From Jason to Freddy, here's how several horror icons have been spending their time since their famous roles.
By Alex Zalben
WASHINGTON (AP) — More than 47 million Americans who receive food stamps will see their benefits go down starting Friday, just as Congress has begun negotiations on further cuts to the program.
Beginning in November, a temporary benefit from the 2009 economic stimulus that boosts food stamp dollars will no longer be available. According to the Agriculture Department, that means a family of four receiving food stamps will start receiving $36 less a month.
The benefits, which go to 1 in 7 Americans, fluctuate based on factors that include food prices, inflation and income. The rolls have swelled as the economy has struggled in recent years, with the stimulus providing higher benefits and many people signing up for the first time.
As a result, the program has more than doubled in cost since 2008, now costing almost $80 billion a year. That large increase in spending has turned the program, now called the Supplemental Nutrition Assistance Program, or SNAP, into a target for House Republicans looking to reduce spending.
Negotiations on a wide-ranging farm bill, including cuts to the SNAP program, began Wednesday. Five-year farm bills passed by both the House and the Senate would cut food stamps, reductions that would come on top of the cut that will go into effect Friday. But the two chambers are far apart on the amounts.
Legislation passed by the GOP-controlled House would cut food stamps by an additional $4 billion annually and tighten eligibility requirements. The House bill would also end government waivers that have allowed able-bodied adults without dependents to receive food stamps indefinitely and allow states to put broad new work requirements in place.
The Senate farm bill would cut a tenth of the House amount, with Democrats and President Barack Obama opposing major cuts.
Farm-state lawmakers have been pushing the farm bill for more than two years, and Wednesday's conference negotiations represented the opening round in final talks. If the bill is not passed by the end of the year and current farm law is not extended, certain dairy supports would expire that could raise the price of milk. Farmers would start to feel more effects next spring.
"It took us years to get here but we are here," House Agriculture Committee Chairman Frank Lucas, R-Okla., said. "Let's not take years to get it done."
The biggest obstacle to a final bill is how far apart the two parties are on food stamps. Lucas said at the conference meeting that he was hoping to find common ground on the issue, but House GOP leaders such as Rep. Eric Cantor, R-Va., have insisted on higher cuts, saying the program should be targeted to the neediest people.
House Minority Leader Nancy Pelosi, D-Calif., sent out a statement as the meeting opened that said food stamp recipients "deserve swift action from Congress to pass a bill that provides the much-needed nutritional support for our children, our seniors, our veterans and our communities."
As Congress debates the cuts to the program, charities say they are preparing for the farm bill reductions as well as the scheduled cuts taking place Friday.
"Charities cannot fill the gap for the cuts being proposed to SNAP," said Maura Daly of Feeding America, a network of the nation's food banks. "We are very concerned about the impact on the charitable system."
Daly says food banks may have to as much as double their current levels of distribution if the House cuts were enacted. The Congressional Budget Office says as many as 3.8 million people could lose their benefits in 2014 if the House bill became law.
___
Follow Mary Clare Jalonick on Twitter at http://twitter.com/mcjalonick
Associated PressSource: http://hosted2.ap.org/APDEFAULT/89ae8247abe8493fae24405546e9a1aa/Article_2013-10-31-Farm%20Bill-Food%20Stamps/id-14cd667a5a8442fc8300240b75998935NEW YORK (AP) — It's not coincidental that the stars of "Scandal" live tweet during episodes. They're encouraged to do so.
When several of the show's actors recently visited New York to promote the premiere of season three, ABC made sure to book Kerry Washington on a return flight to Los Angeles that offered Wi-Fi. Other cast members had their trips extended so they could be available on the social networking site.
Joshua Malina, who plays U.S. attorney David Rosen, relishes having a presence on Twitter. He describes his tweets as "self-promotion and dumb jokes."
A few examples:
—"Okay, how do we make the old chargers obsolete?" — first thing spoken at every Apple meeting about a new product."
—"Please watch Kerry Washington tonight on Kimmel as she continues her courageous battle against underexposure!"
—"If Lamar Odom and Khloe Kardashian can't make it, then ... nothing I can think of."
Malina may love Twitter but he wasn't an early fan.
"My sister was an early adopter. She lives in a remote area and what I could tell used Twitter to let my parents know that she was still alive. ... I thought, 'This thing is not gonna catch on.'"
Now he admits to sometimes crafting tweets and saving them for later.
"Occasionally I'll be driving around trying to formulate," he said. "The beauty of it is the enforced brevity forces you to craft your tweets, if you're attempting to be funny to really sort of pare it down so it's just right. I will work something over and over. Other times I'll read what's going on and instantly react."
Malina has no problem sparring with people who tweet him.
"Certainly these strangers who interact with me aren't holding back. People will tweet, 'You're ugly,'" he laughed. "I also have very, very thick skin ... so I don't mind reading the bad stuff."
He even prefers the negative over the positive.
"The good stuff is in a way less entertaining to read. I mean it's nice but you know ... people who want to really go after you I enjoy interacting with. I don't think I've ever actually been offended by anything anyone has written and I sort of hope people take it in the same spirit."
Malina doesn't hold back with celebs.
"Any celebrity that goes on Twitter and spouts off as if we should care what they say is opening himself or herself up to ridicule by anyone else."
"Scandal" airs Thursdays on ABC at 10 p.m. Eastern.
___
Alicia Rancilio covers entertainment for The Associated Press. Follow her online at http://www.twitter.com/aliciar
___
Online:
http://www.abc.go.com/shows/scandal/
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PUBLIC RELEASE DATE: 31-Oct-2013
ShareContact: NIAID Office of Communications
niaidnews@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
Using protein engineering and two different cutting-edge structural biology imaging techniques, researchers have developed a detailed picture of the protein largely responsible for enabling HIV to enter human immune cells and cause infection. An in-depth understanding of the atomic structure of the HIV envelope trimeror Env, the three-component protein found on HIV's surfaceis critical to better understanding how HIV gains entry into cells and for creating potential HIV vaccines.
