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The two-time Oscar winner has signed on to play Nancy Reagan in The Butler, The Hollywood Reporter has confirmed. The film, directed by Lee Daniels, is a biopic of Eugene Allen, a butler who served in the White House from 1952 to 1986.
Another Oscar winner, Forest Whitaker, is reportedly close to a deal to play Allen in the film.
That Fonda would play the wife of the most famous conservative president raises eyebrows due to her well-documented anti-war and civil rights? activism in the 1960s and '70s. She protested and worked closely with Vietnam Veterans Against the War and traveled to North Vietnam, drawing the ire of some in the military and becoming an icon for liberal Hollywood activism. She has continued to be outspoken, recently saying that the Republicans running for president "scare her."
VIDEO: THR's 2011 Women in Entertainment Breakfast Highlights
hThe film is based on a Washington Post article about Allen written by Wil Haygood. Daniels recently completed work on The Paperboy, starring Zac Efron, Nicole Kidman and John Cusack, which is due out this year.
Fonda most recently starred in 2011's Peace, Love & Misunderstanding, and before that, in 2007's Georgia Rule with Lindsay Lohan. She'll also appear in Aaron Sorkin's upcoming HBO show, The Newsroom, playing the CEO of the cable company that owns the news channel where the show is set.
For the record: A previous version of this post misidentified Fonda's co-star of Georgia Rule as Miley Cyrus.
As much as I love Samsung hardware, I've felt for a long while now that the Galaxy Note was a bit of a mistake. The screen size is just too big for me to wield the device comfortably, and I see no real value in the S-Pen other than having a little fun during bored moments. But a good chunk of people out there in the world apparently disagree with me, as Samsung has just announced that the South Korea-based company has shipped 5 million units of the Galaxy Note phablet. At the start of this month, Samsung had sold 2 million Galaxy Notes globally — a solid stat albeit not equal to Galaxy S II or iPhone 4S sales.
Singer Robin Gibb, who spoke last month of making a "spectacular" recovery from cancer, has had further surgery, according to a statement released to the British media on Wednesday.
The 62-year-old, a founding member of the disco-era hit machine the Bee Gees, has been forced to cancel several commitments due to the operation.
"On Sunday 25 March, Robin Gibb underwent further intestinal surgery," the statement read.
"He is currently recovering in hospital and therefore, for the time-being, all existing commitments prior to the Titanic Requiem concert, have had to be cancelled."
His spokesman was not immediately available for comment.
"The Titanic Requiem" is Gibb's first classical work written with his son Robin-John, and is being released to mark the 100th anniversary of the sinking of the luxury liner on April 15, 1912.
The world premiere of the work is due to take place at Central Hall, Westminster in London on April 10.
Media speculation about Gibb's health was sparked in recent months by his gaunt and frail appearance, but the singer said in February that a growth in his colon had "almost gone" and he was feeling "fantastic."
Findings may lead to new strategies to address insulin resistance
Scientists at the Gladstone Institutes have discovered a key protein that regulates insulin resistancethe diminished ability of cells to respond to the action of insulin and which sets the stage for the development of the most common form of diabetes. This breakthrough points to a new way to potentially treat or forestall type 2 diabetes, a rapidly growing global health problem.
In a paper being published online this week in the Proceedings of the National Academy of Sciences, researchers in the laboratory of Gladstone Investigator Katerina Akassoglou, PhD, describe an unexpected role of the p75 neurotrophin receptor in controlling how the body processes sugar. Called p75NTR, this receptor protein is usually associated with functions in neurons.
"We identified that p75NTR is a unique player in glucose metabolism," said Dr. Akassoglou, who is also an associate professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. "Therapies targeted at p75NTR may represent a new therapeutic approach for diabetes."
The pancreas makes a hormone called insulin that processes glucose, moving it from the bloodstream into the body's cells where it is used for energy. Insulin resistance is a key feature of Type 2 diabetes, in which glucose builds up in the bloodstream and the body's cells are unable to function properly. According to the Centers for Disease Control and Prevention, more than 20 million Americans have type 2 diabetes.
"Type 2 diabetes has become a very serious health problem and it is increasing at an alarming rate," said Lennart Mucke, MD, who directs the institute in which the research was conducted. "These findings provide an important new avenue for developing better therapies to combat this deadly diseasethe seventh leading cause of death in the United States."
