Motivational and Inspirational Quotes

1) A good  companion: A good  companion is not like the rain, Which comes and goes. Its like the air, Some time very quite, 2) Work hard till you succeed:  When U win in ur first attempt  people say its luck, But if U win after a defeat they say as hard work. Work hard till U succeed!!! But constantly hanging around. 3) Truth of life: We make them cry who care for us, We cry for them who never care for us, And we care for them who will never cry for us� 4) Always make your absence: Always make ur absence felt in such a way, That somebody misses U, But let not ur absence be so long, That somebody starts learning 2 live without U!!! 5) Trust me that is true: People die younger, Because god loves them so much, You're still on earth, Because there's someone, Who loves you more than god, Trust me, that is true. 5) Knowing yourself is true wisdom: Knowing others is intelligence, Knowing yourself is true wisdom, Mastering others is strength, Mastering yourself is true power. 6) When someone loves you: When some one loves you, You don't realize it, When you realize it, its too late. You always love the one who leaves you And leave the one who loves you. 7) So much love for you: If U r in luv, accept it, respect it & enjoy it. But if U r not, then don't worry coz Someone, somewhere must be wrapping up So much luv for U. 8) Happiness is a perfume : Happiness is a perfume . You cannot spread on others without getting a few drops on urself. So always be happy to make others happy ! 9) The best is yet to come..: If yesterday didn't end up  the way you planned, Just remember: God created today for you  To start a new one! The best is yet to come! 10) Tackle life with all yur skills: Tackle life with all ur skills Overcome each and every hill If u persist with all ur will U will enjoy ur life and all its thrill's. 11) I want Peace: Somebody asked god, I want peace, god replied. Remove that i as that is ego, And peace will be automatically there 12) Never take someone for granted..:  Never take some one for granted, Hold every person close to your Heart Because you might wake up one day and realize That you have lost a diamond While you were too busy collecting stones 13) Think Postive always: GODISNOWHERE This can be read as GOD IS NO WHERE Or as GOD IS NOW HERE Everything depends on how do u see anything. So think positive 14) Aisa apna muqaam rakhna: Dil main hamari yaad rakhna Chehray par muskurahat rakhna Kabhi koi hara na sakay Aisa apna muqaam rakhna 15) Never break anyone's heart: Never break anyone's heart, While breaking heart of others Think first what will happen When someone will break your heart 16) one day more to hope: Every SUNSET gives us one day less to live But every SUNRISE gives us one day more to hope 17) God Bless you: In times of difficulties don't say,  "god have a big problem" Instead say, "hey problem have a big god" Everything will be yours�.God bless you ********************* ******** Some of the Inspiring Quotes which tell not to give up in life so you can learn something from these Quotes 1) Never expect things to happen.. struggle and make them happen.  never expect yourself to be given a good value create a value of your own 2) If a drop of water falls in lake there is no identity. But if it falls on a leaf of lotus it shine like a pearl. so choose the best place where you would shine.. 3) Falling down is not defeat...defeat is when your refuse to get up... 4) Ship is always safe at shore... but it is not built for it 5) When your successful your well wishers know who you are when you are unsuccessful you know who your well wishers are 6) It is great confidence in a friend to tell him your faults; greater to tell  him/her 7)  "To the world you might be one person, but  to one person you just might be the world 8) "Even the word 'IMPOSSIBLE' says 'I M POSSIBLE' " 9) Effort is important, but knowing where to make an effort in your  life makes all the difference. Never take some one for granted, Hold every person Close to your Heart because you might wake up one day and realize that you have lost a diamond while you were too busy collecting stones." Remember this always in life

Neuroscience: Making connections

The nerve fibres of the author's brain were traced by diffusion spectrum imaging, and coloured to represent their direction.