Atomic-resolution imaging of the Env protein has previously been elusive because of the protein's complex, delicate structure. To capture the image, a team of scientists at The Scripps Research Institute and Weill Medical College of Cornell University engineered a more stable version of the protein. Then, in separate studies, using first cryo-electron microscopy and then X-ray crystallography, the researchers were able to reveal the structure of the Env trimer, how it assembles and how it interacts with broadly neutralizing antibodies that target HIV.
Their research, described in two papers published online today in Science Express, received major support from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
###
ARTICLES:
D. Lyumkis et al. Cryo-EM Structure of a Fully Glycosylated Soluble Cleaved HIV-1 Env Trimer. Science Express DOI: 10.1126/science.1245627 (2013).
J.P. Julien et al. Crystal Structure of a Soluble Dleaved HIV-1 Envelope Trimer. Science Express DOI: 10.1126/science.1245625 (2013).
NIAID Director Anthony S. Fauci, M.D, is available to comment on both papers.
To schedule interviews, please contact the NIAID News Office, (301) 402-1663, niaidnews@niaid.nih.gov.
NIAID conducts and supports researchat NIH, throughout the United States, and worldwideto study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov/.
NIH...Turning Discovery Into Health
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.
PUBLIC RELEASE DATE: 31-Oct-2013
ShareContact: NIAID Office of Communications
niaidnews@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
Using protein engineering and two different cutting-edge structural biology imaging techniques, researchers have developed a detailed picture of the protein largely responsible for enabling HIV to enter human immune cells and cause infection. An in-depth understanding of the atomic structure of the HIV envelope trimeror Env, the three-component protein found on HIV's surfaceis critical to better understanding how HIV gains entry into cells and for creating potential HIV vaccines.
Atomic-resolution imaging of the Env protein has previously been elusive because of the protein's complex, delicate structure. To capture the image, a team of scientists at The Scripps Research Institute and Weill Medical College of Cornell University engineered a more stable version of the protein. Then, in separate studies, using first cryo-electron microscopy and then X-ray crystallography, the researchers were able to reveal the structure of the Env trimer, how it assembles and how it interacts with broadly neutralizing antibodies that target HIV.
Their research, described in two papers published online today in Science Express, received major support from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
###
ARTICLES:
D. Lyumkis et al. Cryo-EM Structure of a Fully Glycosylated Soluble Cleaved HIV-1 Env Trimer. Science Express DOI: 10.1126/science.1245627 (2013).
J.P. Julien et al. Crystal Structure of a Soluble Dleaved HIV-1 Envelope Trimer. Science Express DOI: 10.1126/science.1245625 (2013).
NIAID Director Anthony S. Fauci, M.D, is available to comment on both papers.
To schedule interviews, please contact the NIAID News Office, (301) 402-1663, niaidnews@niaid.nih.gov.
NIAID conducts and supports researchat NIH, throughout the United States, and worldwideto study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov/.
NIH...Turning Discovery Into Health
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.
PUBLIC RELEASE DATE: 31-Oct-2013
ShareContact: Anne A. Oplinger
aoplinger@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
An experimental vaccine to protect against respiratory syncytial virus (RSV), a leading cause of illness and hospitalization among very young children, elicited high levels of RSV-specific antibodies when tested in animals, according to a report in the journal Science.
Early-stage human clinical trials of the candidate vaccine are planned. Scientists from the Vaccine Research Center (VRC), National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, built on their previous findings about the structure of a critical viral protein to design the vaccine. The team was led by Peter D. Kwong, Ph.D., and Barney S. Graham, M.D., Ph.D.
In the United States, RSV infection is the most common cause of bronchiolitis (inflammation of small airways in the lungs) and pneumonia in children less than one year old and the most common cause for hospitalization in children under five. Worldwide, it is estimated that RSV is responsible for nearly 7 percent of deaths in babies aged 1 month to 1 year; only malaria kills more children in this age group. Others at risk for severe disease following RSV infection include adults over age 65 and those with compromised immune systems.
Many common diseases of childhood are now vaccine-preventable, but a vaccine against RSV infection has eluded us for decades, said NIAID Director Anthony S. Fauci, M.D. This work marks a major step forward. Not only does the experimental vaccine developed by our scientists elicit strong RSV-neutralizing activity in animals, but, more broadly, this technique of using structural information to inform vaccine design is being applied to other viral diseases, including HIV/AIDS.
Earlier this year, the VRC team obtained atomic-level details of an RSV proteincalled the fusion (F) glycoproteinbound to a broadly neutralizing human RSV antibody. The protein-antibody complex gave scientists their first look at the F glycoprotein as it appears before it fuses with a human cell. In this pre-fusion shape, F glycoprotein contains a region vulnerable to attack by broadly neutralizing antibodies (antibodies able to block infection from the common strains of RSV).
Once RSV fuses with a cell, this vulnerable area, named antigenic site zero by the researchers, is no longer present on the rearranged F protein. In natural RSV infection, the immune system produces antibodies against both the pre-fusion and post-fusion forms of F glycoprotein, but the antibodies to antigenic site zero, which is only present on the pre-fusion form, have much stronger neutralizing activity. Therefore, a vaccine against RSV would have greater chance of success by eliciting antibodies directed at F glycoprotein in its pre-fusion configuration.
In their current publication, Drs. Kwong and Graham describe how they used this structural information to design and engineer F glycoprotein variants that retained antigenic site zero even when no antibody was bound to it. The goal was to create stable variants that could serve as the foundation for a vaccine capable of eliciting a potent antibody response. The researchers designed more than 100 variants; of these, 3 were shown by X-ray crystallography to retain the desired structure. The engineered variants were then used as vaccines in a series of experiments in mice and rhesus macaques.
