Researchers at Monash University in Melbourne, Australia, have observed atypical neurophysiological activity in amputees who experience synesthetic pain (pain synesthetes) when observing pain in another.
The researchers found that reduced alpha and theta brainwaves in pain synesthetes may reflect inhibition of normal inhibitory mechanisms (neurotransmitters involved in the processing of observed pain) as well as increased synesthetic pain.
The researchers used EEG to record brain activity in eight amputees who experienced both phantom and synesthetic pain, 10 amputees who experienced just phantom pain, and 10 healthy people with no amputations while they looked at images of hands or feet in potentially painful and non-painful situations.
When viewing the images, the researchers found that the pain synesthetes exhibited decreased theta and alpha brainwaves compared with the other volunteers. The researchers said that such a decrease reflects an increase in neural activity, suggesting that their mirror systems (neurons that fire when an animal observes the same action performed by another) are activated more strongly.
They said the traumatic experience associated with losing a limb may heighten the sensitivity of pain synesthetes to others’ pain. When threatened, our body naturally becomes hypervigilant to pain: our pain threshold lowers, which can make even small triggers painful. Pain synesthesia may be a symptom of an abnormal, ongoing hypervigilance, the researchers said.
Wednesday, June 1, 2011
Mining patterns in search data with Google Correlate
Google Correlate has been launched on Google Labs. Users can now upload their own data series and retrieve a list of search terms based on popularity to see what best corresponds with a real world trend.
In the example below, official flu activity data were uploaded from the U.S. CDC over the last several years. The data reveal that people search for terms like [cold or flu] in a pattern similar to actual flu rates. Finding these correlated terms, a Google Flu Trends graph was built.
Users can also enter search terms such as [ribosome] and find other terms with activity that correspond well over time.
A white paper describes the methodology behind Google Correlate. How can Google help with the flu? Find out here.
In the example below, official flu activity data were uploaded from the U.S. CDC over the last several years. The data reveal that people search for terms like [cold or flu] in a pattern similar to actual flu rates. Finding these correlated terms, a Google Flu Trends graph was built.
Users can also enter search terms such as [ribosome] and find other terms with activity that correspond well over time.
A white paper describes the methodology behind Google Correlate. How can Google help with the flu? Find out here.
Gestural interfaces: a step backwards in usability?
Usability researchers from the Nielsen Norman group have pointed out that well-tested and understood standards of interaction design are being “overthrown, ignored, and violated” in the rush to develop natural gestural interfaces that can lead to “usability disaster.”
“The first crop of iPad apps revived memories of Web designs from 1993, when Mosaic first introduced the image map that made it possible for any part of any picture to become a UI element,” said Norman Nielsen. “As a result, graphic designers went wild: anything they could draw could be a UI, whether it made sense or not. It’s the same with iPad apps: anything you can show and touch can be a UI on this device. There are no standards and no expectations.”
“One of the worst designs last year was USA Today‘s section navigation, which required users to touch the newspaper logo despite the complete lack of any perceived affordance that the logo would have this effect….
“I thought I’d driven a stake through splash screens many years ago and eradicated them from the Web, but apparently splash screens are super-vampires that can haunt users from beyond the grave.”
“The first crop of iPad apps revived memories of Web designs from 1993, when Mosaic first introduced the image map that made it possible for any part of any picture to become a UI element,” said Norman Nielsen. “As a result, graphic designers went wild: anything they could draw could be a UI, whether it made sense or not. It’s the same with iPad apps: anything you can show and touch can be a UI on this device. There are no standards and no expectations.”
“One of the worst designs last year was USA Today‘s section navigation, which required users to touch the newspaper logo despite the complete lack of any perceived affordance that the logo would have this effect….
“I thought I’d driven a stake through splash screens many years ago and eradicated them from the Web, but apparently splash screens are super-vampires that can haunt users from beyond the grave.”
Thursday, May 26, 2011
Transformer robot turns into a helicopter
A transformer robot that turns into a helicopter has been developed by researchers at the University of Minnesota’s Center for Distributed Robotics.
The robot uses separate motors to run the wheels and the rotors rather than a complex system. Although the first prototype is fragile, future designs will have simpler and more robust folding mechanisms, according to the researchers, including an extendable boom with a tail rotor, similar to those used by helicopters, to provide more stability in flight.
The robot uses separate motors to run the wheels and the rotors rather than a complex system. Although the first prototype is fragile, future designs will have simpler and more robust folding mechanisms, according to the researchers, including an extendable boom with a tail rotor, similar to those used by helicopters, to provide more stability in flight.
Wednesday, May 25, 2011
‘Survival protein’ protects the brain against effects of stroke
A “survival protein” that protects the brain against the effects of stroke in rodent brain tissue has been discovered by scientists at Johns Hopkins University. The finding has implications for treating stroke as well as Parkinson’s Disease, diabetes, and heart attack.
When brain tissue is subjected to a stressful but not lethal insult, a defense response occurs that protects cells from subsequent insult. The scientists dissected this preconditioning pathway to identify the most critical molecular players, including the Iduna protein. This protein increased three- to four-fold in preconditioned mouse brain tissue following an insult to the tissue, the scientists said.
