New York Giants' Peyton Hillis (44) rushes during the second half of an NFL football game against the Minnesota Vikings Monday, Oct. 21, 2013 in East Rutherford, N.J. (AP Photo/Peter Morgan)
New York Giants' Peyton Hillis (44) rushes during the second half of an NFL football game against the Minnesota Vikings Monday, Oct. 21, 2013 in East Rutherford, N.J. (AP Photo/Peter Morgan)
Minnesota Vikings running back Adrian Peterson (28) breaks a tackle by New York Giants' Jon Beason (52) as Jerome Felton (42) trails the play during the second half of an NFL football game Monday, Oct. 21, 2013 in East Rutherford, N.J. (AP Photo/Bill Kostroun)
Minnesota Vikings running back Adrian Peterson (28) stiff-arms New York Giants' Jon Beason (52) during the second half of an NFL football game Monday, Oct. 21, 2013 in East Rutherford, N.J. (AP Photo/Bill Kostroun)
New York Giants kicker Josh Brown (3) kicks a field goal during the second half of an NFL football game against the Minnesota Vikings Monday, Oct. 21, 2013 in East Rutherford, N.J. (AP Photo/Bill Kostroun)
EAST RUTHERFORD, N.J. (AP) — The New York Giants got their first win of the season Monday night by holding Adrian Peterson in check and converting Minnesota mistakes into a 23-7 victory.
The Giants began the season with six losses in which they were the team turning over the ball and showing little penchant for playing defense. But against the Vikings (1-5), they were efficient enough, if not overwhelming, and had three takeaways.
Peterson, the league's MVP last season, was held to 28 yards rushing five days after his 2-year-old son was buried in South Dakota. The man accused in the death was indicted on second-degree murder and manslaughter charges Monday.
Peterson was not aided by a rusty Josh Freeman, making his debut as Vikings quarterback.
Josh Brown kicked three field goals, Rueben Randle caught a 24-yard TD pass and Peyton Hills ran for a TD for New York (1-6).
Detroit Tigers skipper Jim Leyland told reporters: "I'm going to be 69 years old [on Dec. 15]. I'm not ashamed of that. I'm proud of it. The fuel's getting a little low."
The news comes two days after the Tigers were eliminated by the Boston Red Sox in Game 6 of the American League championship series.
Leyland, who said he'll stay with the Tigers in a job yet to be determined, steps down after eight seasons leading Detroit. Over his career, as NPR's Mike Pesca tells our Newscast Desk, Leyland "won three manager of the year awards, three pennants, more than 1,700 games and a World Series [when he managed the Florida Marlins in 1997]."
The World Series, between the Red Sox and National League champion St. Louis Cardinals, starts Wednesday night in Boston. Over the weekend, Eyder posted on "5 Things To Know About The World Series."
NPR's Mike Pesca on Jim Leyland's decision to step down
WASHINGTON (AP) — President Barack Obama called French President Francois Hollande on Monday to discuss France's anger over reported aggressive surveillance tactics by the National Security Agency.
The call came after a French newspaper said the NSA swept up 70.3 million French phone records in a 30-day period. France summoned the U.S. ambassador to explain and called the practice "totally unacceptable."
The White House says some recent disclosures about the NSA have been distorted but that some raise legitimate questions for U.S. allies about how America's intelligence capabilities are used.
Obama told the French president that the U.S. was reviewing its intelligence-gathering to ensure a balance between security and privacy.
The French president's office said in a statement that Hollande told Obama he strongly condemned the practices and found them unacceptable between allies. Hollande also asked Obama to specify all the information that former NSA systems analyst Edward Snowden may possess. Documents leaked by Snowden have been behind a series of revelations about NSA surveillance programs.
The White House said both presidents agreed they should continue diplomatic discussions about the issue.
A Norfolk Southern Railroad train pulls transport cars full of coal near Goodfield, Ill., on Oct. 9, 2012. The United States cut its energy-related carbon dioxide pollution by 3.8 percent in 2012, the second biggest drop since 1990, the Department of Energy said Monday, Oct. 21, 2013. Energy Department economist Perry Lindstrom said carbon pollution reduction is due to warm winter weather, more efficient cars because of new mileage requirements and an ongoing shift from coal-power to natural gas to produce electricity. (AP Photo/Seth Perlman)
A Norfolk Southern Railroad train pulls transport cars full of coal near Goodfield, Ill., on Oct. 9, 2012. The United States cut its energy-related carbon dioxide pollution by 3.8 percent in 2012, the second biggest drop since 1990, the Department of Energy said Monday, Oct. 21, 2013. Energy Department economist Perry Lindstrom said carbon pollution reduction is due to warm winter weather, more efficient cars because of new mileage requirements and an ongoing shift from coal-power to natural gas to produce electricity. (AP Photo/Seth Perlman)
WASHINGTON (AP) — The United States cut its energy-related carbon dioxide pollution by 3.8 percent last year, the second biggest drop since 1990, the Department of Energy said Monday.