MGH HUMAN CONNECTOME PROJECT ACQUISITION TEAM

A building that once housed a Second World War torpedo factory seems an unlikely location for a project aiming to map the human brain. But the Martinos Center for Biomedical Imaging — an outpost of the Massachusetts General Hospital in an industrialized stretch of Boston's riverfront — is home to an impressive collection of magnetic resonance imaging machines. In January, I slid into the newest of these, head first. The operator ran a few test sequences to see whether I experienced any side effects from the unusually rapid changes in this machine's magnetic field. And, when I didn't — no involuntary muscle twitches or illusory flashes of light in my peripheral vision — we began. The machine hummed, then started to vibrate. For 90 minutes, I held still as it scanned my brain.

That scan would be one of the first carried out by the Human Connectome Project (HCP), a five-year, US$40-million initiative funded by the National Institutes of Health (NIH) in Bethesda, Maryland, to map the brain's long-distance communications network. The network, dubbed the 'connectome', is a web of nerve-fibre bundles that criss-cross the brain in their thousands and form the bulk of the brain's white matter. It relays signals between specialized regions devoted to functions such as sight, hearing, motion and memory, and ties them together into a system that perceives, decides and acts as a unified whole.

The connectome is bewilderingly complex and poorly understood. The HCP proposes to resolve this by using new-generation magnetic resonance imaging (MRI) machines, like that used to scan my brain, to trace the connectomes of more than 1,000 individuals. The hope is that this survey will establish a baseline for what is normal, shed light on what the variations might mean for qualities such as intelligence or sociability, and possibly reveal what happens if the network goes awry. “We increasingly believe that brain disorders — from schizophrenia to depression to post-traumatic stress disorder — are disorders of connectivity,” says Thomas Insel, director of the National Institute of Mental Health (NIMH) in Bethesda and a strong supporter of the HCP. “So it is of vital importance that we have ways of detecting and quantifying these connections.”

Yet many wonder whether the NIH is making a mistake. Researchers have yet to prove that MRI techniques can produce a reliable picture of normal connectivity, never mind the types of abnormal connection likely to be found in brain disorders, and some researchers argue that the techniques have not been adequately validated. “I would do the basic neuroscience before I started running lots of people through MRI scanners,” says David Kleinfeld, a physics and neurobiology researcher at the University of California, San Diego.

The grand challenge

Proponents counter that the HCP is a calculated risk. “No one thinks this is going to produce a wiring diagram like you might have for the electricity in your house,” says Insel. But so little is known about the connectome, he says, that even crude maps would represent a major scientific advance.

The decision to take that risk was made by the NIH's Blueprint for Neuroscience Research, set up in 2004 as a collaboration among the 15 NIH institutes, centres and offices with an interest in nervous-system research. In 2009, after five years of funding smaller projects, the group asked officials from across the NIH to submit ideas for 'grand challenges' in neuroscience: large-scale programmes that, Insel says, “would be both extremely high-impact, and virtually impossible with traditional grant mechanisms”.

The Blueprint group received a dozen submissions, including one from Michael Huerta, then a programme officer at the NIMH and a member of a Blueprint subcommittee. Huerta, now at the NIH's National Library of Medicine, began his research career studying the organization of mammalian brains using old-school anatomical and neural-tracing techniques, which typically require the injection of a tracer compound that migrates along nerve fibres and reveals their routes. So he was all too familiar with the barriers to such studies in humans. For ethical reasons, tracers can only be used post-mortem — when they don't migrate far enough to trace a fibre's full length. “The studies just never panned out,” says Huerta.

Nature Neuropod

Nature’s Kerri Smith discusses the Human Connectome Project at its launch

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In 2007, Huerta became fascinated by two new non-invasive imaging methods that might finally allow researchers to study the finer details of connectivity in the brains of living humans. The first was diffusion-spectrum imaging (DSI), developed in 2005 by Van Wedeen, a radiologist at the Martinos Center, and his colleagues¹. DSI is a refinement of the two-decades-old diffusion tensor imaging technique, which exploits MRI's ability to detect the direction in which water molecules are moving at each point in the brain. Because most of those molecules move along the lengths of nerve fibres, like water through a pipe, the data can be used to reconstruct each fibre's location and trajectory. What DSI adds is a more sophisticated form of signal analysis that allows researchers to continue tracing fibre bundles even when one seems to pass behind another, a situation that posed serious problems for the older technique.

