"Melanoma is the most lethal form of skin cancer and represents a substantial cause of productive years of life lost to cancer, especially when occurring in young persons," the authors write as background information in the study. "Among non-Hispanic white girls and women aged 15 to 39 years in the United States, age-adjusted incidence rates of cutaneous melanoma among adolescents have more than doubled during a 3-decade period (1973-2004), with a 2.7 percent increase annually since 1992."
To assess the relationship between the incidence of melanoma and socioeconomic status and UV-radiation exposure, Amelia K. Hausauer, B.A., of the Cancer Prevention Institute of California and the School of Medicine, University of California San Francisco, and colleagues examined data from the California Cancer Registry. The authors focused on melanoma diagnoses that occurred January 1, 1988 through December 31, 1992 and January 1, 1998 through December 31, 2002.
Data were included from a total of 3,800 non-Hispanic white girls and women between the ages of 15 and 39, in whom 3,842 melanomas were diagnosed. Regardless of the year of diagnosis, adolescent girls and young women living neighborhoods with the highest socioeconomic status were nearly 6-fold more likely to be diagnosed with malignant melanoma than those living in the lowest socioeconomic status.
When examining melanoma incidence by socioeconomic status, diagnosis increased over time in all groups, however these changes were only significant among adolescent girls and young women in the highest three levels of socioeconomic status. Increasing levels of socioeconomic status were positively correlated with higher risks of developing melanoma. Additionally, higher rates of UV-radiation exposure were associated with increased rates of melanoma only among adolescent girls and young women in the highest two levels of socioeconomic status.
Girls and women living in neighborhoods with the highest socioeconomic status and highest UV-radiation exposure experienced 73 percent greater melanoma incidence relative to those from neighborhoods with the lowest socioeconomic status and highest UV-radiation, and an 80 percent greater melanoma incidence relative to those living in neighborhoods with the lowest socioeconomic status and lowest UV-radiation exposure.
"Understanding the ways that socioeconomic status and UV-radiation exposure work together to influence melanoma incidence is important for planning effective prevention and education efforts," the authors conclude. "Interventions should target adolescent girls and young women living in high socioeconomic status and high UV-radiation neighborhoods because they have experienced a significantly greater increase in disease burden."
(http://www.sciencedaily.com/releases/2011/03/110321161908.htm)
Tuesday, March 22, 2011
Monday, March 21, 2011
Batteries Charge Quickly and Retain Capacity, Thanks to New Structure
Braun's group developed a three-dimensional nanostructure for battery cathodes that allows for dramatically faster charging and discharging without sacrificing energy storage capacity. The researchers' findings will be published in the March 20 advance online edition of the journal Nature Nanotechnology.
Aside from quick-charge consumer electronics, batteries that can store a lot of energy, release it fast and recharge quickly are desirable for electric vehicles, medical devices, lasers and military applications.
"This system that we have gives you capacitor-like power with battery-like energy," said Braun, a professor of materials science and engineering. "Most capacitors store very little energy. They can release it very fast, but they can't hold much. Most batteries store a reasonably large amount of energy, but they can't provide or receive energy rapidly. This does both."
The performance of typical lithium-ion (Li-ion) or nickel metal hydride (NiMH) rechargeable batteries degrades significantly when they are rapidly charged or discharged. Making the active material in the battery a thin film allows for very fast charging and discharging, but reduces the capacity to nearly zero because the active material lacks volume to store energy.
Braun's group wraps a thin film into three-dimensional structure, achieving both high active volume (high capacity) and large current. They have demonstrated battery electrodes that can charge or discharge in a few seconds, 10 to 100 times faster than equivalent bulk electrodes, yet can perform normally in existing devices.
This kind of performance could lead to phones that charge in seconds or laptops that charge in minutes, as well as high-power lasers and defibrillators that don't need time to power up before or between pulses.
Braun is particularly optimistic for the batteries' potential in electric vehicles. Battery life and recharging time are major limitations of electric vehicles. Long-distance road trips can be their own form of start-and-stop driving if the battery only lasts for 100 miles and then requires an hour to recharge.
"If you had the ability to charge rapidly, instead of taking hours to charge the vehicle you could potentially have vehicles that would charge in similar times as needed to refuel a car with gasoline," Braun said. "If you had five-minute charge capability, you would think of this the same way you do an internal combustion engine. You would just pull up to a charging station and fill up."
All of the processes the group used are also used at large scales in industry so the technique could be scaled up for manufacturing.
They key to the group's novel 3-D structure is self-assembly. They begin by coating a surface with tiny spheres, packing them tightly together to form a lattice. Trying to create such a uniform lattice by other means is time-consuming and impractical, but the inexpensive spheres settle into place automatically.