In both mice and macaques, the researchers found that the more stable the protein, the higher the levels of neutralizing antibodies elicited by vaccination. The levels of antibody made in response to one of the engineered F glycoproteins were more than 10 times higher than those produced following vaccination with post-fusion F glycoprotein and well above levels needed to protect against RSV infection.
Here is a case in which information gained from structural biology has provided the insight needed to solve an immunological puzzle and apply the findings to address a real-world public health problem, said Dr. Graham. He and the VRC scientists are continuing to refine the engineered F glycoproteins and hope to launch early-stage human clinical trials of a candidate RSV vaccine as soon as clinical grade material can be manufactured, a process that takes about 18 to 24 months to complete.
Previously, structure-based vaccine design held promise at a conceptual level, said Dr. Kwong. This advance delivers on that promise and sets the stage for similar applications of structure-guided design to effective vaccines against other pathogens.
Dr. Fauci added, This latest advance underscores the advantages of the VRCs organizational design, where experts in RSV virology, vaccinology and clinical studies, such as Dr. Graham, are in daily contact with Dr. Kwong and others who are experts in structural biology. Such close collaboration across disciplines allows for rapid testing of new approaches to a given problem.
###
NIAID conducts and supports researchat NIH, throughout the United States, and worldwideto study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
NIH...Turning Discovery Into Health
References:
JS McLellan et al. Structure-based design of a fusion glycoprotein vaccine for respiratory syncytial virus. Science DOI: 10.1126/science.1243283 (2013).
JS McLellan et al. Structure of RSV fusion glycoprotein trimer bound to a prefusion-specific neutralizing antibody. Science DOI: 10.1126/science.1234914 (2013).
PUBLIC RELEASE DATE: 31-Oct-2013
ShareContact: Anne A. Oplinger
aoplinger@niaid.nih.gov
301-402-1663
NIH/National Institute of Allergy and Infectious Diseases
An experimental vaccine to protect against respiratory syncytial virus (RSV), a leading cause of illness and hospitalization among very young children, elicited high levels of RSV-specific antibodies when tested in animals, according to a report in the journal Science.
Early-stage human clinical trials of the candidate vaccine are planned. Scientists from the Vaccine Research Center (VRC), National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, built on their previous findings about the structure of a critical viral protein to design the vaccine. The team was led by Peter D. Kwong, Ph.D., and Barney S. Graham, M.D., Ph.D.
In the United States, RSV infection is the most common cause of bronchiolitis (inflammation of small airways in the lungs) and pneumonia in children less than one year old and the most common cause for hospitalization in children under five. Worldwide, it is estimated that RSV is responsible for nearly 7 percent of deaths in babies aged 1 month to 1 year; only malaria kills more children in this age group. Others at risk for severe disease following RSV infection include adults over age 65 and those with compromised immune systems.
Many common diseases of childhood are now vaccine-preventable, but a vaccine against RSV infection has eluded us for decades, said NIAID Director Anthony S. Fauci, M.D. This work marks a major step forward. Not only does the experimental vaccine developed by our scientists elicit strong RSV-neutralizing activity in animals, but, more broadly, this technique of using structural information to inform vaccine design is being applied to other viral diseases, including HIV/AIDS.
Earlier this year, the VRC team obtained atomic-level details of an RSV proteincalled the fusion (F) glycoproteinbound to a broadly neutralizing human RSV antibody. The protein-antibody complex gave scientists their first look at the F glycoprotein as it appears before it fuses with a human cell. In this pre-fusion shape, F glycoprotein contains a region vulnerable to attack by broadly neutralizing antibodies (antibodies able to block infection from the common strains of RSV).
Once RSV fuses with a cell, this vulnerable area, named antigenic site zero by the researchers, is no longer present on the rearranged F protein. In natural RSV infection, the immune system produces antibodies against both the pre-fusion and post-fusion forms of F glycoprotein, but the antibodies to antigenic site zero, which is only present on the pre-fusion form, have much stronger neutralizing activity. Therefore, a vaccine against RSV would have greater chance of success by eliciting antibodies directed at F glycoprotein in its pre-fusion configuration.
In their current publication, Drs. Kwong and Graham describe how they used this structural information to design and engineer F glycoprotein variants that retained antigenic site zero even when no antibody was bound to it. The goal was to create stable variants that could serve as the foundation for a vaccine capable of eliciting a potent antibody response. The researchers designed more than 100 variants; of these, 3 were shown by X-ray crystallography to retain the desired structure. The engineered variants were then used as vaccines in a series of experiments in mice and rhesus macaques.
In both mice and macaques, the researchers found that the more stable the protein, the higher the levels of neutralizing antibodies elicited by vaccination. The levels of antibody made in response to one of the engineered F glycoproteins were more than 10 times higher than those produced following vaccination with post-fusion F glycoprotein and well above levels needed to protect against RSV infection.
Here is a case in which information gained from structural biology has provided the insight needed to solve an immunological puzzle and apply the findings to address a real-world public health problem, said Dr. Graham. He and the VRC scientists are continuing to refine the engineered F glycoproteins and hope to launch early-stage human clinical trials of a candidate RSV vaccine as soon as clinical grade material can be manufactured, a process that takes about 18 to 24 months to complete.
Previously, structure-based vaccine design held promise at a conceptual level, said Dr. Kwong. This advance delivers on that promise and sets the stage for similar applications of structure-guided design to effective vaccines against other pathogens.
Dr. Fauci added, This latest advance underscores the advantages of the VRCs organizational design, where experts in RSV virology, vaccinology and clinical studies, such as Dr. Graham, are in daily contact with Dr. Kwong and others who are experts in structural biology. Such close collaboration across disciplines allows for rapid testing of new approaches to a given problem.
###
NIAID conducts and supports researchat NIH, throughout the United States, and worldwideto study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
NIH...Turning Discovery Into Health
References:
JS McLellan et al. Structure-based design of a fusion glycoprotein vaccine for respiratory syncytial virus. Science DOI: 10.1126/science.1243283 (2013).