The second method that caught Huerta's attention was resting-state functional MRI (rs-fMRI), in which people think about nothing in particular while their brain activity is measured. This is quite different from conventional functional-imaging studies, in which participants are asked to carry out a specific cognitive task and researchers look for the brain regions that are activated in the process. In rs-fMRI, there is no task, and researchers look for correlations among the activity levels in different areas. The presumption is that any two regions with a consistently high correlation are linked — perhaps by an actual bundle of nerve fibres, but certainly by working together in some way.

The application of both DSI and rs-fMRI had already led to a number of high-profile publications. But Huerta realized that few groups were applying both methods in the same subjects, and most studies used small samples, limiting their generalizability. So he proposed that the Blueprint group fund a Human Connectome Project that would apply both methods to hundreds of people. This would allow the first large-scale comparison to be made between structural connectivity, as determined by DSI, and functional connectivity, as determined by rs-fMRI. “No single neuroimaging approach would give you the type of gold-standard connectivity data you need,” says Huerta, recalling his argument for the dual data sets.

The Blueprint group was intrigued, but was not blind to the problems inherent in these techniques. One obvious issue is DSI's spatial resolution: each fibre bundle in the image contains thousands of neurons, meaning that it would miss a great deal of structure on smaller scales.

Partha Mitra, a neuroscientist at Cold Spring Harbor Laboratory in New York, illustrated the problem to me by displaying a series of high-resolution digital pictures of mouse brain slices, each of which had some of its neurons coloured with a dark brown dye. On one such slice, he showed neurons that originated in the left cortex, then branched out and sent fibres to areas on both the left and the right side of the brain. “The brain is not made up of point-to-point connections,” he said. “It's made up of trees.”

This level of connectome structure is invisible to even the most advanced diffusion-imaging methods, says Mitra, who heads the Mouse Brain Architecture Project, a parallel version of the HCP, funded by the NIH and the W. M. Keck Foundation of Los Angeles, that seeks to generate a whole-brain wiring diagram for the mouse using staining techniques. And the problem is made even worse when the data are converted into a 'connectivity matrix', which seeks to quantify how much every point in the brain is connected to every other point — but can't tell the difference between, say, two separate fibres and one fibre with two branches.

The Blueprint group was also aware of concerns about resting-state scans. As with the more familiar form of fMRI, what is actually measured isn't neural activity itself, but blood flow. The general presumption is that the two quantities are closely related — that blood flow increases in a region of the brain whenever the neurons there are active and need to be supplied with more oxygen. But recently, Kleinfeld points out, several studies have called that assumption into question, showing that some increases in blood flow in the brain occur without an increase in neuronal activity². “There is no simple one-to-one relationship,” he says.

A remaining concern

That makes rs-fMRI studies particularly hard to interpret, Kleinfeld adds, if only because the brain's resting-state activity may fluctuate on the same timescales that its blood vessels do. A recent review³ of rs-fMRI admits that this vascular fluctuation “remains a concern”. Other studies show that even something as simple as a subject's pattern of breathing⁴ or slight movements of the head⁵ can significantly confound rs-fMRI measurements.

Even leaving the technical challenges aside, there was no assurance that collecting the connectomes of hundreds of individuals would lead to interesting generalizations. “You could certainly imagine situations in which everyone's wiring diagrams are quite different,” says Gregory Farber, the programme officer at the NIMH who manages the connectome project. Nonetheless, the Blueprint group was swayed by the argument that imperfect data are better than no data. “The committee asked, 'Will we have better methods in five years?',” recalls Huerta. “I'm sure we would. But if we followed that rule, no science would ever get done.”