Then the researchers fill the space between and around the spheres with metal. The spheres are melted or dissolved, leaving a porous 3-D metal scaffolding, like a sponge. Next, a process called electropolishing uniformly etches away the surface of the scaffold to enlarge the pores and make an open framework. Finally, the researchers coat the frame with a thin film of the active material.
The result is a bicontinuous electrode structure with small interconnects, so the lithium ions can move rapidly; a thin-film active material, so the diffusion kinetics are rapid; and a metal framework with good electrical conductivity.
The group demonstrated both NiMH and Li-ion batteries, but the structure is general, so any battery material that can be deposited on the metal frame could be used.
"We like that it's very universal, so if someone comes up with a better battery chemistry, this concept applies," said Braun, who is also affiliated with the Materials Research Laboratory and the Beckman Institute for Advanced Science and Technology at Illinois. "This is not linked to one very specific kind of battery, but rather it's a new paradigm in thinking about a battery in three dimensions for enhancing properties."
(http://www.sciencedaily.com/releases/2011/03/110320164225.htm)
Aside from quick-charge consumer electronics, batteries that can store a lot of energy, release it fast and recharge quickly are desirable for electric vehicles, medical devices, lasers and military applications.
"This system that we have gives you capacitor-like power with battery-like energy," said Braun, a professor of materials science and engineering. "Most capacitors store very little energy. They can release it very fast, but they can't hold much. Most batteries store a reasonably large amount of energy, but they can't provide or receive energy rapidly. This does both."
The performance of typical lithium-ion (Li-ion) or nickel metal hydride (NiMH) rechargeable batteries degrades significantly when they are rapidly charged or discharged. Making the active material in the battery a thin film allows for very fast charging and discharging, but reduces the capacity to nearly zero because the active material lacks volume to store energy.
Braun's group wraps a thin film into three-dimensional structure, achieving both high active volume (high capacity) and large current. They have demonstrated battery electrodes that can charge or discharge in a few seconds, 10 to 100 times faster than equivalent bulk electrodes, yet can perform normally in existing devices.
This kind of performance could lead to phones that charge in seconds or laptops that charge in minutes, as well as high-power lasers and defibrillators that don't need time to power up before or between pulses.
Braun is particularly optimistic for the batteries' potential in electric vehicles. Battery life and recharging time are major limitations of electric vehicles. Long-distance road trips can be their own form of start-and-stop driving if the battery only lasts for 100 miles and then requires an hour to recharge.
"If you had the ability to charge rapidly, instead of taking hours to charge the vehicle you could potentially have vehicles that would charge in similar times as needed to refuel a car with gasoline," Braun said. "If you had five-minute charge capability, you would think of this the same way you do an internal combustion engine. You would just pull up to a charging station and fill up."
All of the processes the group used are also used at large scales in industry so the technique could be scaled up for manufacturing.
They key to the group's novel 3-D structure is self-assembly. They begin by coating a surface with tiny spheres, packing them tightly together to form a lattice. Trying to create such a uniform lattice by other means is time-consuming and impractical, but the inexpensive spheres settle into place automatically.
Then the researchers fill the space between and around the spheres with metal. The spheres are melted or dissolved, leaving a porous 3-D metal scaffolding, like a sponge. Next, a process called electropolishing uniformly etches away the surface of the scaffold to enlarge the pores and make an open framework. Finally, the researchers coat the frame with a thin film of the active material.
The result is a bicontinuous electrode structure with small interconnects, so the lithium ions can move rapidly; a thin-film active material, so the diffusion kinetics are rapid; and a metal framework with good electrical conductivity.
The group demonstrated both NiMH and Li-ion batteries, but the structure is general, so any battery material that can be deposited on the metal frame could be used.
"We like that it's very universal, so if someone comes up with a better battery chemistry, this concept applies," said Braun, who is also affiliated with the Materials Research Laboratory and the Beckman Institute for Advanced Science and Technology at Illinois. "This is not linked to one very specific kind of battery, but rather it's a new paradigm in thinking about a battery in three dimensions for enhancing properties."
(http://www.sciencedaily.com/releases/2011/03/110320164225.htm)
Sunday, March 13, 2011
Bacteria hijack an immune signaling system to live safely in our guts
By Diana Gitig
Our immune system operates under the basic premise that "self" is different from "non-self." Its primary function lies in distinguishing between these entities, leaving the former alone while attacking the latter. Yet we now know that our guts are home to populations of bacterial cells so vast that they outnumber our own cells, and that these microbiota are essential to our own survival.