JS McLellan et al. Structure of RSV fusion glycoprotein trimer bound to a prefusion-specific neutralizing antibody. Science DOI: 10.1126/science.1234914 (2013).
PUBLIC RELEASE DATE: 31-Oct-2013
ShareContact: Paula Byron
pbyron@vt.edu
540-526-2027
Virginia Tech
Real estate agents emphasize location, location, and once more for good measure location. It's the same in a developing brain, where billions of neurons vie for premium property to make connections. Neurons that stake out early claims often land the best value, even if they don't develop the property until later.
Scientists at the Virginia Tech Carilion Research Institute and the University of Louisville have discovered that during neurodevelopment, neurons from the brain's cerebral cortex extend axons to the edge of the part of the brain dedicated to processing visual signals but then stop. Instead of immediately making connections, the cortical neurons wait for two weeks while neurons from the retina connect to the brain.
Now, in a study to be published in the Nov. 14 issue of the journal Cell Reports, the scientists have discovered how. The retinal neurons stop their cortical cousins from grabbing prime real estate by controlling the abundance of a protein called aggrecan.
Understanding how aggrecan controls the formation of brain circuits could help scientists understand how to repair the injured brain or spinal cord after injury or disease.
"Usually when neuroscientists talk about repairing injured brains, they're thinking about putting neurons, axons, and synapses back in the right place," said Michael Fox, an associate professor at the Virginia Tech Carilion Research Institute and lead author of the study. "It may be that the most important synapses the ones that drive excitation need to get there first. By stalling out the other neurons, they can get the best spots. This study shows that when we think about repairing damaged neural networks, we need to consider more than just where connections need to be made. We also need to think about the timing of reinnervation."
The researchers genetically removed the retinal neurons, which allowed the cortical axons to move into the brain earlier than they normally would.
"We were interested in what environmental molecular cues allow the retinal neurons to control the growth of cortical neurons," said Fox, who is also an associate professor of biological sciences in Virginia Tech's College of Science. "After years of screening potential mechanisms, we found aggrecan."
Aggrecan is a protein that has been well studied in cartilage, bones, and the spinal cord, where it is abundant after injuries. According to Fox, aggrecan may be able to isolate damaged areas of the spinal cord to stop inflammation and prevent further destruction. The downside, however, is that aggrecan inhibits axonal growth, which prevents further repair from taking place.
"Axons see this environment and either stop growing or turn around and grow in the opposite direction," said Fox.
Although it is less studied in the developing brain, aggrecan appears in abundance there. In the new study, the researchers found that retinal neurons control aggrecan in a region that receives ascending signals from retinal cells as well as descending signals from the cerebral cortex.
Once the retinal neurons have made connections, they cause the release of enzymes that break down the aggrecan, allowing cortical neurons to move in.
Fox said it is interesting that the retinal axons can grow in this region of the developing brain, despite the high levels of aggrecan. He suspects that it may be because retinal neurons express a receptor integrin that cortical axons do not express.
###
The study, "A molecular mechanism regulating the timing of corticogeniculate innervation," is by Fox, Jianmin Su, a research assistant professor, and Carl Levy, an undergraduate from Suffolk, Va., all with the Virginia Tech Carilion Research Institute; graduate student Justin Brooks and undergraduate Jessica Wang from Virginia Commonwealth University; and Tania Seabrook, a postdoctoral associate, and William Guido, a professor and the chair of the Department of Anatomical Sciences and Neurobiology, both with the University of Louisville School of Medicine.
Written by Ken Kingery
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.
PUBLIC RELEASE DATE: 31-Oct-2013
ShareContact: Paula Byron
pbyron@vt.edu
540-526-2027
Virginia Tech
Real estate agents emphasize location, location, and once more for good measure location. It's the same in a developing brain, where billions of neurons vie for premium property to make connections. Neurons that stake out early claims often land the best value, even if they don't develop the property until later.
Scientists at the Virginia Tech Carilion Research Institute and the University of Louisville have discovered that during neurodevelopment, neurons from the brain's cerebral cortex extend axons to the edge of the part of the brain dedicated to processing visual signals but then stop. Instead of immediately making connections, the cortical neurons wait for two weeks while neurons from the retina connect to the brain.
Now, in a study to be published in the Nov. 14 issue of the journal Cell Reports, the scientists have discovered how. The retinal neurons stop their cortical cousins from grabbing prime real estate by controlling the abundance of a protein called aggrecan.
Understanding how aggrecan controls the formation of brain circuits could help scientists understand how to repair the injured brain or spinal cord after injury or disease.
"Usually when neuroscientists talk about repairing injured brains, they're thinking about putting neurons, axons, and synapses back in the right place," said Michael Fox, an associate professor at the Virginia Tech Carilion Research Institute and lead author of the study. "It may be that the most important synapses the ones that drive excitation need to get there first. By stalling out the other neurons, they can get the best spots. This study shows that when we think about repairing damaged neural networks, we need to consider more than just where connections need to be made. We also need to think about the timing of reinnervation."
The researchers genetically removed the retinal neurons, which allowed the cortical axons to move into the brain earlier than they normally would.
"We were interested in what environmental molecular cues allow the retinal neurons to control the growth of cortical neurons," said Fox, who is also an associate professor of biological sciences in Virginia Tech's College of Science. "After years of screening potential mechanisms, we found aggrecan."
Aggrecan is a protein that has been well studied in cartilage, bones, and the spinal cord, where it is abundant after injuries. According to Fox, aggrecan may be able to isolate damaged areas of the spinal cord to stop inflammation and prevent further destruction. The downside, however, is that aggrecan inhibits axonal growth, which prevents further repair from taking place.
"Axons see this environment and either stop growing or turn around and grow in the opposite direction," said Fox.
Although it is less studied in the developing brain, aggrecan appears in abundance there. In the new study, the researchers found that retinal neurons control aggrecan in a region that receives ascending signals from retinal cells as well as descending signals from the cerebral cortex.
