It seems like almost every day that we receive a press release announcing Verizon or AT&T is planning to expand its LTE coverage to three, five, eleven new markets. But in some remote pockets of the country, you'd be lucky to latch onto even a solid 3G signal. In a bid to make sure those folks in the boonies get their due, the Federal Communications Commission is establishing a fund to encourage carriers to roll out 3G and 4G service in sparser areas. All told, the agency plans to award up to $300 million to mobile operators, with funds going to the providers offering the lowest rates. The winners will be decided in a sealed, single-round auction, which opens June 27th and is set to close July 11th. As a condition for receiving the funds, carriers must agree to cover at least 75 percent of the road miles within a given census tract. While it's unclear at this early stage which mobile players will take the bait, the FCC's already signaled which parts of the country will be first in line for upgraded service -- namely, Rocky Mountain states like Utah and Idaho, along with Maine, Appalachia and upstate New York.
As the poet once said, "Mo' apps, mo' problems", or something like that. The Windows Phone Marketplace continues to grow and with more eyeballs on it, Microsoft is making sure devs know the rules that will keep their apps in the store instead of on the sideline. Trademark and copyright issues headline the new areas of enforcement, followed up by making sure bulk published apps are in the right categories, packaged with tile images and branding that make it clear which one is which and what they do. Rounding out the list are keywords -- pepper your app with popular, but unrelated terms at your own peril -- and apps that currently overstep the allowed boundary "racy" content. In the end only you, the users, can report if these policies are making it easier to navigate the ever expanding amount of apps so let us know -- are things clogged up with intentionally mislabeled crapware, or is it smooth sailing?
Jennifer Lopez and Enrique Iglesias are about to set off on tour together, as the artists gathered yesterday for a press conference discussing the anticipated concerts. There's just one question:
Who will open? And who will headline?
"Neither Jennifer nor Enrique care who opens or closes," J. Lo's manager tells TMZ. "What we want to do is give the fans the best show possible and whatever that means, that's what we will do."
But is that what Iglesias will do? He pulled out of a Britney Spears tour last year, reportedly, because he did NOT get top billing. Which leads us to ask:
Which of these singers would you rather... see in concert?
How does the immune system fight off threats to the brain? New research yields fresh insight Public release date: 30-Apr-2012 [ | E-mail | Share ]
Contact: Kara Gavin kegavin@umich.edu 734-764-2220 University of Michigan Health System
Finding of an amplification defense mechanism may help research on brain infections, tumors & autoimmune attacks and settle a debate in immunology
ANN ARBOR, Mich. Like a police officer calling for backup while also keeping a strong hold on a suspected criminal, immune cells in the brain take a two-tier approach to fighting off a threat, new research from the University of Michigan Health System finds.
For the first time, the scientists managed to capture that reaction in action, showing how certain immune cells locked onto a model of virus-infected brain cells, while also sending signals to neighboring uninfected cells to let them know about the immune attack.
The findings may help research on how the brain fights off viruses and tumors. It also aids the search for ways to harness the immune response to attack and kill brain tumor cells -- or to calm the overzealous self-attack that occurs in people with certain autoimmune diseases.
Published online today in the Proceedings of the National Academy of Sciences, the findings illuminate how cells called CD8+ T cells, or "killer" T cells, carry out their police-like role. Pedro Lowenstein, M.D., Ph.D., professor in the Department of Neurosurgery at the U-M Medical School, led the research team.
He explains that the research yields new insight into the nature of the "gasket" that forms between killer T cells and their target cells, i.e., infected -- or tumor -- cells. Killer T cells go after cells when they detect the presence of foreign proteins, called antigens, on the cell surface.
The gasket-like structure creates an area between the two cells called an immunological synapse -- and has been thought of by some scientists as a tight seal. Studies, including previous ones by Lowenstein's team, have suggested that it allows the killer T cell to lock on to its target and bombard it first with molecules called cytokines, and then with chemicals that break down the infected cell and kill it.
But other scientists have shown that when killer T cells are attacking infected cells, the cytokines they release seem to cause a reaction in many neighboring, uninfected cells suggesting a very open connection. These latter studies question the role of immunological synapses.
Using a unique live-cell imaging technique developed by the team, the new results show that the gasket connection focuses the T cell attack on the infected cell, but is leaky. This creates a two-tier response when a killer T cell goes after an infection.
"The T cell targets the infected cell preferentially, but it also secretes cytokines that reach a number of other cells in the neighborhood," says Lowenstein. "The immunological synapse fails to restrict how far cytokines can spread."
The research team, including U-M postdoctoral fellow Nicholas Sanderson, Ph.D., made the finding using a live-cell imaging method they developed that allows them to detect how many cells are exposed to the cytokine interferon gamma.
While the immunological synapse "gasket" ensured that the targeted cell was hit first by cytokines, other cells in the area soon showed signs of having received the same cytokine signal.
What's more, the researchers confirmed that the killer T cell carried out its killer function only on the targeted, infected cell it had attached to sparing nearby cells.
"This work disproves the idea that T cells secrete cytokines indiscriminately in the brain, but shows that T cell cytokine secretion affects a larger area beyond the targeted cell," says Lowenstein. "This helps settle the quandary of why widespread response to cytokines are seen, even when immune cells form specific immunological synapses only with target cells."
The finding, he adds, will help illuminate at a molecular level how the brain gets rid of infection. But it also hints at how the body's own T cells might mount the misguided attack on normal healthy brain cells in autoimmune diseases. The findings clarify how widespread effects can be obtained in spite of very specific cell-to-cell interactions.