The only recent year with a bigger percentage drop was in 2009, when America was in a large recession. American cars and factories spewed 5.83 billion tons of carbon dioxide in 2012, down from 6.06 billion in 2011. It is the lowest level for U.S. emissions since 1994. Carbon dioxide is the chief man-made global warming gas.
Energy Department economist Perry Lindstrom said carbon pollution reduction is due to warm winter weather, more efficient cars because of new mileage requirements and an ongoing shift from coal-power to natural gas to produce electricity.
The coal shift is a big factor as is a sluggish economic recovery, said Jay Apt, director of the Carnegie Mellon Electricity Industry Center. He said in 1994 coal provided 52 percent of the U.S. power and now it is down to 37 percent. Burning coal produces far more carbon dioxide than burning natural gas.
Some past cuts in carbon pollution were mostly due to economic factors, such as the 7.1 percent drop in 2009, Lindstrom said. But this drop happened while the U.S. economy was growing 2.8 percent, as reflected by the gross domestic product, and its energy use was dropping by more than 2 percent.
Economists measure energy efficiency and how real reductions are in carbon pollution, by calculating carbon dioxide emissions per unit of GDP. And from 2011 to 2012, the United States carbon pollution per GDP dropped by a record 6.5 percent, Lindstrom said.
That shows this drop was clearly not due to a recession, Lindstrom said.
In 2012, America spewed more than 368,000 pounds of carbon dioxide per second.
"This latest drop in energy-related carbon emissions is reason for cautious optimism that we're already starting to move in the right direction," said Pennsylvania State University climate scientist Michael Mann. "But this alone will not lead us toward the dramatic carbon reductions necessary to avoid dangerous climate change."
The world is heading in the opposite direction. In 2011, the world carbon dioxide emissions jumped 3 percent, because of a large increase by China, the No. 1 carbon polluting country. The U.S. is No. 2 in carbon emissions.
___
Online:
The Department of Energy: http://www.eia.gov/environment/emissions/carbon/
___
Seth Borenstein can be followed at http://twitter.com/borenbears
Controlling the triggers of age-related inflammation could extend 'healthspan'
PUBLIC RELEASE DATE:
21-Oct-2013
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Contact: Karen Peart karen.peart@yale.edu 203-432-1326 Yale University
Inflammation is the common denominator of many chronic age-related diseases such as arthritis, gout, Alzheimer's, and diabetes. But according to a Yale School of Medicine study, even in the absence of a disease, inflammation can lead to serious loss of function throughout the body, reducing healthspan that portion of our lives spent relatively free of serious illness and disability.
Published as the cover article in the October issue of Cell Metabolism, the study found that immune sensor Nlrp3 inflammasome is a common trigger of this inflammation-driven loss of function that manifests itself in insulin-resistance, bone loss, frailty, and cognitive decline in aging.
As the elderly population increases, clinicians are seeing a spike in age-related diseases, but scientists did not fully understand the role of inflammation. What is commonly known is that as we age, our cells change, leading the immune system to produce chronic, low-level inflammation throughout the body. Aging is also a major risk factor for multiple chronic diseases, but according to the researchers, biomedical enterprise spends billions of dollars to tackle each age-dependent disease separately.
"This is the first study to show that inflammation is causally linked to functional decline in aging," said lead author Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine. "There are multiple cellular triggers of inflammation throughout the body, but we've pinpointed Nlrp3 as the specific sensor that activates inflammation with age."
"If aging is indeed a common factor for multiple diseases, the unanswered question is, can we identify the triggers of aging that cause low-level inflammation so that 'switching off' the trigger can slow the onset of multiple chronic diseases that are age-dependent at their onset," Dixit added. "Since aging affects us all, if this goal can be achieved, it is likely to significantly improve the healthspan and may also lower healthcare costs as the aging population increases in the U.S."
Dixit and his colleagues investigated the normal aging process of mice that were free of diseases, and fed a normal diet. The research team found that immune sensor Nlrp3 inflammasome is activated in response to aging. They then tested mice to determine if reducing the activity of Nlrp3 inflammasome lowers inflammation, and aging-associated decline in function. Results showed that animals with lower Nlrp3 activation were protected from many age-related disorders such as dementia, bone loss, glucose intolerance, cataracts, and thymus degeneration. Functionally, the mice also performed better, were less frail, and ran for longer durations. The researchers also tested another immune sensor called caspase11, which is activated in response to certain infections, and found that it was not linked to the age-related inflammation process.
"Now that we've identified this mechanism in the Nlrp3 sensor, we might be able to manipulate this immune sensor to delay, or reduce inflammation," Dixit said. "This could lead to the possibility of prolonging healthspan, potentially leading to an old age relatively free of disease or disability."