The group also liked the fact that the findings would be broadly applicable to clinical, as well as scientific, questions. “We thought we could do something like what we did with the Human Genome Project,” Insel says, “because once you have that map of the brain you can compare it to similar maps across development, or to maps of subjects with different disorders of brain circuitry.”

M.F. GLASSER & D.C. VAN ESSEN, THE HUMAN CONNECTOME PROJECT

A blueprint for the brain

In July 2009, the Blueprint group announced its choice of the HCP as one of three grand challenges — the other two focused on pain and on drugs for nervous-system disorders — and simultaneously put out a request for proposals. On 15 September 2010, the NIH announced that it would be funding two HCP proposals.

The larger of the two is a 5-year, $30-million effort led by David Van Essen, a neurobiologist at Washington University in St Louis, Missouri, and Kamil Ugurbil, an fMRI pioneer at the University of Minnesota in Minneapolis. (Another collaborator is Olaf Sporns, a neuroscientist at Indiana University in Bloomington, a co-author on the 2005 review article that coined the term 'connectome'⁶.) During phase one, now nearing completion in Minneapolis, this team has developed a scanner that will be able to double the resolution of standard MRI.

Once complete, that scanner will be moved to Washington University, where it will immediately begin high-throughput scanning. The plan is to use both DSI and rs-fMRI (see 'Scanning the connectome') to study 1,200 people: 300 identical twins, 300 non-identical twins and 600 non-twin siblings. This will allow researchers to explore how much of the brain's connectivity is mapped out by genes. Volunteers will also complete behavioural tests and other fMRI, magnetoencephalogram and electroencephalogram protocols, so that brain structure can be further correlated with function. All these data will be made public, allowing unaffiliated researchers to answer their own questions, and Van Essen's group plans to release a set of new data-analysis tools. Connectomics, Van Essen says, “has been a cottage industry. But we expect this project to allow for a much richer, more unified approach”.

The smaller HCP project — a 3-year, $8.5-million effort led by Bruce Rosen, a radiologist at the Massachusetts General Hospital, and Arthur Toga, a neurologist at the University of California, Los Angeles — involved building a new fMRI scanner optimized for the collection of fibre-tracking data. The idea was to massively increase the gradient strength of the machine — a measure of how rapidly the MRI's magnetic field varies from point to point in the brain. A more intense gradient is like “a bigger mirror in a telescope”, says Wedeen, who is director of connectomics at the Martinos Center. It simultaneously makes the instrument more sensitive to faint signals, and gives it a higher resolution. The machine has now been built — it is the one that collected images of my brain in January — but will require much more tweaking and testing before it is optimized for routine use. But the researchers have already achieved a tenfold increase in sensitivity to the water-diffusion signal, allowing their scanner to trace connections much more precisely than the best off-the-shelf machines.

In a press release announcing the launch of the HCP in July 2009, Insel said that the project would “map the wiring diagram of the entire, living human brain” and that this map could be linked to “the full spectrum of brain function in health and disease”. Such lofty ambitions may or may not succeed in five years. But the project still has its place, says Sebastian Seung, a computational neuroscientist at the Massachusetts Institute of Technology in Cambridge, who studies brain connectivity at the cellular level. “I think it is a mistake to think we have to look at every cell in every region of the brain to make scientific progress,” says Seung, who is not involved in the HCP.

But he also emphasizes that the HCP's connectivity map will be, at best, a beginning. “That is just going to tell us where to look,” he says. “Then we need to study actual cells to learn more”, to figure out how the brain's networks actually transmit information.

A week after my visit to the Martinos Center, I received my DSI data. Using free software from the centre, it is easy to explore the architecture of my brain. I can clearly see my hippocampus, and the vast array of fibres projecting from the midbrain sensory hubs up to my cerebral cortex. I am overwhelmed by the visible detail and obvious organization. At present, it is just a pretty picture — a novelty to show friends. But, I wonder: once scientists know what 'average' looks like, and once they understand the variations, what, if anything, will this rainbow-coloured highway map of my brain say about me?

