antonio today announced the discovery of the second molecule and said its identification could lead to drugs that disrupt the interaction, and thereby block or slow Alzheimer's onset or progression.
    Alzheimer's disease is an irreversible, progressive brain disease marked by deterioration of nerve cells and eventual complete loss of cognitive functioning – thinking, memory and reason. Many Alzheimer's patients have brain lesions called amyloid plaques, which consist of protein fragments called amyloid-beta. Small aggregates of amyloid-beta are thought to contribute prominently to the degeneration of brain cells in Alzheimer's.
    How genes are activated
    The discovery involves an amyloid beta fragment called AICD. Scientists have known that AICD controls expression of genes that contribute to Alzheimer's, but how it did so was unclear – until now. "We discovered a protein molecule that communicates with AICD to turn on target genes," said Thomas G. Boyer, Ph.D., professor of molecular medicine at the Health Science Center. "We hope to exploit this knowledge to identify compounds or drugs that can disrupt these signals, leading to a novel and effective treatment for this disease."
    Alzheimer's disease is the most common cause of dementia among older people, and estimates indicate that as many as 5.3 million Americans suffer from it. While several drugs approved by the U.S. Food and Drug Administration can temporarily slow worsening symptoms, no treatment is currently available to slow or stop the degeneration of nerve cells that lies at the root of the disease.
    More information: The finding is in the Feb. 4 issue of EMBO Reports.
    Provided by University of Texas Health Science Center at San Antonio
  8. Anonymous Member

    Why do we sleep?

    February 3, 2011 By Marcus Woo
    Credit: Chau Dang, LTD Space
    While we can more or less abstain from some basic biological urges—for food, drink, and sex—we can’t do the same for sleep. At some point, no matter how much espresso we drink, we just crash. And every animal that’s been studied, from the fruit fly to the frog, also exhibits some sort of sleep-like behavior. (Paul Sternberg, Morgan Professor of Biology, was one of the first to show that even a millimeter-long worm called a nematode falls into some sort of somnolent state.) But why do we—and the rest of the animal kingdom—sleep in the first place?
    “We spend so much of our time sleeping that it must be doing something important,” says David Prober, assistant professor of biology and an expert on how genes and neurons regulate sleep. Yes, we snooze in order to rest and recuperate, but what that means at the molecular, genetic, or even cellular level remains a mystery. “Saying that we sleep because we’re tired is like saying we eat because we’re hungry,” Prober says. “That doesn’t explain why it’s better to eat some foods rather than others and what those different kinds of foods do for us.”
    No one knows exactly why we slumber, Prober says, but there are four main hypotheses. The first is that sleeping allows the body to repair cells damaged by metabolic byproducts called free radicals. The production of these highly reactive substances increases during the day, when metabolism is faster. Indeed, scientists have found that the expression of genes involved in fixing cells gets kicked up a notch during sleep. This hypothesis is consistent with the fact that smaller animals, which tend to have higher metabolic rates (and therefore produce more free radicals), tend to sleep more. For example, some mice sleep for 20 hours a day, while giraffes and elephants only need two- to three-hour power naps.
    Another idea is that sleep helps replenish fuel, which is burned while awake. One possible fuel is ATP, the all-purpose energy-carrying molecule, which creates an end product called adenosine when burned. So when ATP is low, adenosine is high, which tells the body that it’s time to sleep. While a postdoc at Harvard, Prober helped lead some experiments in which zebrafish were given drugs that prevented adenosine from latching onto receptor molecules, causing the fish to sleep less. But when given drugs with the opposite effect, they slept more. He has since expanded on these studies at Caltech.
    Sleep might also be a time for your brain to do a little housekeeping. As you learn and absorb information throughout the day, you’re constantly generating new synapses, the junctions between neurons through which brain signals travel. But your skull has limited space, so bedtime might be when superfluous synapses are cleaned out.
    And finally, during your daily slumber, your brain might be replaying the events of the day, reinforcing memory and learning. Thanos Siapas, associate professor of computation and neural systems, is one of several scientists who have done experiments that suggest this explanation for sleep. He and his colleagues looked at the brain activity of rats while the rodents ran through a maze and then again while they slept. The patterns were similar, suggesting the rats were reliving their day while asleep.
    Of course, the real reason for sleep could be any combination of these four ideas, Prober says. Or perhaps only one of these hypotheses might have been true in the evolutionary past, but as organisms evolved, they developed additional uses for sleep.
    Researchers in Prober’s lab look for the genetic and neural systems that affect zebrafish sleeping patterns by tweaking their genes and watching them doze off. An overhead camera records hundreds of tiny zebrafish larvae as they swim in an array of shallow square dishes. A computer automatically determines whether the fish are awake or not based on whether they’re moving or still, and whether they respond to various stimuli. Prober has identified about 500 drugs that affect their sleeping patterns, and now his lab is searching for the relevant genetic pathways. By studying the fish, the researchers hope to better understand sleep in more complex organisms like humans. “Even if we find only a few new genes, that’ll really open up the field,” he says. The future is promising, he adds, and for that, it’ll be well worth staying awake.
    Provided by California Institute of Technology (news : web)
  9. Anonymous Member