Once the retinal neurons have made connections, they cause the release of enzymes that break down the aggrecan, allowing cortical neurons to move in.
Fox said it is interesting that the retinal axons can grow in this region of the developing brain, despite the high levels of aggrecan. He suspects that it may be because retinal neurons express a receptor integrin that cortical axons do not express.
###
The study, "A molecular mechanism regulating the timing of corticogeniculate innervation," is by Fox, Jianmin Su, a research assistant professor, and Carl Levy, an undergraduate from Suffolk, Va., all with the Virginia Tech Carilion Research Institute; graduate student Justin Brooks and undergraduate Jessica Wang from Virginia Commonwealth University; and Tania Seabrook, a postdoctoral associate, and William Guido, a professor and the chair of the Department of Anatomical Sciences and Neurobiology, both with the University of Louisville School of Medicine.
Written by Ken Kingery
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.
NEW YORK (AP) — In her teenage dream? Mick Jagger says he never hit on Katy Perry when she was 18.
During an interview with an Australian radio show this week, the pop star said she sang backing vocals for Jagger's 2004 song "Old Habits Die Hard." Perry said she had dinner with the veteran rocker and that "he hit on me when I was 18."
In a statement Thursday, a representative for Jagger says he "categorically denies that he has ever made a pass at Katy Perry." The rep adds: "Perhaps she is confusing him with someone else."
Perry was one of the singers to make a guest appearance on the Rolling Stones' tour this year. The 29-year-old singer also said in the interview that the 70-year-old Jagger has been "very kind" to her.
WASHINGTON (AP) — Obama administration officials defended U.S. efforts in Syria Thursday against blistering criticism from Republicans who claim Washington has goals, but no strategy to find a solution that would end the bloody conflict affecting nations throughout the Mideast.
Robert Ford, U.S. ambassador to Syria, testifying to the Senate Foreign Relations Committee, said the United States is proud of the humanitarian and other assistance it has provided to the Syrian opposition trying to topple President Bashar Assad's government. He acknowledged that the Syrian people were "deeply disappointed" when the U.S. did not take military action against the Syrian regime, but said the administration is working furiously to arrange a conference in Geneva next month to set up a transitional government and end the bloodshed.
Ford had tense exchanges with two of the committee's harshest GOP critics.
"You continue to call this a civil war, Ambassador Ford," said Sen. John McCain, R-Arizona. "This isn't a civil war anymore; this is a regional conflict. It's spread to Iraq. We now have al-Qaida resurgence in Iraq. It's destabilizing Jordan. Iran is all in. Hezbollah has 5,000 troops there. For you to describe this as a quote, 'civil war,' of course, is a gross distortion of the facts, which again makes many of us question your fundamental strategy because you are — you don't describe the realities on the ground."
Ford said he does not think that Assad can win militarily and only has the advantage in a few places like around Aleppo in northern Syria. He said Assad has a disadvantage on the battleground in other places, including some in the east and south.
McCain was not satisfied, saying Assad's killing of civilians remained unchecked.
"Come on. ... The fact is that he was about to be toppled a year ago, or over a year ago. Then Hezbollah came in. Then the Russians stepped up their effort. Then the Iranian Revolutionary Guard intervened in what you call a, quote, 'civil war,' and he turned the tide. And he continues to maintain his position of power and slaughtering innocent Syrian civilians. And you are relying on a Geneva conference, right?"
The prospects for an international peace conference in Geneva to end the war are unclear.
Assad told the Arab League-U.N. envoy Wednesday that foreign support for the armed opposition must end if any political solution to the country's conflict is to succeed.
The United States, Russia and the United Nations have been trying for months to bring the Syrian government and the opposition together in Geneva to attempt to negotiate a political resolution to the conflict. After repeated delays, efforts renewed in earnest last month to organize the conference, but the Syrian opposition remains deeply divided over whether to attend, while the government refuses to sit down with the armed opposition.
Meanwhile, fighting continued to rage in Syria. And the Britain-based Syrian Observatory for Human Rights increased its estimate of the death toll of the war now in its third year. It said more than 120,000 people have been killed since the start of conflict, up from the previous estimate of 100,000. The new estimate said more than 61,000 of the dead were civilians.
"The problem itself is tragic ... and we want to help them," Ford said in one exchange with Sen. Bob Corker of Tennessee, the top Republican on the committee. "But ultimately, Senator, Syrians must fix this problem, and ultimately, Senator, it's going to require them to sit down at a table. The sooner they start, the better. But in the meantime, we will keep helping the opposition, Senator."
Corker, who has long been critical of the slow pace of aid to Syria, said he thinks the U.S. assistance to Syrian opposition has been an "embarrassment."
"I find it appalling that you would sit here and act as if we're doing the things we said we would do three months ago, six months ago, nine months ago," said Corker. "The London 11 (group of countries that support the opposition) has to look at us as one of the most feckless nations they've ever dealt with."
Sen. Ed Markey, D-Mass., cautioned that the U.S. should approach the situation in Syria "with a lot of humility, given what we've learned after we intervened in Iraq, in Libya, in Afghanistan; after what we've seen go on in Egypt."
"We should just have a little humility in the United States in terms of our ability to control events on the ground in these countries," he said.
Sen. Robert Menendez, D-N.J., the Foreign Relations panel's chairman, said in prepared remarks that progress toward destroying Syria's chemical weapons was "the only positive note" in the worsening crisis.
He referred to the announcement earlier Thursday by the Organization for the Prohibition of Chemical Weapons that Syria had completed the destruction of equipment used to produce chemical weapons, meeting another deadline in an ambitious timeline to eliminate the country's entire stockpile by mid-2014.
But Menendez lamented the worsening humanitarian crisis caused by the war, noting it has created more than 2 million refugees, and he said lack of progress on a negotiated political settlement portends continued bloodshed and suffering.
___
Associated Press Writer Deb Riechmann in Washington contributed to this report.