As a recent study in Nature Immunology notes, "An equilibrium is established between the microbiota and the immune system that is fundamental to intestinal homeostasis." How does the immune system achieve this equilibrium, neither overacting and attacking the symbiotic bacteria nor being lax and allowing pathogens to get through? It turns out that our gut bacteria manipulate the immune system to keep things from getting out of hand.
Like many stories of immune regulation, this one is a tale of many interleukins (ILs). Interleukins are a subset of cytokines, signaling molecules used by the immune system to control processes such as inflammation and the growth and differentiation of different classes of immune cells. IL-22 is known to be important in defense, both ridding the intestines of bacterial pathogens and protecting the colon from inflammation.
IL-22 is produced by the subset of T cells defined by their expression of IL-17, known as TH17 cells, as well as by innate lymphoid cells. Sawa et al. report that in the intestine, most of the IL-22 is produced by a specific subset of innate lymphoid cells that live there, and not TH17 cells.
Microbiota can repress this expression of IL-22 by inducing the expression of IL-25 in the epithelial cells lining the walls of the intestine. The researchers deduced this because IL-22 expression goes down in mice after weaning, when microbial colonization of the intestine dramatically increases. When adult mice were treated with antibiotics, IL-22 production went up again. IL-22 production also increased during inflammation.
Microbiota also induce the generation of TH17 cells and, even though these normally make IL-22, this induction further depresses its production. The TH17 ended up competing with the innate lymphoid cells for the same pool of regulatory cytokines; as a result, all of them got less and became less active.
These innate lymphoid cells thus play a critical role in maintaining intestinal homeostasis. They make IL-22, which induces the production of antibacterial peptides by the lining and protects the intestine from pathological inflammation. Symbiotic microbiota make a safe home by tamping down the production of IL-22 by inducing IL-25. The TH17 cells can contribute to this tamping down by competing for regulators. The authors conclude by stating that “this complex regulatory network… demonstrates the subtle interaction between the microbiota and the various forces of the vertebrate immune system in maintaining intestinal homeostasis.”
http://arstechnica.com/science/news/2011/03/a-signaling-pathway-helps-the-immune-system-interact-safely-with-gut-microbes.ars
Our immune system operates under the basic premise that "self" is different from "non-self." Its primary function lies in distinguishing between these entities, leaving the former alone while attacking the latter. Yet we now know that our guts are home to populations of bacterial cells so vast that they outnumber our own cells, and that these microbiota are essential to our own survival.
As a recent study in Nature Immunology notes, "An equilibrium is established between the microbiota and the immune system that is fundamental to intestinal homeostasis." How does the immune system achieve this equilibrium, neither overacting and attacking the symbiotic bacteria nor being lax and allowing pathogens to get through? It turns out that our gut bacteria manipulate the immune system to keep things from getting out of hand.
Like many stories of immune regulation, this one is a tale of many interleukins (ILs). Interleukins are a subset of cytokines, signaling molecules used by the immune system to control processes such as inflammation and the growth and differentiation of different classes of immune cells. IL-22 is known to be important in defense, both ridding the intestines of bacterial pathogens and protecting the colon from inflammation.
IL-22 is produced by the subset of T cells defined by their expression of IL-17, known as TH17 cells, as well as by innate lymphoid cells. Sawa et al. report that in the intestine, most of the IL-22 is produced by a specific subset of innate lymphoid cells that live there, and not TH17 cells.
Microbiota can repress this expression of IL-22 by inducing the expression of IL-25 in the epithelial cells lining the walls of the intestine. The researchers deduced this because IL-22 expression goes down in mice after weaning, when microbial colonization of the intestine dramatically increases. When adult mice were treated with antibiotics, IL-22 production went up again. IL-22 production also increased during inflammation.
Microbiota also induce the generation of TH17 cells and, even though these normally make IL-22, this induction further depresses its production. The TH17 ended up competing with the innate lymphoid cells for the same pool of regulatory cytokines; as a result, all of them got less and became less active.
These innate lymphoid cells thus play a critical role in maintaining intestinal homeostasis. They make IL-22, which induces the production of antibacterial peptides by the lining and protects the intestine from pathological inflammation. Symbiotic microbiota make a safe home by tamping down the production of IL-22 by inducing IL-25. The TH17 cells can contribute to this tamping down by competing for regulators. The authors conclude by stating that “this complex regulatory network… demonstrates the subtle interaction between the microbiota and the various forces of the vertebrate immune system in maintaining intestinal homeostasis.”
http://arstechnica.com/science/news/2011/03/a-signaling-pathway-helps-the-immune-system-interact-safely-with-gut-microbes.ars
Saturday, March 12, 2011
Scientists already making discoveries in wake of Japan's temblor
By Eryn Brown
Here's what experts have learned about the earthquake thus far.