    Brain development may be influenced by bacteria in the gut

    February 1, 2011

    A team of scientists from across the globe have found that gut bacteria may influence mammalian brain development and adult behavior. The study is published in the scientific journal PNAS, and is the result of an ongoing collaboration between scientists at Karolinska Institutet in Sweden and the Genome Institute of Singapore.
    The research team compared behavior and gene expression in two groups of mice - those raised with normal microorganisms, and those raised in the absence of microorganisms (or germ-free mice). The scientists observed that adult germ-free mice displayed different behavior from mice with normal microbiota, suggesting that gut bacteria may have a significant effect on the development of the brain in mammals.
    The adult germ-free mice were observed to be more active and engaged in more 'risky' behavior than mice raised with normal microorganisms. When germ-free mice were exposed to normal microorganisms very early in life, as adults they developed the behavioral characteristics of those exposed to microorganisms from birth. In contrast, colonizing adult germ-free mice with bacteria did not influence their behavior.
    Subsequent gene profiling in the brain identified genes and signaling pathways involved in learning, memory and motor control that were affected by the absence of gut bacteria, highlighting the profound changes in the mice that developed in the absence of microorganisms. This suggests that, over the course of evolution, colonization of the gut by microorganisms (in total 1.5 kilograms) in early infancy became integrated into early brain development.
    "The data suggests that there is a critical period early in life when gut microorganisms affect the brain and change the behavior in later life", says Dr. Rochellys Diaz Heijtz, first author of the study.
    "Not only are signal substances like serotonin and dopamine subject to regulation by bacteria, synapse function also appears to be regulated by colonizing bacteria", continues Prof. Sven Pettersson, coordinator of the study. "However, it is important to note that this new knowledge can be applied only to mice, and that it is too early to say anything about the effect of gut bacteria on the human brain."
    In addition to Sven Pettersson and Rochellys Diaz Heijtz, Prof. Hans Forssberg at Stockholm Brain Institute and Karolinska Institutet, and Dr. Martin Hibberd from the Genome Institute of Singapore (GIS) where involved in the research project. The findings presented are a result of a long-standing and ongoing collaboration between Karolinska Institutet and the GIS in Singapore aimed at exploring host-microbe interactions in a systematic manner.
    More information: Rochellys Diaz Heijtz, et al. Normal gut microbiota modulates brain development and behavior. PNAS, online early edition 31 January - 4 February 2011
    Provided by Karolinska Institutet (news : web)
  10. Anonymous Member

    Scientists reveal key mechanism governing nicotine addiction

    January 30, 2011

    Scientists from the Florida campus of The Scripps Research Institute have identified a pathway in the brain that regulates an individual's vulnerability to the addictive properties of nicotine. The findings suggest a new target for anti-smoking therapies.
    The study appeared January 30, 2011, in an advance, online issue of the journal Nature.
    In the study, the scientists examined the effects of a part of a receptor (a protein molecule to which specific signaling molecules attach) that responds to nicotine in the brain. The scientists found that animal models with a genetic mutation inhibiting this receptor subunit consumed far more nicotine than normal. This effect could be reversed by boosting the subunit's expression.
    "We believe that these new data establish a new framework for understanding the motivational drives in nicotine consumption and also the brain pathways that regulate vulnerability to tobacco addiction," said Scripps Research Associate Professor Paul Kenny, who led the study. "These findings also point to a promising target for the development of potential anti-smoking therapies."
    Specifically, the new study focused on the nicotinic receptor subunit α5, in a discrete pathway of the brain called the habenulo-interpeduncular tract. The new findings suggest that nicotine activates nicotinic receptors containing this subunit in the habenula, triggering a response that acts to dampen the urge to consume more of the drug.
    "It was unexpected that the habenula, and brain structures into which it projects, play such a profound role in controlling the desire to consume nicotine," said Christie Fowler, the first author of the study and research associate in the Kenny laboratory. "The habenula appears to be activated by nicotine when consumption of the drug has reached an adverse level. But if the pathway isn't functioning properly, you simply take more. Our data may explain recent human data showing that individuals with genetic variation in the α5 nicotinic receptor subunit are far more vulnerable to the addictive properties of nicotine, and far more likely to develop smoking-associated diseases such as lung cancer and chronic obstructive pulmonary disease."
    A Previously Unknown Pathway Inhibits Motivation
    Tobacco smoking is one of the leading causes of death worldwide, with more than five million people dying each year as a result of it, according to statistics cited in the study. Smoking is considered the cause of more than 90 percent of lung cancer deaths. Scientists have established that a tendency towards smoking can be inherited – more than 60 percent of the risk of becoming addicted to nicotine can be laid at the door of genetic factors.
    Nicotine is the major addictive component of tobacco smoke, and nicotine acts in the brain by stimulating proteins called nicotinic acetylcholine receptors (nAChRs). These nAChRs are made up of different types of subunits, one of which is the α5 subunit—the focus of the new study.
    In their experiments, the Scripps Research scientists set out to determine the role of nAChRs-containing α5 subunits (α5* nAChRs) in regulating nicotine consumption.
    First, the team assessed the addictive properties of nicotine in genetically altered mice lacking α5* nAChRs. The results showed that when these "knockout" mice were given access to high doses of nicotine, they consumed much larger quantities than normal mice. Next, to determine if the subunit was responsible for the sudden shift in appetite for nicotine, the scientists used a virus that "rescued" the expression of α5* nAChRs only in the medial habenula and areas of the brain into which it projects. The results showed the nicotine consumption patterns of the knockout mice returned to a normal range.
    The scientists repeated the experiments with rats and produced similar results. In this case, the scientists used a virus to "knock out" α5 nAChR subunits in the medial habenula. When the α5* nAChRs were decreased, the animals were more aggressive in seeking higher doses of nicotine. When the subunit remained unaltered, the animals showed more restraint.
    The scientists then worked out the biochemical mechanisms through which α5* nAChRs operate in the medial habenula to control the addictive properties of nicotine. They found that α5* nAChRs regulate just how responsive the habenula is to nicotine, and that the habenula is involved in some of the negative responses to nicotine consumption. So when α5* nAChRs do not function properly, the habenula is less responsive to nicotine and much more of the drug can be consumed without negative feedback from the brain.
    The scientists are optimistic that their findings may one day lead to help for smokers who want to kick the habit. Based on the new findings, the Scripps Florida scientists have started a new program of research in collaboration with scientists at the University of Pennsylvania to develop new drugs to boost α5* nAChR signaling and decrease the addictive properties of nicotine.
    Provided by The Scripps Research Institute (news : web)
  11. an0nim0uz Member

    ScnTo is no longer the most annoying person ITT.
    • Like Like x 6
  12. Anonymous Member

    How does anesthesia disturb self-perception?