Associated PressSource: http://hosted2.ap.org/APDEFAULT/cae69a7523db45408eeb2b3a98c0c9c5/Article_2013-10-31-Congress-Syria/id-50d5f64823f3431d9230d306210769a7BRUNSWICK, Ga. (AP) — Spared from a possible death sentence by a deal among lawyers, A Georgia man convicted of beating his father and seven others to death inside the mobile home they shared was sentenced Thursday to life in prison without possibility of parole.
Guy Heinze Jr. was sentenced less than a week after a Glynn County jury found him guilty of malice murder for the Aug. 29, 2009, slayings. Prosecutors spared 26-year-old Heinze from a possible death sentence last week as part of a deal with defense attorneys that allowed them to avoid a hung jury.
Under Georgia law, Heinze faced an automatic life sentence once the death penalty was off the table. The only thing Superior Court Judge Stephen Scarlett had to decide was whether the defendant would ever be eligible for parole.
Heinze's attorneys have insisted he is innocent.
In a frantic 911 call made the morning the bodies were discovered, Heinze cried out: "My whole family is dead!"
Heinze's trial almost ended with a hung jury last week during the third day of deliberations. But prosecutors last Friday dropped the death penalty in a deal with Heinze's lawyers to allow the trial judge to dismiss one juror and replace him with an alternate. A guilty verdict was returned four hours later. Afterward, prosecutors said only that there had been "a situation" with the dismissed juror that contributed to the deadlock.
Prosecutors said Heinze had been smoking crack cocaine when he killed his father and the other victims, all members of an extended family. They said he killed the first victim in a dispute over a bottle of prescription painkillers he wanted to steal, then killed the others to avoid getting caught.
Each of the victims died from multiple crushing blows to the head from what police believe was a shotgun barrel, jurors heard. Autopsies showed they suffered a combined total of more than 220 wounds. The murder weapon was never found.
Although the attack happened in the middle of the night and most of the victims were found in bed, defense attorneys argued a single assailant couldn't possibly have inflicted such carnage. They insisted that Heinze would not kill loved ones over a bottle of weak prescription pills and that police ignored evidence and alternate suspects in a rush to accuse him.
Heinze had told police he found the victims' bodies after returning from a late night away from home.
The dead included Heinze's father, Guy Heinze Sr., 45. Rusty Toler Sr., 44, was slain along with his four children: Chrissy Toler, 22; Russell D. Toler Jr., 20; Michael Toler, 19; and Michelle Toler, 15. Also killed was the elder Toler's sister, Brenda Gail Falagan, 49, and Joseph L. West, the 30-year-old boyfriend of Chrissy Toler. Her 3-year-old son, Byron Jimerson Jr., ended up the sole survivor but suffered severe head injuries.
Heinze told police his father went to live with the elder Toler's family when they were both teenagers. The suspect said he considered Rusty Toler Sr. to be his uncle, and the man's children were his cousins.
Associated PressSource: http://hosted2.ap.org/APDEFAULT/386c25518f464186bf7a2ac026580ce7/Article_2013-10-31-Mobile%20Home%20Slayings/id-6c59fb2807e44cd69bf71f116f9fbefdBoston Red Sox's Mike Napoli hits an RBI single during the fourth inning of Game 6 of baseball's World Series against the St. Louis Cardinals Wednesday, Oct. 30, 2013, in Boston. (AP Photo/David J. Phillip)
Boston Red Sox's Mike Napoli hits an RBI single during the fourth inning of Game 6 of baseball's World Series against the St. Louis Cardinals Wednesday, Oct. 30, 2013, in Boston. (AP Photo/David J. Phillip)
Boston Red Sox catcher Jarrod Saltalamacchia watches as home plate umpire Dana DeMuth calls St. Louis Cardinals' Allen Craig safe on an obstruction during the ninth inning of Game 3 of baseball's World Series Saturday, Oct. 26, 2013, in St. Louis. The Cardinals won 5-4 to take a 2-1 lead in the series. (AP Photo/David J. Phillip)
Boston Red Sox starting pitcher Jon Lester gets the ball back as St. Louis Cardinals left fielder Matt Holliday runs the bases after hitting a home run during the fourth inning of Game 5 of baseball's World Series Monday, Oct. 28, 2013, in St. Louis. (AP Photo/Matt Slocum)
Boston Red Sox's Jacoby Ellsbury gets past St. Louis Cardinals relief pitcher Kevin Siegrist as he makes it safely back to first on a rundown during the fifth inning of Game 6 of baseball's World Series Wednesday, Oct. 30, 2013, in Boston. (AP Photo/David J. Phillip)
BOSTON (AP) — The Boston Red Sox built a World Series champion in 2013 by avoiding the expensive free agents they've made mistakes on in the past.
They'll have to do it again this winter.
Center fielder Jacoby Ellsbury is a free agent, as are first baseman Mike Napoli, shortstop Stephen Drew and catcher Jarrod Saltalamacchia. The team will almost certainly prevent pitcher Jon Lester from becoming a free agent by picking up his $13 million option.
Expect the team to avoid trying to make a big splash on players like they did when they overpaid for Adrian Gonzalez and Carl Crawford. Instead, general manager Ben Cherington will follow up on a strategy that brought in Shane Victorino, Jonny Gomes and Koji Uehara — all key parts of this year's title.
Associated PressSource: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2013-10-31-BBA-Red-Sox-Future/id-2f9593f6cb6741498366415174cea632Intel has been talking about 4G LTE in mobile devices for a while, but now the chipmaker is walking the walk with its first multi-mode 4G LTE modem.
Asian and European versions of Samsung’s Galaxy Tab 3 will be the first to feature Intel’s new ZMM 7160 processor.
The ZMM 7160 model will allow phones and tablets—presumably those with Intel chips inside—to connect to 4G LTE networks in North America, Asia, and Europe. The chip will first appear in the Asia and Europe versions of Samsung’s Galaxy Tab 3, and Intel says it’s now commercially available to other vendors as well.
