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.
Thursday, May 26, 2011
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.
‘Master switch’ gene for obesity and diabetes discovered
A gene linked to type 2 diabetes and cholesterol levels is in fact a “master regulator” gene that controls the behavior of other genes found within fat in the body, researchers at King’s College London and the University of Oxford have found.
The researchers examined over 20,000 genes in subcutaneous fat biopsies from 800 UK female twin volunteers.
They found an association between the KLF14 gene (inherited from the mother) and the expression levels of multiple distant genes found in fat tissue. This means that it acts as a master switch to control these genes, the researchers said. This was then confirmed in a further independent sample of 600 subcutaneous fat biopsies from Icelandic subjects.
Other genes controlled by KLF14 are in fact linked to a range of metabolic traits, including body-mass index (obesity), cholesterol, insulin and glucose levels, highlighting the interconnectedness of metabolic traits, the researchers said.
The researchers examined over 20,000 genes in subcutaneous fat biopsies from 800 UK female twin volunteers.
They found an association between the KLF14 gene (inherited from the mother) and the expression levels of multiple distant genes found in fat tissue. This means that it acts as a master switch to control these genes, the researchers said. This was then confirmed in a further independent sample of 600 subcutaneous fat biopsies from Icelandic subjects.
Other genes controlled by KLF14 are in fact linked to a range of metabolic traits, including body-mass index (obesity), cholesterol, insulin and glucose levels, highlighting the interconnectedness of metabolic traits, the researchers said.
Wednesday, May 4, 2011
Removable ‘cloak’ for nanoparticles helps them target tumors
A new type of drug-delivery nanoparticle that could target nearly any type of tumor and carry virtually any type of drug has been developed by chemists at MIT.
The new nanoparticles are cloaked in a polymer layer that protects them from being degraded by the bloodstream and can survive in the bloodstream for up to 24 hours.
This outer layer falls off after entering the slightly more acidic environment near a tumor, revealing another layer that is able to penetrate individual tumor cells.
The tumor acidity is a byproduct of the tumor’s intensified metabolism. Tumor cells grow and divide much more rapidly than normal cells, and that metabolic activity uses up a lot of oxygen, which increases acidity. As the tumor grows, the tissue becomes more and more acidic.
To build their targeted particles, the researchers used a technique called “layer-by-layer assembly.” This means each layer can be tailored to perform a specific function.
When the outer layer (made of polyethylene glycol, or PEG) breaks down in the tumor’s acidic environment, a positively charged middle layer is revealed, allowing the nanoparticle to penetrate the negatively charged cell membrane.
The nanoparticles’ innermost layer can be a polymer that carries a cancer drug, or a quantum dot that could be used for imaging, or virtually anything else that the designer might want to deliver.
These particles are the first that have been successfully tested in living animals by targeting acidity, the researchers said.
The new nanoparticles are cloaked in a polymer layer that protects them from being degraded by the bloodstream and can survive in the bloodstream for up to 24 hours.
This outer layer falls off after entering the slightly more acidic environment near a tumor, revealing another layer that is able to penetrate individual tumor cells.
The tumor acidity is a byproduct of the tumor’s intensified metabolism. Tumor cells grow and divide much more rapidly than normal cells, and that metabolic activity uses up a lot of oxygen, which increases acidity. As the tumor grows, the tissue becomes more and more acidic.
To build their targeted particles, the researchers used a technique called “layer-by-layer assembly.” This means each layer can be tailored to perform a specific function.
When the outer layer (made of polyethylene glycol, or PEG) breaks down in the tumor’s acidic environment, a positively charged middle layer is revealed, allowing the nanoparticle to penetrate the negatively charged cell membrane.
The nanoparticles’ innermost layer can be a polymer that carries a cancer drug, or a quantum dot that could be used for imaging, or virtually anything else that the designer might want to deliver.
These particles are the first that have been successfully tested in living animals by targeting acidity, the researchers said.
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