Q: What caused it?
A: The earthquake occurred because a portion of the Pacific Plate is being pushed into and underneath the North American plate, forming a so-called subduction zone that built up so much pressure it ruptured, slipping as much as 60 feet.
"This was a planetary monster," said Thomas Jordan, director of the Southern California Earthquake Center at USC.
The earthquake occurred along a patch of an undersea fault that's about 220 miles long and 60 miles wide. Because the fault broke at a shallow depth, it shifted the sea floor, triggering tsunamis throughout the Pacific Ocean.
Q: Was it a surprise?
A: Yes and no. Seismologists said the quake was larger than they thought was possible in that part of the world. "We thought about the Big One as an 8.5 or so," said Susan Hough, a seismologist at the U.S. Geological Survey in Pasadena, Calif. Such an earthquake would have been about one-third as strong as an 8.9 quake.
"But it's not like an 8.9 hit Kansas," she added. "We know Japan is an active subduction zone."
What tripped scientists up was a lack of recent activity in the area, Jordan said. The last earthquake of this magnitude along this plate boundary occurred in the year 869. Seismologists had been debating the fault's potential to break, but they had little data to go on.
"The question was whether that section had locked - accumulating strain - or was it slipping slowly," Jordan said. "We now know that this is a plate boundary that was locked."
Q: You mean there were no hints at all?
A: Brian Atwater, a USGS seismologist based in Seattle, said that Japanese GPS data collected since the 1990s showed that the coast of Japan was being pulled inland at a rate of about 25 feet per century, another indication that the plates were stuck and energy was building between them.
(http://www.physorg.com/news/2011-03-scientists-discoveries-japan-temblor.html)
Here's what experts have learned about the earthquake thus far.
Q: What caused it?
A: The earthquake occurred because a portion of the Pacific Plate is being pushed into and underneath the North American plate, forming a so-called subduction zone that built up so much pressure it ruptured, slipping as much as 60 feet.
"This was a planetary monster," said Thomas Jordan, director of the Southern California Earthquake Center at USC.
The earthquake occurred along a patch of an undersea fault that's about 220 miles long and 60 miles wide. Because the fault broke at a shallow depth, it shifted the sea floor, triggering tsunamis throughout the Pacific Ocean.
Q: Was it a surprise?
A: Yes and no. Seismologists said the quake was larger than they thought was possible in that part of the world. "We thought about the Big One as an 8.5 or so," said Susan Hough, a seismologist at the U.S. Geological Survey in Pasadena, Calif. Such an earthquake would have been about one-third as strong as an 8.9 quake.
"But it's not like an 8.9 hit Kansas," she added. "We know Japan is an active subduction zone."
What tripped scientists up was a lack of recent activity in the area, Jordan said. The last earthquake of this magnitude along this plate boundary occurred in the year 869. Seismologists had been debating the fault's potential to break, but they had little data to go on.
"The question was whether that section had locked - accumulating strain - or was it slipping slowly," Jordan said. "We now know that this is a plate boundary that was locked."
Q: You mean there were no hints at all?
A: Brian Atwater, a USGS seismologist based in Seattle, said that Japanese GPS data collected since the 1990s showed that the coast of Japan was being pulled inland at a rate of about 25 feet per century, another indication that the plates were stuck and energy was building between them.
(http://www.physorg.com/news/2011-03-scientists-discoveries-japan-temblor.html)
Thursday, March 10, 2011
Scientists Discover Anti-Anxiety Circuit in Brain Region Considered the Seat of Fear
Stimulation of a distinct brain circuit that lies within a brain structure typically associated with fearfulness produces the opposite effect: Its activity, instead of triggering or increasing anxiety, counters it.
That's the finding in a paper by Stanford University School of Medicine researchers to be published online March 9 in Nature. In the study, Karl Deisseroth, MD, PhD, and his colleagues employed a mouse model to show that stimulating activity exclusively in this circuit enhances animals' willingness to take risks, while inhibiting its activity renders them more risk-averse. This discovery could lead to new treatments for anxiety disorders, said Deisseroth, an associate professor of bioengineering and of psychiatry and behavioral science.
The investigators were able to pinpoint this particular circuit only by working with a state-of-the-art technology called optogenetics, pioneered by Deisseroth at Stanford, which allows brain scientists to tease apart the complex circuits that compose the brain so these can be studied one by one.
"Anxiety is a poorly understood but common psychiatric disease," said Deisseroth, who is also a practicing psychiatrist. More than one in four people, in the course of their lives, experience bouts of anxiety symptoms sufficiently enduring and intense to be classified as a full-blown psychiatric disorder. In addition, anxiety is a significant contributing factor in other major psychiatric disorders from depression to alcohol dependence, Deisseroth said.