Nature 483, 394–396 ( 22 March 2012 ) doi :10.1038/483394a

References

1. Wedeen, V. J., Hagmann, P., Tseng, W. Y., Reese, T. G. & Weisskoff, R. M. Magn. Reson. Med. 54, 1377–1386 (2005).
2. Sirotin, Y. B. & Das, A. Nature 457, 475–479 (2009).
3. Kelly, C., Biswal, B. B., Craddock, R. C., Castellanos, F. X. & Milham, M. P. Trends Cogn. Sci. 16, 181–188 (2012).
4. Di, X., Kannurpatti, S. S., Rypma, B. & Biswal, B. B. Cerebral Cortex http://dx.doi.org/10.1093/cercor/bhs001 (2012).
5. Power, J. D., Barnes, K. A., Snyder, A. Z., Schlaggar, B. L. & Petersen, S. E. Neuroimage 59, 2142–2154 (2012).
6. Sporns, O., Tononi, G. & Kötter, R. PLoS Comput. Biol. 1, e42 (2005).

Source: Nature
http://www.nature.com/news/neuroscience-making-connections-1.10260

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Robert Karl Stonjek

Study shines light on brain mechanism that controls reward enjoyment

What characterizes many people with depression, schizophrenia and some other mental illnesses is anhedonia: an inability to gain pleasure from normally pleasurable experiences.

Exactly why this happens is unclear. But new research led by neuroscientists at the University of North Carolina at Chapel Hill School of Medicine may have literally shined a light on the answer, one that could lead to the discovery of new mental health therapies. A report of the study appears March 22 in the journal Neuron.

The study used a combination of genetic engineering and laser technology to manipulate the wiring of a specific population of brain cells deep in a portion of a midbrain area that's known to promote behavioral responses to reward.

"For many years it's been known that dopamine neurons in the ventral midbrain, the ventral tegmental area, or VTA, are involved in reward processing and motivation. For example, they're activated during exposure to drugs of abuse and to naturally rewarding experiences," said study lead author Garret D. Stuber, PhD, assistant professor in the departments of Psychiatry and Cell and Molecular Physiology, and the UNC Neuroscience Center.

"The major focus in our lab is to determine what other sorts of neural circuits or genetically defined neural populations might be modulating the activity of those neurons, whether it's increasing or decreasing their activity," Stuber said. "In our study we found that activation of the nearby VTA GABAergic neurons directly inhibit the function of dopamine neurons, which is something that's never been shown before."

In the past, researchers have tried to get a glimpse into the inner workings of the brain using electrical stimulation or drugs, but those techniques couldn't quickly and specifically change only one type of cell or one type of connection. But optogenetics, a technique that emerged about six years ago, can.

In this study, the scientists used a transgenic animal with a foreign gene that has been inserted into its genome to express a bacterial enzyme that can cause DNA recombination only in GABA neurons and not dopamine cells. Using a gene transfer method developed at UNC and with the animal anesthetized, the Stuber team transferred light-sensitive proteins called "opsins" – derived from algae or bacteria that need light to grow – into the VTA, targeting GABA cells. The presence of these foreign opsins in GABA neurons allows researchers to excite or inhibit them by pumping light from a laser into brain tissue.

The animals were then tested in different reward situations, simple tasks in which they were trained to associate a cue with a sugar water reward from a bottle or were given the opportunity to drink the reward by "free licking," where they could drink as much as they want.

Then, via optical fibers, the researchers shined laser beams onto the genetically manipulated GABA neurons, activating them for 5 seconds during the cue period followed by reward. And on another day, they activated the neurons during reward consumption, when the animals were actively engaged in drinking the sugar water.

"And what we saw when we activated the cells during the cue period, or reward anticipation, it didn't do anything to the behavioral response at all; they showed no difference compared to non-stimulated animals," Stuber explained.