Dixit said additional studies are needed to explore whether the Nlrp3 mechanism can be safely manipulated without impairing the immune system. He points out that although there are several anti-inflammatory drugs available, none seem to be effective in expanding the healthspan. "One of our long-term goals is to develop therapies or specific diets that could dampen the excessive inflammation process as a means to prevent chronic diseases," he said.
###
Other authors on the study include Yun-Hee Youm, Ryan W. Grant, Laura R. McCabe, Diana C. Albarado, Kim Yen Nguyen, Anthony Ravussin, Paul Pistell, Susan Newman, Renee Carter, Amanda Lague, Heike Munzberg, Clifford J. Rosen, Donald K. Ingram, and J. Michael Salbaum.
The study was supported by the National Institutes of Health (AG043608, AI105097, and DK090556, P20RR02195, HD055528); The Genomics and Core CBB Core facilities supported by Pennington Center of Biomedical Research Excellence (NIH 8P20 GM 103528) and Nutrition and Obesity Research Center (NIH P30DK072476).
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.
Controlling the triggers of age-related inflammation could extend 'healthspan'
PUBLIC RELEASE DATE:
21-Oct-2013
[
| E-mail
]
Share
Contact: Karen Peart karen.peart@yale.edu 203-432-1326 Yale University
Inflammation is the common denominator of many chronic age-related diseases such as arthritis, gout, Alzheimer's, and diabetes. But according to a Yale School of Medicine study, even in the absence of a disease, inflammation can lead to serious loss of function throughout the body, reducing healthspan that portion of our lives spent relatively free of serious illness and disability.
Published as the cover article in the October issue of Cell Metabolism, the study found that immune sensor Nlrp3 inflammasome is a common trigger of this inflammation-driven loss of function that manifests itself in insulin-resistance, bone loss, frailty, and cognitive decline in aging.
As the elderly population increases, clinicians are seeing a spike in age-related diseases, but scientists did not fully understand the role of inflammation. What is commonly known is that as we age, our cells change, leading the immune system to produce chronic, low-level inflammation throughout the body. Aging is also a major risk factor for multiple chronic diseases, but according to the researchers, biomedical enterprise spends billions of dollars to tackle each age-dependent disease separately.
"This is the first study to show that inflammation is causally linked to functional decline in aging," said lead author Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine. "There are multiple cellular triggers of inflammation throughout the body, but we've pinpointed Nlrp3 as the specific sensor that activates inflammation with age."
"If aging is indeed a common factor for multiple diseases, the unanswered question is, can we identify the triggers of aging that cause low-level inflammation so that 'switching off' the trigger can slow the onset of multiple chronic diseases that are age-dependent at their onset," Dixit added. "Since aging affects us all, if this goal can be achieved, it is likely to significantly improve the healthspan and may also lower healthcare costs as the aging population increases in the U.S."
Dixit and his colleagues investigated the normal aging process of mice that were free of diseases, and fed a normal diet. The research team found that immune sensor Nlrp3 inflammasome is activated in response to aging. They then tested mice to determine if reducing the activity of Nlrp3 inflammasome lowers inflammation, and aging-associated decline in function. Results showed that animals with lower Nlrp3 activation were protected from many age-related disorders such as dementia, bone loss, glucose intolerance, cataracts, and thymus degeneration. Functionally, the mice also performed better, were less frail, and ran for longer durations. The researchers also tested another immune sensor called caspase11, which is activated in response to certain infections, and found that it was not linked to the age-related inflammation process.
"Now that we've identified this mechanism in the Nlrp3 sensor, we might be able to manipulate this immune sensor to delay, or reduce inflammation," Dixit said. "This could lead to the possibility of prolonging healthspan, potentially leading to an old age relatively free of disease or disability."
Dixit said additional studies are needed to explore whether the Nlrp3 mechanism can be safely manipulated without impairing the immune system. He points out that although there are several anti-inflammatory drugs available, none seem to be effective in expanding the healthspan. "One of our long-term goals is to develop therapies or specific diets that could dampen the excessive inflammation process as a means to prevent chronic diseases," he said.
###
Other authors on the study include Yun-Hee Youm, Ryan W. Grant, Laura R. McCabe, Diana C. Albarado, Kim Yen Nguyen, Anthony Ravussin, Paul Pistell, Susan Newman, Renee Carter, Amanda Lague, Heike Munzberg, Clifford J. Rosen, Donald K. Ingram, and J. Michael Salbaum.
The study was supported by the National Institutes of Health (AG043608, AI105097, and DK090556, P20RR02195, HD055528); The Genomics and Core CBB Core facilities supported by Pennington Center of Biomedical Research Excellence (NIH 8P20 GM 103528) and Nutrition and Obesity Research Center (NIH P30DK072476).