    January 19, 2011

    An Inserm research team in Toulouse, led by Dr Stein Silva, working with the "Modelling tissue and nociceptive stress" Host Team (MATN IFR 150), were interested in studying the illusions described by many patients under regional anaesthetic. In their work, to be published in the journal Anesthesiology, the researchers demonstrated that anaesthetising an arm affects brain activity and rapidly impairs body perception.
    The ultimate aim of the work is to understand how neuronal circuits are reorganised at this exact moment in time and to take advantage of anaesthesia to reconfigure them correctly following trauma. This would allow anaesthetic techniques to be used in the future to treat pain described by amputated patients in what are known as "phantom limbs".
    Neuroscience research in recent years has shown that the brain is a dynamic structure. Phenomena such as learning, memorising or recovery from stroke are made possible by the brain's plastic properties. Brain plasticity does not, however, always have a beneficial effect.
    For example, some amputated patients suffering from chronic pain (known as phantom limb pain) feel as though their missing limb were "still there". Such "phantom limb" illusions are related to the appearance in the brain of incorrect representations of the missing body part.
    Persons under regional anaesthetic describe these very same false images.
    Based on these observations, Inserm's researchers wished to discover whether anaesthesia could, in addition to fulfilling its primary function, induce comparable phenomena in the brain. If this were so, anaesthetics could be used as new therapeutic tools capable of modulating brain activity.
    With this in mind, a team headed by Dr Stein Silva monitored 20 patients who were to have one of their arms anaesthetised before surgery. The patients were shown 3D images of the hand, shot from different angles, and their ability to distinguish the right hand from the left was assessed. Results showed how anaesthesia affected the patients' ability to perceive their body correctly.
    The researchers observed three phenomena based on these tests:
    • All the patients described false sensations in their arm (swelling, difference in size and shape, imagined posture).
    • In general, patients under anaesthetic took longer to distinguish between a left and right hand and made far more mistakes than persons not under anaesthetic.
    • The best results were obtained when the anaesthetised limb was visible.
    In other words, anaesthetising the hand (peripheral deafferentation ) modifies brain activity and rapidly changes the way we perceive the outside world and our own body.
    The teams are now using functional brain imaging to characterise the regions concerned in the brain. They also hope that it will be possible to use anaesthesia for therapeutic purposes in the future by modulating post-lesional plasticity (chronic pain in amputated patients, improved recovery in those suffering from brain lesions).
    Inserm researcher Stein Silva, an anaesthetist and the chief author of the study, believes that it will no doubt be necessary to develop new anaesthetic techniques to inhibit or directly stimulate the brain images associated with painful phenomena.
    More information: Anesthesiology, January 2011 - … 3e31820164f1
    Provided by INSERM
  13. Anonymous Member

    Study uses new technology to peek deep into the brain

    January 18, 2011

    Changes within deep regions of the brain can now be visualized at the cellular level, based on research on mice, which was funded by the National Institutes of Health. Published Sunday in Nature Medicine, the study used a groundbreaking technique to explore cellular-level changes over a period of weeks within deep brain regions, providing a level of detail not possible with previously available methods. The study was supported by the National Institute on Drug Abuse (NIDA), the National Cancer Institute, and the National Institute of Neurological Disorders and Stroke.
    Researchers at Stanford University used time-lapse fluorescence microendoscopy, a technique that uses miniature probes to directly visualize specific cells over a period of time, to explore structural changes that occur in neurons as a result of tumor formation and increased stimulation in the mouse brain. This could lead to greater information on how the brain adapts to changing situations, including repeated drug exposure.
    "Continued drug use leads to changes in neuronal circuits that are evident well after a person stops taking an addictive substance," said Dr. Nora D. Volkow, director of NIDA. "This study demonstrates an innovative technique that allows for a glimpse of these cellular changes within the brain regions implicated in drug reward, providing an important tool in our understanding and treatment of addiction."
    Investigators focused on two brain regions within the study, the hippocampus and striatum. The striatum, a brain region important for motor function and habit formation, is also a major target for abused drugs. Some researchers believe that a shift in activity within the striatum is at least partly responsible for the progression from voluntary drug-taking to addiction. This new technique could allow a better understanding of how these processes occur at the cellular level, leading to insights into mechanisms underlying addictive behaviors.
    "The results should now allow neuroscientists to track longitudinally in the living brain the effects of drugs of abuse at the levels of neural circuitry, the individual neuron, and neuronal dendrites," said Dr. Mark Schnitzer, corresponding author for the article. "For example, our imaging methods work well in the dorsal striatum, which we have followed with microscopic resolution over weeks in the live brain. This should permit researchers interested in the reward system to address a range of issues that were previously out of reach."
    More information: The study can be found online at … 1038/nm.2292
    Provided by National Institutes of Health
  14. Anonymous Member

    New technique to see neurons of the deep brain for months at a time developed

    January 16, 2011
    This is a diagram of the experimental setup. (left) Tiny optical instruments called microendoscopes are inserted into glass imaging guide tubes, which maintain a precise position in the brain. This allows researchers to view the exact same neuron with a microscope (right) again and again, a new technique for brain researchers. Scientists can also compare diseased tissue, such as a tumor, to healthy tissue in the same animal. Credit: Modified image courtesy Mark Schnitzer and Nature Medicine.
    Travel just one millimeter inside the brain and you'll be stepping into the dark.
    Standard light microscopes don't allow researchers to look into the interior of the living brain, where memories are formed and diseases such as dementia and cancer can take their toll.
    But Stanford scientists have devised a new method that not only lets them peer deep inside the brain to examine its neurons but also allows them to continue monitoring for months.
    The technique promises to improve understanding of both the normal biology and diseased states of this hidden tissue.
    Other recent advances in micro-optics had enabled scientists to take a peek at cells of the deep brain, but their observations captured only a momentary snapshot of the microscopic changes that occur over months and years with aging and illness.
    The Stanford development appears online Jan. 16 in the journal Nature Medicine. It also will appear in the February 2011 print edition.