"And when they were actively engaging with the sucrose, we did see we could disrupt their reward consumption when we activated those cells. They immediately disengaged from drinking, stopped drinking the sucrose solution. And when the stimulus stopped, they would then return back and continue to drink it again."

During the "free licking" sessions, optical stimulation of GABA neurons resulted in disruption of sucrose consumption. The animals stopped drinking.

Using sophisticated electrophysiology and cell chemistry measures, the study team could monitor the activity of the GABA and dopamine neurons. They found a direct link between GABA activation and dopamine suppression.

"So basically, it appears that these GABA neurons located in the VTA are just microns away from dopamine and are negative regulators of dopamine function," Stuber proposes.

"When they become active, their basic job is to suppress dopamine release. A dysfunction in these GABA neurons might potentially underlie different aspects of neuropsychiatric illness, such as depression. Thus, we could think of them as a new physiological target for various aspects of neuropsychiatric diseases."

Provided by University of North Carolina School of Medicine

"Study shines light on brain mechanism that controls reward enjoyment." March 21st, 2012. http://medicalxpress.com/news/2012-03-brain-mechanism-reward-enjoyment.html

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Robert Karl Stonjek

Study may lead to new treatments for prostate cancer

 by Biomechanism 

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A recent study conducted at Marshall University may eventually help scientists develop new treatments for prostate cancer, the most common malignancy in American men.

The study, which focused on the effects of cadmium on the prostate, was conducted by Dr. Pier Paolo Claudio, an associate professor in the Biomedical Sciences Graduate Program and Department of Biochemistry and Microbiology at the university’s Joan C. Edwards School of Medicine, and an international team of colleagues from the University of L’Aquila and the National Cancer Institute in Italy, and the University of Colorado Denver and the National Institute of Environmental Health Sciences in the United States.

An extremely toxic metal found in industrial workplaces, cadmium is commonly used in electroplating and is a key component in batteries and some paints. It is also found in cigarettes and some food supplies.

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According to Claudio, scientists believe the prostate may be a target for cancer caused by cadmium, although the underlying mechanisms have been unclear.

“In our study, we investigated the effects of cadmium exposure in normal and in tumor cells derived from human prostate tissue,” he said. “We were able to demonstrate the molecular mechanisms cadmium uses to induce carcinogenesis in the prostate.”

Claudio, who said he has spent the last 15 years conducting research to understand the crosstalk between the factors that contribute to cancer progression versus those that protect from it, says this study is important because once those molecular mechanisms are understood, new therapies can be tailored to treat prostate cancer.

He added, “The focus of work in our laboratory is to understand the molecular mechanisms governing malignant transformation in order to tailor novel therapeutic strategies. To effectively design novel biological drugs, a thorough understanding of the mechanism of cancer pathogenesis is required. Our study will contribute to the body of knowledge available to science and may lead to exciting new treatments for this common cancer.”

The research was published today in the journal PLoS ONE. The full article, “Cadmium Induces p53-Dependent Apoptosis in Human Prostate Epithelial Cells,” is available online here: Cadmium Induces p53-Dependent Apoptosis in Human Prostate Epithelial Cells

Can a traumatic brain injury explain a killing spree?

Massacre in Afghanistan throws spotlight on the brain at war.

Sharon Weinberger

 

Why a U.S. Army soldier suspected of killing 16 civilians in Afghanistan did what he did is still unclear, but one thing is certain: his lawyers are likely to invoke emerging science about the effects of war on the brain to aid in his defense.

In fact, even before Staff Sgt. Robert Bales' identity was revealed, unnamed US officials were telling major news outlets that the suspect had suffered a traumatic brain injury, or TBI. Shortly thereafter, Bales’ lawyer publicly suggested that his client suffered from Post-Traumatic Stress Disorder (PTSD), even though it does not appear to have been previously diagnosed.

JOHANNES EISELE/AFP/Getty Images

How much either TBI or PTSD could explain a pre-planned rampage is up for debate, however.