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.
Almost all patients suffering from head and neck squamous cell carcinoma (HNSCC) develop canker sores, a complication resulting from different modalities of treatment, namely stem cell transplantation, chemotherapy, and radiotherapy. Canker sore is divided in five grades (zero to four) by the World Health Organization (WHO), with severe cases (grades 3 and 4) being associated with pain, weight loss, poor quality of life, and higher hospital costs due to increased healthcare needs. Severe canker sore can also lead to treatment interruption, which may decrease the patient's chances of surviving the cancer.
No effective preventative strategy is currently available for canker sore, but prospective trials of low-level laser therapy (LLLT) done in HNSCC patients undergoing chemoradiotherapy showed promising results. However, additional trials detected a high incidence of canker sore among patients, leaving the question of whether LLLT can effectively prevent canker sore still open.
Now, a group of scientists led by Dr. Heliton Spindola Antunes at the National Cancer Institute (INCA) in Rio de Janeiro, Brazil, has successfully performed a definitive trial showing that LLLT reduces the occurrence of canker sore in HNSCC patients undergoing concurrent chemoradiotherapy and improves patient's quality of life.
The trial was performed with 94 HNSCC patients undergoing chemoradiotherapy. They were divided into two groups of 47 individuals, one of which received LLLT while the other received placebo. Researchers observed a significant difference in the incidence of canker sore grades 3 and 4 between groups. For instance, while in the group of patients receiving LLLT only three patients developed severe cases of canker sore, in the group receiving the placebo this number was 19. There were also significant differences in the absence of canker sore (grades 0-1), with the LLLT group having 59.6% of patients free of canker sore as opposed to 21.3% in the placebo group. The LLLT group had less severe oral pain and, as a result, used fewer opioid analgesics. They were also less likely to require gastrostomy (a surgical opening into the stomach for nutritional support) throughout the cancer treatment.
"For ethical reasons," says Dr Antunes, "all patients who developed canker sore grades 3 or 4 in the placebo arm were then offered the option of receiving LLLT. They all improved to grade 2 or lower, supporting the evidence that LLLT is an effective choice to prevent or treat canker sore in these patients."
###
The article entitled "Phase III trial of low-level laser therapy to prevent oral mucositis in head and neck patients treated with concurrent chemoradiation" has been published ahead of print in Radiotherapy & Oncology and is available at http://dx.doi.org/10.1016/j.radonc.2013.08.010
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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.
Almost all patients suffering from head and neck squamous cell carcinoma (HNSCC) develop canker sores, a complication resulting from different modalities of treatment, namely stem cell transplantation, chemotherapy, and radiotherapy. Canker sore is divided in five grades (zero to four) by the World Health Organization (WHO), with severe cases (grades 3 and 4) being associated with pain, weight loss, poor quality of life, and higher hospital costs due to increased healthcare needs. Severe canker sore can also lead to treatment interruption, which may decrease the patient's chances of surviving the cancer.
No effective preventative strategy is currently available for canker sore, but prospective trials of low-level laser therapy (LLLT) done in HNSCC patients undergoing chemoradiotherapy showed promising results. However, additional trials detected a high incidence of canker sore among patients, leaving the question of whether LLLT can effectively prevent canker sore still open.
Now, a group of scientists led by Dr. Heliton Spindola Antunes at the National Cancer Institute (INCA) in Rio de Janeiro, Brazil, has successfully performed a definitive trial showing that LLLT reduces the occurrence of canker sore in HNSCC patients undergoing concurrent chemoradiotherapy and improves patient's quality of life.
The trial was performed with 94 HNSCC patients undergoing chemoradiotherapy. They were divided into two groups of 47 individuals, one of which received LLLT while the other received placebo. Researchers observed a significant difference in the incidence of canker sore grades 3 and 4 between groups. For instance, while in the group of patients receiving LLLT only three patients developed severe cases of canker sore, in the group receiving the placebo this number was 19. There were also significant differences in the absence of canker sore (grades 0-1), with the LLLT group having 59.6% of patients free of canker sore as opposed to 21.3% in the placebo group. The LLLT group had less severe oral pain and, as a result, used fewer opioid analgesics. They were also less likely to require gastrostomy (a surgical opening into the stomach for nutritional support) throughout the cancer treatment.
"For ethical reasons," says Dr Antunes, "all patients who developed canker sore grades 3 or 4 in the placebo arm were then offered the option of receiving LLLT. They all improved to grade 2 or lower, supporting the evidence that LLLT is an effective choice to prevent or treat canker sore in these patients."
###
The article entitled "Phase III trial of low-level laser therapy to prevent oral mucositis in head and neck patients treated with concurrent chemoradiation" has been published ahead of print in Radiotherapy & Oncology and is available at http://dx.doi.org/10.1016/j.radonc.2013.08.010
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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.
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