    This video is not supported by your browser at this time.
    Stanford researchers have developed a new technique that allows them to monitor the tiny branches of neurons in a live brain for months at a time. Neuroscientists will now be able to monitor the microscopic changes that occur over the course of progressive brain disease. Credit: Jack Hubbard, Stanford University News Service
    Scientists study many diseases of the deep brain using mouse models, mice that have been bred or genetically engineered to have diseases similar to human afflictions.
    "Researchers will now be able to study mouse models in these deep areas in a way that wasn't available before," said senior author Mark Schnitzer, associate professor of biology and of applied physics.
    Because light microscopy can only penetrate the outermost layer of tissues, any region of the brain deeper than 700 microns or so (about 1/32 of an inch) cannot be reached by traditional microscopy techniques. Recent advances in micro-optics had allowed scientists to briefly peer deeper into living tissues, but it was nearly impossible to return to the same location of the brain and it was very likely that the tissue of interest would become damaged or infected.
    With the new method, "Imaging is possible over a very long time without damaging the region of interest," said Juergen Jung, operations manager of the Schnitzer lab. Tiny glass tubes, about half the width of a grain of rice, are carefully placed in the deep brain of an anaesthetized mouse. Once the tubes are in place, the brain is not exposed to the outside environment, thus preventing infection. When researchers want to examine the cells and their interactions at this site, they insert a tiny optical instrument called a microendoscope inside the glass guide tube. The guide tubes have glass windows at the ends through which scientists can examine the interior of the brain.
    "It's a bit like looking through a porthole in a submarine," said Schnitzer.
    The guide tubes allow researchers to return to exactly the same location of the deep brain repeatedly over weeks or months. While techniques like MRI scans could examine the deep brain, "they couldn't look at individual cells on a microscopic scale," said Schnitzer. Now, the delicate branches of neurons can be monitored during prolonged experiments.
    To test the use of the technique for investigating brain disease, the researchers looked at a mouse model of glioma, a deadly form of brain cancer. They saw hallmarks of glioma growth in the deep brain that were previously known in tumors described as surficial (on or near the surface).
    The severity of glioma tumors depends on their location. "The most aggressive brain tumors arise deep and not superficially," said Lawrence Recht, professor of neurology and neurological sciences. Why the position of glioma tumors affects their growth rate isn't understood, but this method would be a way to explore that question, Recht said.
    In addition to continuing their studies of brain disease and the neuroscience of memory, the researchers hope to teach other researchers how to perform the technique.
    Provided by Stanford University (news : web)
  15. Anonymous Member

    New microscope records firing of thousands of individual neurons in 3-D

    January 12, 2011 By Mark Wheeler
    STEM microscope designed at UCLA . Photo credit: UCLA
    ( -- Some disorders of the brain are obvious -- the massive death of brain cells after a stroke, the explosion in the growth of cells that marks a tumor. Other disorders, such as autism, schizophrenia and mental retardation show no physical signs of damage and are believed to be caused by problems in how brain cells communicate with one another.
    To understand the root of the problem of these latter diseases, visualizing brain activity is key. But even the best imaging devices available -- fMRIs and PET scans -- can only give a "coarse" picture of brain activity.
    UCLA neuroscientists have now collaborated with physicists to develop a non-invasive, ultra–high-speed microscope that can record in real time the firing of thousands of individual neurons in the brain as they communicate, or miscommunicate, with each other.
    "In our view, this is the world's fastest two-photon excitation microscope for three-dimensional imaging in vivo," said UCLA physics professor Katsushi Arisaka, who designed the new optical imaging system with UCLA assistant professor of neurology and neurobiology Dr. Carlos Portera-Cailliau and colleagues.
    Their research appears in the Jan. 9 edition of the journal Nature Methods.
    Because neuropsychiatric diseases like autism and mental retardation often display no physical brain damage, it's thought they are caused by conductivity problems — neurons not firing properly. Normal cells have patterns of electrical activity, said Portera-Cailliau, but abnormal cell activity as a whole doesn't generate relevant information the brain can use.
    "One of the greatest challenges for neuroscience in the 21st century is to understand how the billions of neurons that form the brain communicate with one another to produce complex behaviors," he said. "The ultimate benefit from this type of research will come from deciphering how dysfunctional patterns of activity among neurons lead to devastating symptoms in a variety of neuropsychiatric disorders."
    For the last few years, Portera-Cailliau has been using calcium imaging, a technique that uses fluorescent dyes that are taken up by neurons. When the cells fire, they "blink like lights in a Christmas tree," he said. "Our role now is to decipher the code that neurons use, which is buried in those blinking light patterns."
    But that technique had its limitations, according to Portera-Cailliau.
    "The signal of the calcium-based fluorescent dye we used faded as we imaged deeper into the cortex. We couldn't image all the cells," he said.
    Another problem was speed. Portera-Cailliau and his colleagues were concerned they were missing information because they couldn't image a large enough portion of the brain fast enough to measure the group-firing of individual neurons. That was the driving impulse behind the collaboration with Arisaka and one of his graduate students, Adrian Cheng, to find a better way to record neuronal activity faster.
    The imaging technology they developed is called multifocal two-photon microscopy with spatio-temporal excitation-emission multiplexing — STEM for short. The researchers modified two-photon laser-scanning microscopes to image fluorescent calcium dyes inside the neurons, and came up with a way to split the main laser beam into four smaller beamlets. This allowed them to record four times as many brain cells as the earlier version, or four times faster. In addition, they used a different beam to record neurons at different depths inside the brain, giving a 3-D effect, which had never been done previously.
    "Most video cameras are designed to capture an image at 30 pictures per second. What we did was speed that up by 10 times to roughly 250 pictures per second," Arisaka said. "And we are working on making it even faster."
    The result, he said, "is a high-resolution three-dimensional video of neuronal circuit activity in a living animal."
    The use of calcium imaging in research is already providing dividends. Portera-Cailliau studies Fragile X syndrome, a form of autism. By comparing the cortex of a normal mouse with a Fragile X mutant mouse, his group has discerned the misfiring that occurs in the Fragile X brain.
    Other authors of this study included co-first authors Cheng and J. Tiago Goncalves, and Peyman Golshani, all of UCLA. Funding for the research was provided by the National Institutes of Health. The authors report no conflicts of interest.
    Provided by University of California Los Angeles (news : web)
  16. Anonymous Member