According to Dr. James Giordano, director of the Center for Neurotechnology Studies at the Potomac Institute for Policy Studies in Arlington, Virginia,  TBI manifests itself through a variety of complaints, which may range from mild to moderate. These could include disorientation, ringing in the ears, vertigo, and headaches, as well as a more profound constellation of severe neurological and psychological symptoms, such as impaired impulse control, acting out and aggressive behavior. “What we're seeing is that TBI presents as spectrum disorder with a variety of effects,” says Giordano.

In fact, some people make a complete recovery from TBI, while others develop more severe conditions down the road, and it’s difficult to predict which injuries will persist, according to Giordano. “One would think the milder the injury, the less severe the symptoms,” says Giordano. “That’s not always the case.”

The Pentagon estimates that over 230,000 troops have suffered some form of TBI over the past 10 years. That statistic, though shocking on its own, could also be understated, according to a RAND study, since many mild TBIs go unreported.

Along with a greater understanding about the extent of TBI injuries, there is also a growing body of evidence that many of these TBIs could lead to later emotional and cognitive problems, and even violent behavior.

Kevin Kit Parker, a biomedical engineering professor at Harvard University, points to ongoing work by the Veterans Administration looking at sports players who have suffered from TBI, many of whom suffered behavioral problems, or even violent outbursts, prior to their death. “This is long-noted in anecdotal data in professional athletes and in soldiers,” says Parker, who is working on research to understand the mechanisms that result in a TBI. “When someone has a brain injury, behavioral issues are often emergent after some period,” he says.

What kinds of issues depends on the part of the brain that is injured. So-called 'executive function problems' — which involve the ability to function and plan — are frequently seen when the injury affects the front lobes says David Hovda, director of the Brain Injury Research Center at the University of California, Los Angeles. “Frontal lobes are needed in order for us to act appropriately in public, or in a delicate situation, like a date,” says Hovda. “If we don’t have working frontal lobes, we may say and do things that are bizarre and inappropriate.”

And if the injury is in the right spot, it can also effect inhibitions, which can be linked to violent behavior, according to Hovda.

Of course, at issue with the killings in Afghanistan is whether the soldier might have succumbed to violent impulses because of his prior brain injury. On that point, most experts are hesitant to speculate on the specific case, but Hovda and others point out that the types of violent behavior that typically result from a TBI don’t seem to mesh with what is known about the Afghanistan killings, which have been described as methodical and pre-planned.

That may be why Bales’ lawyer is already talking about PTSD, which can lead to a much wider constellation of symptoms, including destructive behavior such drinking. Moreover, emerging research suggests that TBI makes the brain more susceptible to developing PTSD, delivering a sort of medical double-whammy with the potential for a wide array of symptomatic behavior.

Hovda suggest that the suspect’s lawyer could argue that the TBI contributed to PTSD, and as a result of PTSD, Bales became “depressed, anxious, angry at his environment, and took that out on other people.”

While a TBI could certainly contribute to violent behavior, to claim that a brain injury alone explains a methodical killing spree is “a bit of a stretch,” says Hovda.

Nature doi :10.1038/nature.2012.10252

 

Source: Nature
http://www.nature.com/news/can-a-traumatic-brain-injury-explain-a-killing-spree-1.10252?WT.ec_id=NEWS-20120320

 

Posted by
Robert Karl Stonjek

Can War Injuries Spawn Massacres?

Recent research on the neurological effects of combat might play a role in the defense trial of a US Army soldier who is accused killed 16 Afghan civilians.

By Bob Grant | 

Wikimedia Commons, TheBrain

On March 11, Staff Sergeant Robert Bales allegedly went on a door-to-door killing spree in the Panjwayi district of Afghanistan. By the end of it, according to reports, 5 civilians were injured and 16 were dead. Nine of the deceased were children. Though investigators are still sifting through the details of Bales’s case, there have been indications that his defense team may introduce evidence that uses post traumatic stress disorder (PTSD) or traumatic brain injury (TBI) to help explain the soldier’s alleged actions.