Most current anti-anxiety medications work by suppressing activity in the brain circuitry that generates anxiety or increases anxiety levels. Many of these drugs are not very effective, and those that are have significant side effects such as addiction or respiratory suppression, Deisseroth said. "The discovery of a novel circuit whose action is to reduce anxiety, rather than increase it, could point to an entire strategy of anti-anxiety treatment," he added.
Ironically, the anti-anxiety circuit is nestled within a brain structure, the amygdala, long known to be associated with fear. Generally, stimulating nervous activity in the amygdala is best known to heighten anxiety. So the anti-anxiety circuit probably would have been difficult if not impossible to locate had it not been for optogenetics, a new technology in which nerve cells in living animals are rendered photosensitive so that action in these cells can be turned on or off by different wavelengths of light. The technique allows researchers to selectively photosensitize particular sets of nerve cells. Moreover, by delivering pulses of light via optical fibers to specific brain areas, scientists can target not only particular nerve-cell types but also particular cell-to-cell connections or nervous pathways leading from one brain region to another. The fiber-optic hookup is both flexible and pain-free, so experimental animals' actual behavior as well as their brain activity can be monitored.
In contrast, older research approaches involve probing brain areas with electrodes to stimulate nerve cell firing. But an electrode stimulates not only all the nerve cells that happen to be in the neighborhood but even fibers that are just passing through on the way to somewhere else. Thus, any effect from stimulating the newly discovered anti-anxiety circuit would have been swamped by the anxiety-increasing effects of the dominant surrounding circuitry.
In December 2010, the journal Nature Methods bestowed its "Method of the Year" title on optogenetics.
In the new Nature study, the researchers photosensitized a set of fibers projecting from cells in one nervous "switchboard" to another one within the amygdala. By carefully positioning their light-delivery system, they were able to selectively target this projection, so that it alone was activated when light was pulsed into the mice's brains. Doing so led instantaneously to dramatic changes in the animals' behavior.
"The mice suddenly became much more comfortable in situations they would ordinarily perceive as dangerous and, therefore, be quite anxious in," said Deisseroth. For example, rodents ordinarily try to avoid wide-open spaces such as fields, because such places leave them exposed to predators. But in a standard setup simulating both open and covered areas, the mice's willingness to explore the open areas increased profoundly as soon as light was pulsed into the novel brain circuit. Pulsing that same circuit with a different, inhibitory frequency of light produced the opposite result: the mice instantly became more anxious. "They just hunkered down" in the relatively secluded areas of the test scenario, Deisseroth said.
Standard laboratory gauges of electrical activity in specific areas of the mice's amygdalas confirmed that the novel circuit's activation tracked the animals' increased risk-taking propensity.
Deisseroth said he believes his team's findings in mice will apply to humans as well. "We know that the amygdala is structured similarly in mice and humans," he said. And just over a year ago a Stanford team led by Deisseroth's associate, Amit Etkin, MD, PhD, assistant professor of psychiatry and behavioral science, used functional imaging techniques to show that human beings suffering from generalized anxiety disorder had altered connectivity in the same brain regions within the amygdala that Deisseroth's group has implicated optogenetically in mice.
The study was funded by the National Institutes of Health, the National Institute of Mental Health, the National Institute on Drug Abuse, the National Science Foundation, NARSAD, a Samsung Scholarship, and the McKnight, Woo, Snyder, and Yu foundations. Kay Tye, PhD, a postdoctoral researcher in the Deisseroth laboratory, and Rohit Prakash, Sung-Yon Kim and Lief Fenno, all graduate students in that lab, shared first authorship. Other co-authors are graduate student Logan Grosenick, undergraduate student Hosniya Zarabi, postdoctoral researcher Kimberly Thompson, PhD, and research associates Viviana Gradinaru and Charu Ramakrishnan, all of the Deisseroth lab.
(http://www.sciencedaily.com/releases/2011/03/110309131930.htm)
That's the finding in a paper by Stanford University School of Medicine researchers to be published online March 9 in Nature. In the study, Karl Deisseroth, MD, PhD, and his colleagues employed a mouse model to show that stimulating activity exclusively in this circuit enhances animals' willingness to take risks, while inhibiting its activity renders them more risk-averse. This discovery could lead to new treatments for anxiety disorders, said Deisseroth, an associate professor of bioengineering and of psychiatry and behavioral science.
The investigators were able to pinpoint this particular circuit only by working with a state-of-the-art technology called optogenetics, pioneered by Deisseroth at Stanford, which allows brain scientists to tease apart the complex circuits that compose the brain so these can be studied one by one.