    Setting his sights on a cure

    January 11, 2011 By Tom Vasich
    Photo: Steve Zylius
    For poets and lovers, the eyes are windows to the soul. But for researchers like Dr. Henry Klassen, they provide unparalleled access to the central nervous system.
    With this access, the UC Irvine assistant professor of ophthalmology is discovering new ways to use stem cells to repair the retina — the only part of the body’s intricate central nervous system that can be viewed without surgery. In doing so, Klassen is gleaning information about stem cells that goes beyond eye disease.
    “The eye is an important proving ground for stem cell-based therapies,” he says, “and provides a stepping stone to many otherwise incurable diseases of the brain and spinal cord.”
    For nearly 25 years, Klassen — who came to UCI in 2006 — has focused on regenerating damaged retinal tissue to restore sight to people suffering from retinitis pigmentosa and macular degeneration, which affect millions of Americans. He serves as research director for the retinal regeneration program at UCI’s Gavin Herbert Eye Institute and is affiliated with the Sue & Bill Gross Stem Cell Research Center. The Discovery Eye Foundation, which aids many UCI efforts to find cures and treatments for corneal and retinal eye disease, also supports his work.
    In addition to his medical degree, Klassen holds a doctorate in neurobiology and has delved into the retina’s unique architecture to understand how to repair the neural system. The retina lines the inner surface of the eye and converts light images into nerve impulses that are sent to vision centers in the brain.
    In October, Klassen received $3.85 million from the California Institute for Regenerative Medicine — the state’s stem cell research funding agency — to standardize a method for creating photoreceptor progenitor stem cells from immature retinas and transplanting them into the eye to repair or replace damaged light-sensing cells. The CIRM reviewers gave Klassen’s proposal the highest scientific score — 93 on a scale of 100 — among all applicants in this round of grants.
    “Stem cell research on the eye is moving quite quickly,” says Ingrid Caras, a CIRM science officer. “The eye is an attractive study target – it’s a small, contained area with no immune rejection of implanted cells, and it’s much easier to monitor what’s happening in the eye.”
    Retinitis pigmentosa is marked by the slow decay of the photoreceptors — in the shape of rods and cones — that perform the initial detection of light. The disease is caused by mutations in genes important to photoreceptor function. Eventually, the rods die, followed by the cones. People with retinitis pigmentosa first experience night blindness, then tunnel vision and, ultimately, legal blindness.
    Klassen’s objective is to introduce stem cells that supplant damaged and dying rods and also resuscitate moribund cones, thus reversing the course of retinitis pigmentosa even at relatively advanced stages. The current CIRM funding makes clinical trials a possibility within three years.
    “We believe it’s possible to replace rods and rejuvenate cones in the degenerated retina,” Klassen says. “Our methods have been validated, and I’m optimistic that stem cell-based treatments can help people with eye diseases restore their fading vision.”
    Provided by University of California, Irvine (news : web)
  17. Anonymous Member

    'Timing is everything' in ensuring healthy brain development

    January 6, 2011

    Work published today shows that brain cells need to create links early on in their existence, when they are physically close together, to ensure successful connections across the brain throughout life.
    In people, these long-distance connections enable the left and right side of the brain to communicate and integrate different kinds of information such as sound and vision. A change in the number of these connections has been found in many developmental brain disorders including autism, epilepsy and schizophrenia.
    The Newcastle University researchers Dr Marcus Kaiser and Mrs Sreedevi Varier carried out a sophisticated computer analysis relating birth-time associated data to connectivity patterns of nerve cells in the roundworm, Caenorhabditis elegans. They demonstrated that when two nerve cells develop close together, they form a connection which then stretches out when the two nerve cells move apart as the organism grows. This creates a link across the brain known as a long-distance connection.
    Publishing today in PLoS Computational Biology, the researchers have demonstrated for the first time that this is the most frequent successful mechanism by which long distance connections are made.