And, significant for the U-M team's work on brain tumor physiology, the new result helps build knowledge that could be used in attempts to attack and kill brain tumor cells while sparing normal cells. "What we want to know is how T cells work, how they interact with target cells and how we can make this process more efficient," Lowenstein explains.
Such an approach is the goal of the team led by Lowenstein and Maria Castro, Ph.D., who is a co-author on this paper.
###
The research was funded by the National Institute for Neurological Disorders and Stroke, part of the National Institutes of Health. Lowenstein credits Neurosurgery chair Karin Muraszko, M.D., for recruiting the team to U-M last year, and fostering their work on brain tumors. Lowenstein and Castro also hold faculty appointments in the Medical School's department of Cell and Developmental Biology.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
How does the immune system fight off threats to the brain? New research yields fresh insight Public release date: 30-Apr-2012 [ | E-mail | Share ]
Contact: Kara Gavin kegavin@umich.edu 734-764-2220 University of Michigan Health System
Finding of an amplification defense mechanism may help research on brain infections, tumors & autoimmune attacks and settle a debate in immunology
ANN ARBOR, Mich. Like a police officer calling for backup while also keeping a strong hold on a suspected criminal, immune cells in the brain take a two-tier approach to fighting off a threat, new research from the University of Michigan Health System finds.
For the first time, the scientists managed to capture that reaction in action, showing how certain immune cells locked onto a model of virus-infected brain cells, while also sending signals to neighboring uninfected cells to let them know about the immune attack.
The findings may help research on how the brain fights off viruses and tumors. It also aids the search for ways to harness the immune response to attack and kill brain tumor cells -- or to calm the overzealous self-attack that occurs in people with certain autoimmune diseases.
Published online today in the Proceedings of the National Academy of Sciences, the findings illuminate how cells called CD8+ T cells, or "killer" T cells, carry out their police-like role. Pedro Lowenstein, M.D., Ph.D., professor in the Department of Neurosurgery at the U-M Medical School, led the research team.
He explains that the research yields new insight into the nature of the "gasket" that forms between killer T cells and their target cells, i.e., infected -- or tumor -- cells. Killer T cells go after cells when they detect the presence of foreign proteins, called antigens, on the cell surface.
The gasket-like structure creates an area between the two cells called an immunological synapse -- and has been thought of by some scientists as a tight seal. Studies, including previous ones by Lowenstein's team, have suggested that it allows the killer T cell to lock on to its target and bombard it first with molecules called cytokines, and then with chemicals that break down the infected cell and kill it.
But other scientists have shown that when killer T cells are attacking infected cells, the cytokines they release seem to cause a reaction in many neighboring, uninfected cells suggesting a very open connection. These latter studies question the role of immunological synapses.
Using a unique live-cell imaging technique developed by the team, the new results show that the gasket connection focuses the T cell attack on the infected cell, but is leaky. This creates a two-tier response when a killer T cell goes after an infection.
"The T cell targets the infected cell preferentially, but it also secretes cytokines that reach a number of other cells in the neighborhood," says Lowenstein. "The immunological synapse fails to restrict how far cytokines can spread."
The research team, including U-M postdoctoral fellow Nicholas Sanderson, Ph.D., made the finding using a live-cell imaging method they developed that allows them to detect how many cells are exposed to the cytokine interferon gamma.
While the immunological synapse "gasket" ensured that the targeted cell was hit first by cytokines, other cells in the area soon showed signs of having received the same cytokine signal.
What's more, the researchers confirmed that the killer T cell carried out its killer function only on the targeted, infected cell it had attached to sparing nearby cells.
"This work disproves the idea that T cells secrete cytokines indiscriminately in the brain, but shows that T cell cytokine secretion affects a larger area beyond the targeted cell," says Lowenstein. "This helps settle the quandary of why widespread response to cytokines are seen, even when immune cells form specific immunological synapses only with target cells."
The finding, he adds, will help illuminate at a molecular level how the brain gets rid of infection. But it also hints at how the body's own T cells might mount the misguided attack on normal healthy brain cells in autoimmune diseases. The findings clarify how widespread effects can be obtained in spite of very specific cell-to-cell interactions.
And, significant for the U-M team's work on brain tumor physiology, the new result helps build knowledge that could be used in attempts to attack and kill brain tumor cells while sparing normal cells. "What we want to know is how T cells work, how they interact with target cells and how we can make this process more efficient," Lowenstein explains.
Such an approach is the goal of the team led by Lowenstein and Maria Castro, Ph.D., who is a co-author on this paper.
###
The research was funded by the National Institute for Neurological Disorders and Stroke, part of the National Institutes of Health. Lowenstein credits Neurosurgery chair Karin Muraszko, M.D., for recruiting the team to U-M last year, and fostering their work on brain tumors. Lowenstein and Castro also hold faculty appointments in the Medical School's department of Cell and Developmental Biology.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Richibrown Organic Natox has just been launched to provide the cosmetic industry with a quality Botox alternative. Natox was created and works on the same principle as Botox but without the use of any injectable substances. Botulinum toxin injections are often considered as an unpleasant anti-wrinkle method but many people resort to it because of its effectiveness.
Natox manufacturers claim that this new anti-wrinkle cream can work as a Botox alternative and it can offer:
Improved skin texture
Reduction of deep wrinkles
Elimination of fine lines
Younger looking appearance
Easy application ? just like any other face cream
A natural product without side effects
Affordable price
Fast visible results
Increased production of collagen
Although Organic Natox is a new product on the market, several ageing celebrities used it privately as a Botox alternative in the past. Natox has been the secret anti-ageing weapon of Hollywood stars and according to their testimonials, this anti-wrinkle cream gave them a younger and fresher look without wrinkles and fine lines.
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Public release date: 30-Apr-2012
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