"Anxiety is a poorly understood but common psychiatric disease," said Deisseroth, who is also a practicing psychiatrist. More than one in four people, in the course of their lives, experience bouts of anxiety symptoms sufficiently enduring and intense to be classified as a full-blown psychiatric disorder. In addition, anxiety is a significant contributing factor in other major psychiatric disorders from depression to alcohol dependence, Deisseroth said.
Most current anti-anxiety medications work by suppressing activity in the brain circuitry that generates anxiety or increases anxiety levels. Many of these drugs are not very effective, and those that are have significant side effects such as addiction or respiratory suppression, Deisseroth said. "The discovery of a novel circuit whose action is to reduce anxiety, rather than increase it, could point to an entire strategy of anti-anxiety treatment," he added.
Ironically, the anti-anxiety circuit is nestled within a brain structure, the amygdala, long known to be associated with fear. Generally, stimulating nervous activity in the amygdala is best known to heighten anxiety. So the anti-anxiety circuit probably would have been difficult if not impossible to locate had it not been for optogenetics, a new technology in which nerve cells in living animals are rendered photosensitive so that action in these cells can be turned on or off by different wavelengths of light. The technique allows researchers to selectively photosensitize particular sets of nerve cells. Moreover, by delivering pulses of light via optical fibers to specific brain areas, scientists can target not only particular nerve-cell types but also particular cell-to-cell connections or nervous pathways leading from one brain region to another. The fiber-optic hookup is both flexible and pain-free, so experimental animals' actual behavior as well as their brain activity can be monitored.
In contrast, older research approaches involve probing brain areas with electrodes to stimulate nerve cell firing. But an electrode stimulates not only all the nerve cells that happen to be in the neighborhood but even fibers that are just passing through on the way to somewhere else. Thus, any effect from stimulating the newly discovered anti-anxiety circuit would have been swamped by the anxiety-increasing effects of the dominant surrounding circuitry.
In December 2010, the journal Nature Methods bestowed its "Method of the Year" title on optogenetics.
In the new Nature study, the researchers photosensitized a set of fibers projecting from cells in one nervous "switchboard" to another one within the amygdala. By carefully positioning their light-delivery system, they were able to selectively target this projection, so that it alone was activated when light was pulsed into the mice's brains. Doing so led instantaneously to dramatic changes in the animals' behavior.
"The mice suddenly became much more comfortable in situations they would ordinarily perceive as dangerous and, therefore, be quite anxious in," said Deisseroth. For example, rodents ordinarily try to avoid wide-open spaces such as fields, because such places leave them exposed to predators. But in a standard setup simulating both open and covered areas, the mice's willingness to explore the open areas increased profoundly as soon as light was pulsed into the novel brain circuit. Pulsing that same circuit with a different, inhibitory frequency of light produced the opposite result: the mice instantly became more anxious. "They just hunkered down" in the relatively secluded areas of the test scenario, Deisseroth said.
Standard laboratory gauges of electrical activity in specific areas of the mice's amygdalas confirmed that the novel circuit's activation tracked the animals' increased risk-taking propensity.
Deisseroth said he believes his team's findings in mice will apply to humans as well. "We know that the amygdala is structured similarly in mice and humans," he said. And just over a year ago a Stanford team led by Deisseroth's associate, Amit Etkin, MD, PhD, assistant professor of psychiatry and behavioral science, used functional imaging techniques to show that human beings suffering from generalized anxiety disorder had altered connectivity in the same brain regions within the amygdala that Deisseroth's group has implicated optogenetically in mice.
The study was funded by the National Institutes of Health, the National Institute of Mental Health, the National Institute on Drug Abuse, the National Science Foundation, NARSAD, a Samsung Scholarship, and the McKnight, Woo, Snyder, and Yu foundations. Kay Tye, PhD, a postdoctoral researcher in the Deisseroth laboratory, and Rohit Prakash, Sung-Yon Kim and Lief Fenno, all graduate students in that lab, shared first authorship. Other co-authors are graduate student Logan Grosenick, undergraduate student Hosniya Zarabi, postdoctoral researcher Kimberly Thompson, PhD, and research associates Viviana Gradinaru and Charu Ramakrishnan, all of the Deisseroth lab.
(http://www.sciencedaily.com/releases/2011/03/110309131930.htm)
Tuesday, March 8, 2011
NASA says 'no support' for claim of alien microbes
by Kerry Sheridan Kerry Sheridan
WASHINGTON (AFP) – Top NASA scientists said Monday there was no scientific evidence to support a colleague's claim that fossils of alien microbes born in outer space had been found in meteorites on Earth.