    This video is not supported by your browser at this time.
    The animation shows the growth of the neuronal network with neurons being added at each stage. There are four different views, shown in succession, for each of the six identified stages of development.
    Dr Marcus Kaiser, at Newcastle University, says: "You can draw parallels with childhood friendships carrying on into adulthood. For example, two children living close to each other could become friends through common activities like school or playing at the park. The friendship can last even if one of them moves further away, while, beginning a lasting friendship with someone already far away, is much more difficult."
    Mrs Sreedevi Varier adds: "Although it's too early for this research to have direct clinical applications, it adds to our understanding of the structural changes in the brain and raises some interesting questions as to how these connections can become faulty. In further studying this mechanism, we may eventually contribute towards insights into the diagnosis and possibly the treatment of patients with epilepsy and autism."
    It has long been understood that the first connections in the brain created in the early days of development can be formed over long distances using guidance signals to direct nerve fibres to their correct positions – known as axonal guidance. Subsequently, other connections can follow those pioneer fibres to a target location creating connections between distant parts of the brain. Through these long-distance connections different kinds of information, such as sound and vision, can be integrated.
    This EPSRC-funded research showed that most neurons are able to create a connection early on in their development when they were physically close together, potentially giving them more time to host and establish connections. These developed into a long-distance connection, the two cells pulling apart as the organism grows larger.
    Studying the connections in the neuronal network of the roundworm Caenorhabditis elegans the Newcastle scientists - who are also affiliated with Seoul National University, Korea - found that most neurons with a long-distance connection had developed in this way.
    This new mechanism differs from the previous model for long-distance connectivity. An axon is a fibre that is extended from one nerve cell and, after travelling through the tissue, can contact several other nerve cells. Normally, axons would grow in a straight line. For several targets, however, the axon has to travel around obstacles, as a straight connection is not possible. In such cases, cells along the way can release guidance cues that either attract or repulse the travelling axon. One example of bended fibres is the visual pathway that at several points takes a sharp 90-degree turn to arrive at the correct target position.
    Instead, establishing potential links early on when neurons are spatially nearby might reduce the need for such guidance cues. This reduces costs in producing guidance cues but potentially also for genetically encoding a wider range of cues. An early mechanism opens up the possibility that changes in long-distance brain connectivity, that are observed in children and young adults with brain disorders, arise earlier during brain development than previously thought. These are questions that the team continue to work on through data analysis and computer simulations of brain development.
    More information: Neural development features: Spatio-temporal development of the Caenorhabditis elegans neuronal network, Sreedevi Varier and Marcus Kaiser Published in: PLoS Computational Biology
    Provided by Newcastle University
  18. Anonymous Member

    Autism-vaccine study was 'fraud' says journal (Update)

    January 5, 2011

    A 1998 study that linked childhood autism to a vaccine was branded an "elaborate fraud" by the British Medical Journal (BMJ) Thursday, but its lead author said he was the victim of a smear campaign by drug manufacturers.
    In an interview late Wednesday with CNN, Andrew Wakefield denied inventing data and blasted a reporter who apparently uncovered the falsifications as a "hit man" doing the bidding of a powerful pharmaceutical industry.
    "It's a ruthless pragmatic attempt to crush any investigation into valid vaccine safety concerns," Wakefield said.
    He insisted the "truth" was in his book about the scandal: "The book is not a lie, the study is not a lie...I did not make up the diagnoses of autism."

    Follow up: Autism study doctor says victim of smears

    Blamed for a disastrous boycott of the measles, mumps and rubella (MMR) vaccine in Britain, the study was retracted by The Lancet last year and Wakefield was disgraced on the grounds of conflict of financial interest and unethical treatment of some children involved in the research.
    Wakefield, then a consultant in experimental gastro-enterology at London's Royal Free Hospital, and his team suggested they had found a "new syndrome" of autism and bowel disease among 12 children.
    They linked it to the MMR vaccine, which they said had been administered to eight of the youngsters shortly before the symptoms emerged.
    But other scientists swiftly cautioned the study was only among a tiny group, without a comparative "control" sample, and the dating of when symptoms surfaced was based on parental recall, which is notoriously unreliable.
    Experts said the study's results have never been replicated.
    When asked why 10 of his co-authors retracted the interpretations of the study, Wakefield said: " I'm afraid the pressure has been put on them to do so."
    "People get very, very frightened. You're dealing with some very powerful interests here."
    The BMJ charged that hundreds of thousands of children in Britain are now unshielded against these three diseases. In 2008, measles was declared endemic, or present in the wider population much like chicken pox, in England and Wales.
    None of the 12 cases, as reported in the study, tallied fully with the children's official medical records, the journal said.
    Some diagnoses had been misrepresented and dates faked in order to draw a convenient link with the MMR jab, it said.
    Of nine children described by Wakefield as having "regressive autism," only one clearly had this condition and three were not even diagnosed with autism at all, it said.
    The findings had been skewed in advance, as the patients had been recruited via campaigners opposed to the MMR vaccine, the journal added.
    And, said the BMJ, Wakefield had been confidentially paid hundreds of thousands of pounds (dollars, euros) through a law firm under plans to launch "class action" litigation against the vaccine.
    Wakefield, who still retains a vocal band of supporters, reportedly left Britain to work in the United States.
    Wakefield has previously accused Britain's General Medical Council (GMC) of seeking to "discredit and silence" him and shield the British government from responsibility in what he calls a "scandal."
    The Lancet told AFP it would not comment on the BMJ accusations.
    Autism is the term for an array of conditions ranging from poor social interaction to repetitive behaviours and entrenched silence. The condition is rare, predominantly affecting boys, although its causes are fiercely debated.
    (c) 2011 AFP
  19. Anonymous Member