This isn’t Intel’s first 4G LTE modem, but a previous single-mode chip was unable to fall back on older 3G and 2G networks. The ZMM 7160 can connect to both GSM and HSPA networks, so it’s a much better fit for wireless carrier support.
Still, Intel has one disadvantage over ARM-based rival Qualcomm: The modem itself is a discrete chip, not integrated with Intel’s application processors. Integrated modems allow for longer battery life, so perhaps no surprise that the first product to feature the ZMM 7160 is a tablet, which should be better than a smartphone at absorbing any hits to battery life.
So far, Intel hasn’t made any commitments on integrating the modem with its application processors. “We will do it when the time is right,” Herman Eul, general manager for Intel’s Mobile and Communications Group, said during an August preview of multimode LTE chips.
For now, having 4G LTE and older network support all rolled into a single modem could clear the way for more Bay Trail-powered Windows tablets with mobile broadband support. As for laptops, Intel is introducing a PCIe module with support for 4G and older networks. Intel says we’ll see connected Ultrabooks as well as laptops with this module next year.
Hot daddy-to-be! Jamie Dornan stepped out for the first time with his pregnant wife Amelia Warner since being cast in Fifty Shades of Grey on Saturday, Oct. 26. Dornan -- set to star as Christian Grey in the E.L. James' film adaption -- went for a quiet walk with Warner in London.
Strolling arm and arm, the couple dressed casual during their outing. Dornan, 31, dressed in jeans, a pink t-shirt and a blue peacoat, as British actress and singer-songwriter Warner went without makeup in a loose-fitted top, leggings and a navy cardigan. The pair also held on to individual hot beverage cups.
Dornan and the brunette beauty, also 31, married in April 2013, and confirmed in June that they are expecting their first child together.
Earlier this week, the Irish actor and model officially accepted the role of Grey, replacing Sons of Anarchy's Charlie Hunnam. He's yet to comment on the new S&M role, but James couldn't help but chime in. "Stow your twitchy palms ladies...our man is here. Welcome to #TeamFifty @JamieDornan1 x," the author wrote via Twitter on Oct. 24.
PHOTOS: Remember these breakout stars?
Dornan will be playing opposite Dakota Johnson, as she takes on the role of Anastasia Steele. "Jamie has a really good reputation as someone easy to work with, easy going and is seen as someone who will very appreciative of this role," an insider revealed to Us Weekly on why he ultimately won the role. "It's his charm and personality that is winning people over."
See ya, Snooks. In yet another upset, Nicole "Snooki" Polizzi was sent home -- per viewer's votes, or lack thereof -- on the Monday, Oct. 28 episode of Dancing with the Stars. The Jersey Shore standout, 25, had consistently earned high scores during her time on the ABC dance competition, so when she learned her fate -- lowest-scoring couple Bill Engvall and Emma Slater made it through -- Polizzi was visibly distraught.
PHOTOS: Snooki's body evolution
"I can't even talk right now," the engaged mom to Lorenzo, 14 months, said on camera, looking tearful. "I love everybody here, so it sucks."
During the post-show interviews, the reformed party girl vainly choked back tears as she chatted with reporters. "I definitely didn't think I was going to to go home yet and I'm not ready to go home. This experience has been amazing. Sasha's amazing," she began before bursting into tears.
"I don't want to go," she said. What she'll miss most? "I just love everybody on the show!" she added, admitted she never thought she'd fall in love so deeply with dancing. "I'm a lot stronger than I thought I was," she concluded.
Standouts of the evening including Amber Riley and Derek Hough, who danced through a back injury to score 29 points for a Paso Doble plus Jack Osbourne and Cheryl Burke, who nabbed their first 10 of the season, garnering a 27 for their jive.
Tell Us: Did Snooki really deserve to go home?
The story of the iPad, continuing with the iPad 2, which introduced not only a sleeker design, but a more focused purpose
On March 2, 2011, Steve Jobs returned to the keynote stage after a long period of medical leave. It was the second-to-last keynote he'd ever conduct, and he received a long, loud standing evasion. He and Apple had been working on something for a long time, and he didn't want to miss it. The original iPad was supposed to have been magical, but no one, not even Apple, had known exactly how it would weave its spell. A year later and they had a much, much better idea. Where previously they'd known they'd had something, now they were beginning to understand just exactly what they had. It was thinner. It was lighter. It was faster. It was more smartly covered. And it could hold an entire band in its garage. It was the iPad 2.
“With more than 15 million iPads sold, iPad has defined an entirely new category of mobile devices,” said Steve Jobs, Apple’s CEO. “While others have been scrambling to copy the first generation iPad, we’re launching iPad 2, which moves the bar far ahead of the competition and will likely cause them to go back to the drawing boards yet again.”
During the iPad 2 event, Steve Jobs said people had made fun of Apple for using the word "magical" to describe their tablet, but that it had turned out to be just that. He proclaimed 2010 as the year of the iPad. He teased 2011 as the year of the copycats before announcing what he thought it really was: the year of the iPad 2.
The iPad 2, code named K94 and model number iPad 2,1, has the same 9.7-inch, 1024x768, 132ppi screen as the original, and came in the same Wi-Fi and Wi-Fi + 3G HSPA/EVDO Rev. A - hello Verizon! - models. It was considerably faster, however, sporting a new Apple A5 chipset with dual-core 1GHz ARM Cortex A9 processors, dual-core PowerVR SGX543MP2 graphics processors, and double the RAM at 512MB. It was up to twice as fast for CPU, and up to 9 times as fast for GPU tasks.
16, 32, and 64GB of NAND Flash storage remained the same as well, as did the 25 watt-hour battery. Bluetooth stayed at 2.1 + EDR, by a gyroscope joined the sensor array.