The US space agency formally distanced itself from the paper by NASA scientist Richard Hoover, whose findings were published Friday in the peer-reviewed Journal of Cosmology, which is available free online.
"That is a claim that Mr Hoover has been making for some years," said Carl Pilcher, director of NASA's Astrobiology Institute.
"I am not aware of any support from other meteorite researchers for this rather extraordinary claim that this evidence of microbes was present in the meteorite before the meteorite arrived on Earth and and was not the result of contamination after the meteorite arrived on Earth," he told AFP.
"The simplest explanation is that there are microbes in the meteorites; they are Earth microbes. In other words, they are contamination."
Pilcher said the meteorites that Hoover studied fell to Earth 100 to 200 years ago and have been heavily handled by humans, "so you would expect to find microbes in these meteorites."
Paul Hertz, chief scientist of NASA's Science Mission Directorate in Washington, also issued a statement saying NASA did not support Hoover's findings.
"While we value the free exchange of ideas, data and information as part of scientific and technical inquiry, NASA cannot stand behind or support a scientific claim unless it has been peer-reviewed or thoroughly examined by other qualified experts," Hertz said.
"NASA also was unaware of the recent submission of the paper to the Journal of Cosmology or of the paper's subsequent publication."
He noted that the paper did not complete the peer-review process after being submitted in 2007 to the International Journal of Astrobiology.
According to the study, Hoover sliced open fragments of several types of carbonaceous chondrite meteorites, which can contain relatively high levels of water and organic materials, and looked inside with a powerful microscope, Field Emission Scanning Electron Microscopy (FESEM).
He found bacteria-like creatures, calling them "indigenous fossils" that originated beyond Earth and were not introduced here after the meteorites landed.
Hoover "concludes these fossilized bacteria are not Earthly contaminants but are the fossilized remains of living organisms which lived in the parent bodies of these meteors, e.g. comets, moons and other astral bodies," said the study.
"The implications are that life is everywhere, and that life on Earth may have come from other planets."
The journal's editor-in-chief, Rudy Schild of the Harvard-Smithsonian Center for Astrophysics, hailed Hoover as a "highly respected scientist and astrobiologist with a prestigious record of accomplishment at NASA."
The publication invited experts to weigh in on Hoover's claim, and both sceptics and supporters began publishing their commentaries on the journal's website Monday.
"While the evidence clearly indicates that the meteorites was eons ago populated with bacterial life, whether the meteorites are of actual extra-terrestrial origin might debatable," wrote Patrick Godon of Villanova University in Pennsylvania.
Michael Engel of the University of Oklahoma wrote: "Given the importance of this finding, it is essential to continue to seek new criteria more robust than visual similarity to clarify the origin(s) of these remarkable structures."
The journal did not immediately respond to requests for comment.
Pilcher described Hoover as a "NASA employee" who works in a solar physics branch of a NASA lab in the southeastern state of Alabama.
"He clearly does some very interesting microscopy. The actual measurements on these meteorites are very nice measurements, but I am not aware of any other qualification that Mr Hoover has in analysis of meteorites or in astrobiology," Pilcher said.
A NASA-funded study in December suggested that a previously unknown form of bacterium, found deep in a California lake, could thrive on arsenic, adding a new element to what scientists have long considered the six building blocks of life.
That study drew hefty criticism, particularly after NASA touted the announcement as evidence of extraterrestrial life. Scientists are currently attempting to replicate those findings.
(http://news.yahoo.com/s/afp/20110307/ts_alt_afp/usspacebiologyastrobiologynasa_20110307213642)
WASHINGTON (AFP) – Top NASA scientists said Monday there was no scientific evidence to support a colleague's claim that fossils of alien microbes born in outer space had been found in meteorites on Earth.
The US space agency formally distanced itself from the paper by NASA scientist Richard Hoover, whose findings were published Friday in the peer-reviewed Journal of Cosmology, which is available free online.
"That is a claim that Mr Hoover has been making for some years," said Carl Pilcher, director of NASA's Astrobiology Institute.
"I am not aware of any support from other meteorite researchers for this rather extraordinary claim that this evidence of microbes was present in the meteorite before the meteorite arrived on Earth and and was not the result of contamination after the meteorite arrived on Earth," he told AFP.
"The simplest explanation is that there are microbes in the meteorites; they are Earth microbes. In other words, they are contamination."
Pilcher said the meteorites that Hoover studied fell to Earth 100 to 200 years ago and have been heavily handled by humans, "so you would expect to find microbes in these meteorites."
Paul Hertz, chief scientist of NASA's Science Mission Directorate in Washington, also issued a statement saying NASA did not support Hoover's findings.