    Scientist haunted by misuse of drugs he invented

    January 5, 2011 By SETH BORENSTEIN , AP Science Writer
    This handout photo provided by Purdue University shows David Nichols in a lab at the university in West Lafayette, Ind., Wednesday, Jan. 5, 2011. Nichols studies the way psychedelic drugs act in the brains of rats. But he's haunted by how his work is being hijacked by humans selling street drugs. (AP Photo/Purdue University, Mark Simons)
    David Nichols studies the way psychedelic drugs act in the brains of rats. But he's haunted by how humans hijack his work to make street drugs, sometimes causing overdose deaths.
    Nichols makes chemicals roughly similar to ecstasy and LSD that are supposed to help explain how parts of the brain function. Then he publishes the results for other scientists, hoping his work one day leads to treatments for depression or Parkinson's disease.
    But Nichols' findings have not stayed in purely scientific circles. They've also been exploited by black market labs to make cheap and marginally legal recreational drugs.
    "You try to work for something good, and it's subverted in a way," Nichols said. "I try not to think about it."
    Now the 66-year-old chairman of the Purdue University pharmacology department is speaking out in one of the world's most prestigious scientific journals to describe an ethical struggle seldom discussed by brain researchers.
    "You can't control what people do with what you publish, but yeah, I felt it personally," he said in a phone interview, explaining that his struggles are probably somewhat similar to those faced by the inventor of the machine gun, although not as severe. The journal Nature published his essay online Wednesday.
    "What if a substance that seems innocuous is marketed and becomes wildly popular on the dance scene, but then millions of users develop an unusual type of kidney damage that proves irreversible and difficult to treat, or even life-threatening or fatal?" Nichols wrote. "That would be a disaster of immense proportions. This question, which was never part of my research focus, now haunts me."
    Nichols has studied psychedelic drugs for more than 40 years, concentrating on serotonin. That's a basic chemical "that goes to every part of the brain. It's involved in appetite, sleep, sex, aggression, you name it," Nichols said in the interview with The Associated Press. "It really plays a key role in brain activation, the difference between being awake and being asleep."
    Nichols estimates that at least five of his compounds - out of hundreds - have been turned into street drugs.
    His drug work used to be a joking matter. People would ask him if he needed human test subjects, and he would respond: "No, it's just rat stuff."
    "I never thought of these getting out of the lab," he told the AP. Sure, the field includes research into LSD and other hallucinogens, but Nichols never imagined his work escaping the lab and causing death. The worst would be maybe someone getting high on stuff they shouldn't, he figured.
    "Every time we make a molecule now, I do think, 'Is this the one that's going to be a problem?' I never used to think that before," Nichols said.
    One chemical was so potent that "I just stopped and said, 'We're not going to study this one. This stuff would hit the market big-time,'" he said.
    That wasn't the case almost 20 years ago, when he developed something similar to ecstasy - but not nearly as potent. Back then it was a little-known street drug. He published his study, found little interest from pharmaceutical companies in his chemical, called MTA, and moved on.
    But somebody in the illicit world of drug abuse read his research and synthesized that drug into tablets for street use. It was eerily called "flatliners." But it really didn't provide much of a high. "Flatline implies that you're brain dead," Nichols said. "Why would anyone take it?"
    People did. They took too much. Their brains were flooded with serotonin, and they died. The first time Nichols was told about it, only two people had died.
    "I sat in my office and thought. 'Wow, if you shoot somebody with a gun, you know you killed them, but if technology escapes and someone dies," Nichols said, his voice trailing off. "You're kind of disconnected from it."
    At least five or six people died from that first drug. A second drug, a hallucinogenic called bromo-dragonfly, has killed two others. It could have been worse because it was chemically similar to a potent toxin that causes liver cancer, Nichols said.
    A story last year in the Wall Street Journal said Nichols' published research is a favorite for European chemists who make black market street drugs. That hit him hard, but didn't surprise him. In the past year or so, he's been getting inquiries about his research from investigators and forensic labs.
    Johns Hopkins University behavioral biology professor Roland Griffiths struggles with the same ethical questions when he studies the chemicals behind hallucinogenic mushrooms. But Griffiths believes the key to scientific progress is the free exchange of ideas, saying it's better than no information.
    University of Pennsylvania bioethicist Art Caplan said there are times when you can share too much scientific information - with nuclear weapons, biological weapons and the like - despite the desire for open research. And this may be one of those cases given the large black market out there, he said.
    Caplan said Nichols' essay "should lead to more careful thinking about the unintended consequences of scientific advances."
    More information: Nature:
    ©2010 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
  20. Anonymous Member

    In Brief: The cocktail party problem

    January 4, 2011

    People can identify a repeating sound in a noisy room, but only when the noise includes mixtures of distinct distracting sounds, according to a study published this week in the Proceedings of the National Academy of Sciences.
    Sound researchers have pondered this so-called "cocktail party problem," which underlies the ability to focus on a specific, unfamiliar sound.
    To determine how the auditory system parses sound seemingly effortlessly, Josh H. McDermott and colleagues presented listeners with a synthesized audio recording that resembled everyday sounds, such as spoken words and animal vocalizations.
    When the target sound was presented with one other sound, the listeners heard the mixture as a single sound and were unable to identify the target correctly.
    However, when the target sound was presented repeatedly, mixed with a distinct distracting sound each time, the listeners developed an impression of the repeating target and identified it in the mixtures.
    Further, the listeners' ability to recognize the target sound depended on the number of different mixtures in the audio recording, not the number of times the target was presented.
    Hence, the authors suggest, the auditory system detects sounds based on patterns of time and frequency, such as might be produced by feet pounding on pavement or by branches swaying in the wind, and interprets the patterns as sound sources.
    More information: "Recovering sound sources from embedded repetition," by Josh H. McDermott, David Wrobleski, and Andrew J. Oxenham, Proceedings of the National Academy of Sciences, January 2010.
    Provided by Proceedings of the National Academy of Sciences
  21. Anonymous Member