Thinner and lighter was taken care of by an all-new design that reduced it from 0.53- to 0.34-inches - making it 33% thinner - and from 1.5 to 1.33lbs. Jobs made sure to mention several times on stage that the numbers were deceptive and at those tiny sizes and weights, small reductions made for big differences in how it felt. It wasn't a breakthrough, certainly nothing that changed it from a 2-handed to a 1-handed device, or made it easier to use for long periods of time without resting it on a surface, but it was a significant improvement.
The iPad 2 also added cameras. Two of them. a rear-facing 1.3 megapixel/720p camera (what Apple now markets as iSight), and a front-facing 0.3 megapixel/VGA camera (FaceTime). They were... terrible. But they were cameras. It also added a second color. In addition to black and aluminum, you could get the iPad 2 with an iPhone 4-style white front plate instead.
Prices stayed exactly the same, starting at $499.
There were, however, some new accessories. First was a $29 HDMI to 30-pin Dock connector dongle allowed for mirroring the display to an HDTV. Second, was the Smart Cover. It could fold into a typing or viewing stand, and thanks to magnets embedded into the cover and the iPad 2, it stuck on and aligned automatically, and it could wake the iPad when it opened and sleep it again when it closed. They came in polyurethane for $39 and leather for $69, and in a variety of colors.
It shipped with iOS 4.3, which added a few new features in addition to what iOS 4 had brought to the iPhone. They included the Nitro JavaScript engine for Safari, Home Sharing for iTunes streaming from OS X to iOS, improvements to AirPlay, and a return of the hardware orientation lock as a hardware switch option. It also added FaceTime for video calls, and an iOS version of Photo Booth to the built-in apps.
Also debuting at the same event as the iPad 2, adding to the 65,000 tablet-optimized apps that were already in the App Store - were two new Apple apps, mobile versions of Apple's iLife mainstays, iMovie and GarageBand. They were, to put it mildly, a revelation. Randy Ubillos showed off iMovie, with an old time movie theater main screen, and what would become Apple's new, signature, editing interface. It was precise, it was multitrack. It was amazing. GarageBand was perhaps even more impressive. You could plug in and use real instruments, but it also supported touch instruments right on the iPad. Xander Soren handled that demo, and immediately set a new standard for mobile apps. They showed, arguably for the first time, what the iPad really meant for the future of personal computing. It mean very personal computing. or as Apple had come to call it, post-PC.
Jobs ended the event by focusing on that, and repeating his belief that "technology alone was not enough", while standing at the crossroads of technology and liberal arts.
The iPad 2 launched on March 11 in the U.S., and 25 additional countries on March 25. Apple:
While competitors are still struggling to catch up with our first iPad, we’ve changed the game again with iPad 2,” said Steve Jobs, Apple’s CEO. “We’re experiencing amazing demand for iPad 2 in the US, and customers around the world have told us they can't wait to get their hands on it. We appreciate everyone’s patience and we are working hard to build enough iPads for everyone.
Reviewers like the new . Ed Baig, USA Today:
The headline additions to iPad 2 are front- and rear-facing cameras, the absence of which was my biggest disappointment with version one. Now you can plunge into FaceTime, Apple's nifty video chat program previously available only on the iPhone 4, iPod Touch and some Macintosh computers. With a brand new Apple A5 dual-core processor, the iPad 2 is snappier, too, though it's not as if the first-generation model was a laggard. Apple claims the graphics in the new machine have nine times the horsepower of the original. That's difficult to measure, but Epic Citadel, a stunning, graphics-rich game, played smoothly in my tests.
Jason Snell of Macworld:
For Apple’s competitors in the tablet-device market, the iPad 2 is a bucket of water to the face. After more than a year of struggling to catch up to the original iPad, here’s a new model that addresses many of the iPad’s deficiencies, dramatically improves its speed, and doesn’t cede any ground on price, features, or battery life. The iPad 2 raises the bar Apple set a year ago—and it’s time for the rest of the industry to scramble again to catch up.
For everyone else, the iPad 2 is a triumph, an iPad that’s even more iPad than the original. And the original one was really good. The first iPad was a bolt from the blue, a device that defined an entire category, and a tough act to follow. The iPad 2 follows it with aplomb.
Yours truly, for iMore:
I used my original iPad a lot... until iPhone 4 was released. I still kept most of my apps and games on iPad but because iPhone 4 was so much faster I just picked it up far more often. iPad 2 has changed that paradigm again. The combination of the big screen and Apple A5 processor has made it my go-to device once more (when I'm not in feet-down mobile, of course.) It's by no means perfect, and we've listed many of the most glaring and frustrating imperfections above, but iPad 2 looks better, it feels better, and it just works better.
Cliched as it sounds, the iPad 2 was the first complete iPad, and the template from which all others have followed.
The iPad's competitors remained confused. They saw the tablet post-iPad the way they'd seen it pre-iPad - as simply another form factor for the traditional PC. Like a laptop or netbook was simply a smaller PC, so too they felt the tablet was simply a smaller laptop or netbook. It was evident in their marketing. "Amateur hour is over." "Tell your wife it has a dual-core processor."
Competitors told people they could have a more traditional PC experience than the iPad. They could have multiple windows and desktops. They could have Flash. They could have everything the vast majority of them never, not ever wanted.
Despite Apple having spent over a year teaching the world just exactly how to sell hundreds of thousands of tablets, no one else seemed able to leave the PC behind. Yet that's exactly what mainstream customers wanted. The PC alienated them. It was intimidating and inaccessible, and more of the same was the so much less appealing, they stayed away in droves. They brought specs to an experience fight, and their primary use case ended up being preventing warehouse shelves from floating up off the floor.
To this day, it's a lessen very few outside Apple have learned, and one Apple themselves don't always remember - The tablet wasn't meant to replace the PC for mainstream users. It was meant to succeed it.
Apple sold 15 million iPads in 2010, more than all Tablet PCs sold in history before that. They sold 15.4 million iPad 2 tablets in Q4 2011 alone. Almost 30 million from March to December. From 65,000 tablet-optimized apps, they reached 200,000. Year of the iPad 2 indeed...
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