"While we value the free exchange of ideas, data and information as part of scientific and technical inquiry, NASA cannot stand behind or support a scientific claim unless it has been peer-reviewed or thoroughly examined by other qualified experts," Hertz said.
"NASA also was unaware of the recent submission of the paper to the Journal of Cosmology or of the paper's subsequent publication."
He noted that the paper did not complete the peer-review process after being submitted in 2007 to the International Journal of Astrobiology.
According to the study, Hoover sliced open fragments of several types of carbonaceous chondrite meteorites, which can contain relatively high levels of water and organic materials, and looked inside with a powerful microscope, Field Emission Scanning Electron Microscopy (FESEM).
He found bacteria-like creatures, calling them "indigenous fossils" that originated beyond Earth and were not introduced here after the meteorites landed.
Hoover "concludes these fossilized bacteria are not Earthly contaminants but are the fossilized remains of living organisms which lived in the parent bodies of these meteors, e.g. comets, moons and other astral bodies," said the study.
"The implications are that life is everywhere, and that life on Earth may have come from other planets."
The journal's editor-in-chief, Rudy Schild of the Harvard-Smithsonian Center for Astrophysics, hailed Hoover as a "highly respected scientist and astrobiologist with a prestigious record of accomplishment at NASA."
The publication invited experts to weigh in on Hoover's claim, and both sceptics and supporters began publishing their commentaries on the journal's website Monday.
"While the evidence clearly indicates that the meteorites was eons ago populated with bacterial life, whether the meteorites are of actual extra-terrestrial origin might debatable," wrote Patrick Godon of Villanova University in Pennsylvania.
Michael Engel of the University of Oklahoma wrote: "Given the importance of this finding, it is essential to continue to seek new criteria more robust than visual similarity to clarify the origin(s) of these remarkable structures."
The journal did not immediately respond to requests for comment.
Pilcher described Hoover as a "NASA employee" who works in a solar physics branch of a NASA lab in the southeastern state of Alabama.
"He clearly does some very interesting microscopy. The actual measurements on these meteorites are very nice measurements, but I am not aware of any other qualification that Mr Hoover has in analysis of meteorites or in astrobiology," Pilcher said.
A NASA-funded study in December suggested that a previously unknown form of bacterium, found deep in a California lake, could thrive on arsenic, adding a new element to what scientists have long considered the six building blocks of life.
That study drew hefty criticism, particularly after NASA touted the announcement as evidence of extraterrestrial life. Scientists are currently attempting to replicate those findings.
(http://news.yahoo.com/s/afp/20110307/ts_alt_afp/usspacebiologyastrobiologynasa_20110307213642)
Surgeon creates new kidney on TED stage
"It's like baking a cake," Anthony Atala of the Wake Forest Institute of Regenerative Medicine said as he cooked up a fresh kidney on stage at a TED Conference in the California city of Long Beach.
Scanners are used to take a 3-D image of a kidney that needs replacing, then a tissue sample about half the size of postage stamp is used to seed the computerized process, Atala explained.
The organ "printer" then works layer-by-layer to build a replacement kidney replicating the patient's tissue.
College student Luke Massella was among the first people to receive a printed kidney during experimental research a decade ago when he was just 10 years old.
He said he was born with Spina Bifida and his kidneys were not working.
"Now, I'm in college and basically trying to live life like a normal kid," said Massella, who was reunited with Atala at TED.
"This surgery saved my life and made me who I am today."
About 90 percent of people waiting for transplants are in need of kidneys, and the need far outweighs the supply of donated organs, according to Atala.
"There is a major health crisis today in terms of the shortage of organs," Atala said. "Medicine has done a much better job of making us live longer, and as we age our organs don't last."
(http://www.physorg.com/news/2011-03-surgeon-kidney-ted-stage.html)
Scanners are used to take a 3-D image of a kidney that needs replacing, then a tissue sample about half the size of postage stamp is used to seed the computerized process, Atala explained.
The organ "printer" then works layer-by-layer to build a replacement kidney replicating the patient's tissue.
College student Luke Massella was among the first people to receive a printed kidney during experimental research a decade ago when he was just 10 years old.
He said he was born with Spina Bifida and his kidneys were not working.
"Now, I'm in college and basically trying to live life like a normal kid," said Massella, who was reunited with Atala at TED.
"This surgery saved my life and made me who I am today."
About 90 percent of people waiting for transplants are in need of kidneys, and the need far outweighs the supply of donated organs, according to Atala.
"There is a major health crisis today in terms of the shortage of organs," Atala said. "Medicine has done a much better job of making us live longer, and as we age our organs don't last."
(http://www.physorg.com/news/2011-03-surgeon-kidney-ted-stage.html)
Subscribe to:
Posts (Atom)