    Uncovering the neurobiological basis of general anesthesia

    December 30, 2010

    The use of general anesthesia is a routine part of surgical operations at hospitals and medical facilities around the world, but the precise biological mechanisms that underlie anesthetic drugs' effects on the brain and the body are only beginning to be understood. A review article in the December 30 New England Journal of Medicine brings together for the first time information from a range of disciplines, including neuroscience and sleep medicine, to lay the groundwork for more comprehensive investigations of processes underlying general anesthesia.
    "A key point of this article is to lay out a conceptual framework for understanding general anesthesia by discussing its relation to sleep and coma, something that has not been done in this way before," says Emery Brown, MD, PhD, of the Massachusetts General Hospital (MGH) Department of Anesthesia, Critical Care and Pain Medicine, lead author of the NEJM paper. "We started by stating the specific physiological states that comprise general anesthesia – unconsciousness, amnesia, lack of pain perception and lack of movement while stable cardiovascular, respiratory and thermoregulatory systems are maintained – another thing that has never been agreed upon in the literature; and then we looked at how it is similar to and different from the states that are most similar – sleep and coma."
    After laying out their definition, Brown and his co-authors – Ralph Lydic, PhD, a sleep expert from the University of Michigan, and Nicholas Schiff, MD, an expert in coma from Weill Cornell Medical College – compare the physical signs and electroencephalogram (EEG) patterns of general anesthesia to those of sleep. While it is common to describe general anesthesia as going to sleep, there actually are significant differences between the states, with only the deepest stages of sleep being similar to the lightest phases of anesthesia induced by some types of agents.
    While natural sleep normally cycles through a predictable series of phases, general anesthesia involves the patient being taken to and maintained at the phase most appropriate for the procedure, and the phases of general anesthesia at which surgery is performed are most similar to states of coma. "People have hesitated to compare general anesthesia to coma because the term sounds so harsh, but it really has to be that profound or how could you operate on someone?" Brown explains. "The key difference is this is a coma that is controlled by the anesthesiologist and from which patients will quickly and safely recover."
    In detailing how different anesthetic agents act on different brain circuits, the authors point out some apparently contradictory information – some drugs like ketamine actually activate rather than suppress neural activity, an action that can cause hallucinations at lower doses. Ketamine blocks receptors for the excitatory transmitter glutamate, but since it has a preference for receptors on certain inhibitory neurons, it actually stimulates activity when it blocks those inhibitors. This excess brain activity generates unconsciousness through a process similar to what happens when disorganized data travels through an electronic communication line and blocks any coherent signal. A similar mechanism underlies seizure-induced unconsciousness.
    Brown also notes that recent reports suggest an unexpected use for ketamine – to treat depression. Very low doses of the drug have rapidly reduced symptoms in chronically depressed patients who had not responded to traditional antidepressants. Ketamine is currently being studied to help bridge the first days after a patient begins a new antidepressant – a time when many may be at risk of suicide – and the drug's activating effects may be akin to those of electroconvulsive therapy.
    Another unusual situation the authors describe is the case of a brain-injured patient in a minimally conscious state who actually recovered some functions through administration of the sleep-inducing drug zolpidem (Ambien). That patient's case, analyzed previously by Schiff, mirrors a common occurrence called paradoxical excitation, in which patients in the first stage of general anesthesia may move around or vocalize. The authors describe how zolpidem's suppression of the activity of a brain structure called the globus pallidus – which usually inhibits the thalamus – stimulates activity in the thalamus, which is a key neural control center. They hypothesize that a similar mechanism may underlie paradoxical excitation.
    "Anesthesiologists know how to safely maintain their patients in the states of general anesthesia, but most are not familiar with the neural circuit mechanisms that allow them to carry out their life-sustaining work," Brown says. "The information we are presenting in this article – which includes new diagrams and tables that don't appear in any anesthesiology textbook – is essential to our ability to further understanding of general anesthesia, and this is the first of several major reports that we anticipate publishing in the coming year."
    Schiff adds, "We think this is, conceptually, a very fresh look at phenomena we and others have noticed and studied in sleep, coma and use of general anesthesia. By reframing these phenomena in the context of common circuit mechanisms, we can make each of these states understandable and predictable."
    Provided by Massachusetts General Hospital (news : web)
  22. BrakTalk Member

    I'm almost beginning to suspect that whoever is making all these posts is using some kind of bot to do it, which grabs data from a few predetermined websites' tags and automatically pastes them in here. There's no way s/he is copy and pasting all these manually this fast.
    • Like Like x 3
  23. Natter Bored Member

    I like ^
  24. Anonymous Member

    You can't have a conversation with a computer virus.
    • Like Like x 1
  25. Anonymous Member

    Could be a team.

    I like how the posts/walls of text emphasize the work science is doing, mostly in the medical fields.

    Where are all the brilliant scientologist scientists? After 60 fucking years of this dianetic/scientology crap, there aren't any. And there will never be any.

    There will only be a bunch of stupefied people, on a bridge to nowhere, obtaining imaginary freedom, getting their minds destroyed by science-fiction. Oops.
    • Like Like x 9
  26. BrakTalk Member

    You can if you can decompile it and you know the programming language it was written in.
  27. Tooo bad ScnTo doesn't even use .00000001 % of its brain :(
    also: cawks
  28. BrakTalk Member

    You don't need a brain. It doesn't do anything. Don't you remember? The brain just takes you back into the ethereal realm of times passed on the space-time continuum. That's where all the memories and information actually reside. Psh. Don't you know ANYTHING? It's right there, documented for you in Dianetics chapter 4, entitled "The Way to Bullshit", on page 86. In black and white.
  29. Anonymous Member

    You can't have a conversation with a computer virus.
  30. but... i kinda really like mah brain. :'(
  31. BrakTalk Member

    Oh, I've had my fair share of conversations with them. They usually break the ice with a popup message saying "Viagra! $25 per bottle!". Then I say "no" by clicking the little X at the top to close the popup, then it tries to change the topic to "Enlarge your penis!"
    • Like Like x 2
  32. Anonymous Member

    You can't have a conversation with a computer virus.
  33. BrakTalk Member

    But it just weighs down your head. It could be safely removed and all your cognitive abilities will remain intact. L. Ron said so, so it must be true. How else would you be able to remember past lives where your current brain wasn't present? It's the only logical conclusion.
    • Like Like x 1
  34. BrakTalk Member

    You can't have a conversation with a Scientologist either. Their methods are almost the same as the popup ads: "Solve all your problems for only $xxx,xxx.xx!"
  35. BrakTalk Member

    • Like Like x 1
  36. or alot o' free tits ass and cawk!!!!!
    • Like Like x 1
  37. aww brak you just gone and upset mah brain....
    • Like Like x 1
  38. slobeck Member

    • Like Like x 3
  39. slobeck Member

    FIFY again
    • Like Like x 2
  40. Oh you.
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