But current research is not definitive on whether those two disorders, which are increasingly diagnosed in today’s fighting troops, could contribute to what seemed to be a pre-meditated massacre, such as the one of which Bales is accused.

“When someone has a brain injury, behavioral issues are often emergent after some period,” Kevin Kit Parker, Harvard University biomedical engineering, told Nature.

While “most experts are hesitant to speculate on the specific case” of Bales, as details are still scant, according to the Nature report, they do admit that violent behaviors can result from both TBI and PTSD.

Bales’s lawyer, John Henry Browne, told NBC’s TODAY last week that the soldier suffered a “concussive head injury” and was cleared of PTSD after “minimal” testing during an earlier deployment in Iraq, and that he and the rest of Bales’s defense team would likely focus on PTSD when the case goes to trial. Also, Browne told Sky News HD that Bales has “some memories of before the incident and he has some memories of after the incident. In between, very little.”

Source: TheScientist
http://the-scientist.com/2012/03/21/can-war-injuries-spawn-massacres/

Posted by
Robert Karl Stonjek

'Emerald-cut' galaxy discovered

SWINBURNE UNIVERSITY OF TECHNOLOGY

The emeral-cut galaxy is extremely unusual as most galaxies exist in three forms: disc-like, spheroidal or lumpy and irregular in appearance. Image: Swinburne University of Technology An international team of astronomers has discovered a rare square galaxy with a striking resemblance to an emerald-cut diamond. The astronomers - from Australia, Germany, Switzerland and Finland - discovered the rectangular shaped galaxy within a group of 250 galaxies some 70 million light years away. "In the Universe around us, most galaxies exist in one of three forms: spheroidal, disc-like, or lumpy and irregular in appearance," said Associate Professor Alister Graham from Swinburne University of Technology He said the rare rectangular-shaped galaxy was a very unusual object. "It's one of those things that just makes you smile because it shouldn't exist, or rather you don't expect it to exist. "It's a little like the precarious Leaning Tower of Pisa or the discovery of some exotic new species which at first glance appears to defy the laws of nature." The unusually shaped galaxy was detected in a wide field-of-view image taken with the Japanese Subaru Telescope for an unrelated program by Swinburne astrophysicist Dr Lee Spitler. The astronomers suspect it is unlikely that this galaxy is shaped like a cube. Instead, they believe that it may resemble an inflated disc seen side on, like a short cylinder. Support for this scenario comes from observations with the giant Keck Telescope in Hawaii, which revealed a rapidly spinning, thin disc with a side on orientation lurking at the centre of the galaxy. The outermost measured edge of this galactic disc is rotating at a speed in excess of 100,000 kilometres per hour. "One possibility is that the galaxy may have formed out of the collision of two spiral galaxies," said Swinburne's Professor Duncan Forbes, co author of the research. "While the pre-existing stars from the initial galaxies were strewn to large orbits creating the emerald cut shape, the gas sank to the mid plane where it condensed to form new stars and the disc that we have observed." Despite its apparent uniqueness, partly due to its chance orientation, the astronomers have managed to glean useful information for modelling other galaxies. While the outer boxy shape is somewhat reminiscent of galaxy merger simulations which don't involve the production of new stars, the disc-like structure is comparable with merger simulations involving star formation. "This highlights the importance of combining lessons learned from both types of past simulation for better understanding galaxy evolution in the future," said Associate Professor Graham. "One of the reasons this emerald cut galaxy was hard to find is due to its dwarf-like status: it has 50 times less stars than our own Milky Way galaxy, plus its distance from us is equivalent to that spanned by 700 Milky Way galaxies placed end-to-end. "Curiously, if the orientation was just right, when our own disc-shaped galaxy collides with the disc-shaped Andromeda galaxy about three billion years from now we may find ourselves the inhabitants of a square looking galaxy." The results will be published in The Astrophysical Journal. Editor's Note: Original news release can be found here.