The team exposed mouse brain cells to short bursts of a toxic chemical, and then screened these “preconditioned” cells for genes that turned on as a result of the insult. Focusing on Iduna, the researchers turned up the gene’s activity in the cells during exposure to the toxic chemical, which induced preconditioning. Cells deficient in Iduna did not survive, but those with more Iduna did.
The scientists found that the Iduna protein interferes with a particular kind of cell death that’s implicated in complications from diabetes and heart attack as well as stroke. By binding with a molecule known as PAR polymer, Iduna prevents the movement of cell-death-inducing factor (AIF) into a cell’s nucleus.
“Apparently, what doesn’t kill you makes you stronger,” says Valina Dawson, Ph.D. “This protective response was broad in its defense of neurons and glia and blood vessels — the entire brain. It’s not just a delay of death, but real protection that lasts for about 72 hours.”
When brain tissue is subjected to a stressful but not lethal insult, a defense response occurs that protects cells from subsequent insult. The scientists dissected this preconditioning pathway to identify the most critical molecular players, including the Iduna protein. This protein increased three- to four-fold in preconditioned mouse brain tissue following an insult to the tissue, the scientists said.
The team exposed mouse brain cells to short bursts of a toxic chemical, and then screened these “preconditioned” cells for genes that turned on as a result of the insult. Focusing on Iduna, the researchers turned up the gene’s activity in the cells during exposure to the toxic chemical, which induced preconditioning. Cells deficient in Iduna did not survive, but those with more Iduna did.
The scientists found that the Iduna protein interferes with a particular kind of cell death that’s implicated in complications from diabetes and heart attack as well as stroke. By binding with a molecule known as PAR polymer, Iduna prevents the movement of cell-death-inducing factor (AIF) into a cell’s nucleus.
“Apparently, what doesn’t kill you makes you stronger,” says Valina Dawson, Ph.D. “This protective response was broad in its defense of neurons and glia and blood vessels — the entire brain. It’s not just a delay of death, but real protection that lasts for about 72 hours.”
Monday, May 16, 2011
Tiny variation in one gene may have led to crucial changes in human brain
A tiny variation within a single gene may determine the formation of brain convolutions, the deep fissures and convolutions that increase its surface area and allow for rational and abstract thoughts, researchers at Yale University have discovered.
A genetic analysis of a Turkish patient whose brain lacks the characteristic convolutions in part of his cerebral cortex revealed that the deformity was caused by the deletion of two genetic letters from 3 billion in the human genetic alphabet. Similar variations of the same gene, called laminin gamma3 (LAMC3), were discovered in two other patients with similar abnormalities.
An analysis of the gene shows that it is expressed during the embryonic period. This period is vital to the formation of dendrites, which form synapses or connections between brain cells, the researchers said.
They said that although the same gene is present in lower organisms with smooth brains, such as mice, somehow over time it has evolved to gain novel functions that are fundamental for human occipital cortex formation. Its mutation leads to the loss of surface convolutions, a hallmark of the human brain, the researchers said.
A genetic analysis of a Turkish patient whose brain lacks the characteristic convolutions in part of his cerebral cortex revealed that the deformity was caused by the deletion of two genetic letters from 3 billion in the human genetic alphabet. Similar variations of the same gene, called laminin gamma3 (LAMC3), were discovered in two other patients with similar abnormalities.
An analysis of the gene shows that it is expressed during the embryonic period. This period is vital to the formation of dendrites, which form synapses or connections between brain cells, the researchers said.
They said that although the same gene is present in lower organisms with smooth brains, such as mice, somehow over time it has evolved to gain novel functions that are fundamental for human occipital cortex formation. Its mutation leads to the loss of surface convolutions, a hallmark of the human brain, the researchers said.
Tiny variation in one gene may have led to crucial changes in human brain
A tiny variation within a single gene may determine the formation of brain convolutions, the deep fissures and convolutions that increase its surface area and allow for rational and abstract thoughts, researchers at Yale University have discovered.
A genetic analysis of a Turkish patient whose brain lacks the characteristic convolutions in part of his cerebral cortex revealed that the deformity was caused by the deletion of two genetic letters from 3 billion in the human genetic alphabet. Similar variations of the same gene, called laminin gamma3 (LAMC3), were discovered in two other patients with similar abnormalities.
An analysis of the gene shows that it is expressed during the embryonic period. This period is vital to the formation of dendrites, which form synapses or connections between brain cells, the researchers said.
They said that although the same gene is present in lower organisms with smooth brains, such as mice, somehow over time it has evolved to gain novel functions that are fundamental for human occipital cortex formation. Its mutation leads to the loss of surface convolutions, a hallmark of the human brain, the researchers said.
A genetic analysis of a Turkish patient whose brain lacks the characteristic convolutions in part of his cerebral cortex revealed that the deformity was caused by the deletion of two genetic letters from 3 billion in the human genetic alphabet. Similar variations of the same gene, called laminin gamma3 (LAMC3), were discovered in two other patients with similar abnormalities.
An analysis of the gene shows that it is expressed during the embryonic period. This period is vital to the formation of dendrites, which form synapses or connections between brain cells, the researchers said.
They said that although the same gene is present in lower organisms with smooth brains, such as mice, somehow over time it has evolved to gain novel functions that are fundamental for human occipital cortex formation. Its mutation leads to the loss of surface convolutions, a hallmark of the human brain, the researchers said.
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