Complex signaling interactions between several different types of tissueincluding fat, liver, muscle and brainregulate glucose metabolism. Because p75NTR is found in fat and muscle tissue and participates in many important functions in the cell, Gladstone scientists hypothesized that p75NTR might also help to regulate glucose metabolism.
To study this, the researchers used mice that lacked the genes for p75NTR. They compared these mice to normal mice and discovered that those lacking p75NTR were more responsive to insulin when fed a normal diet. Second, they used some molecular biology tricks to block the action of the p75NTR protein in fat cells. This also resulted in increased glucose absorption in response to insulin. In contrast, when they caused the fat cells to make more p75NTR, glucose absorption was reduced. Additionally, the researchers found that another important regulatory molecule, Rab5, played a key role in p75NTR's impact on metabolism.
"Importantly, regulation by p75NTR enhanced insulin's effectiveness in normal lean mice on a normal diet," said Bernat Baeza-Raja, PhD, postdoctoral fellow and lead author of the study. "Because these mice already process glucose efficiently, the actions of p75NTR on glucose transport indicate a direct role of this protein in the regulation of glucose metabolism."
"Our studies of p75NTR's unanticipated role in regulating glucose metabolism suggest a new target for drug therapies," said Dr. Akassoglou. "Future work is needed to test whether this finding may translate into a potential treatment."
###
This study was a collaborative work between scientists at Gladstone, the University of California, San Diego (UCSD), the University of Michigan and the University of Houston. Other scientists who participated in this research at Gladstone include Natacha Le Moan, PhD, Christian Schachtrup, PhD, Dimitrios Davalos, PhD, and Eirini Vagena. Jerrold Olefsky, PhD, and Pingping Li, PhD, at UCSD were co-senior and co-first authors, respectively. Funding was provided by a variety of sources, including the National Institutes of Health, the University of California San Francisco Liver Center and Diabetes and Endocrinology Center and the R. A. Welch Foundation.
About the Gladstone Institutes
Gladstone is an independent and nonprofit biomedical-research organization dedicated to accelerating the pace of scientific discovery and innovation to prevent, treat and cure cardiovascular, viral and neurological diseases. Gladstone is affiliated with the University of California, San Francisco.
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Gladstone Scientists identify key mechanism involved in Type 2 diabetesPublic release date: 28-Mar-2012 [ | E-mail | Share ]
Findings may lead to new strategies to address insulin resistance
Scientists at the Gladstone Institutes have discovered a key protein that regulates insulin resistancethe diminished ability of cells to respond to the action of insulin and which sets the stage for the development of the most common form of diabetes. This breakthrough points to a new way to potentially treat or forestall type 2 diabetes, a rapidly growing global health problem.
In a paper being published online this week in the Proceedings of the National Academy of Sciences, researchers in the laboratory of Gladstone Investigator Katerina Akassoglou, PhD, describe an unexpected role of the p75 neurotrophin receptor in controlling how the body processes sugar. Called p75NTR, this receptor protein is usually associated with functions in neurons.
"We identified that p75NTR is a unique player in glucose metabolism," said Dr. Akassoglou, who is also an associate professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. "Therapies targeted at p75NTR may represent a new therapeutic approach for diabetes."
The pancreas makes a hormone called insulin that processes glucose, moving it from the bloodstream into the body's cells where it is used for energy. Insulin resistance is a key feature of Type 2 diabetes, in which glucose builds up in the bloodstream and the body's cells are unable to function properly. According to the Centers for Disease Control and Prevention, more than 20 million Americans have type 2 diabetes.
"Type 2 diabetes has become a very serious health problem and it is increasing at an alarming rate," said Lennart Mucke, MD, who directs the institute in which the research was conducted. "These findings provide an important new avenue for developing better therapies to combat this deadly diseasethe seventh leading cause of death in the United States."
Complex signaling interactions between several different types of tissueincluding fat, liver, muscle and brainregulate glucose metabolism. Because p75NTR is found in fat and muscle tissue and participates in many important functions in the cell, Gladstone scientists hypothesized that p75NTR might also help to regulate glucose metabolism.
To study this, the researchers used mice that lacked the genes for p75NTR. They compared these mice to normal mice and discovered that those lacking p75NTR were more responsive to insulin when fed a normal diet. Second, they used some molecular biology tricks to block the action of the p75NTR protein in fat cells. This also resulted in increased glucose absorption in response to insulin. In contrast, when they caused the fat cells to make more p75NTR, glucose absorption was reduced. Additionally, the researchers found that another important regulatory molecule, Rab5, played a key role in p75NTR's impact on metabolism.
"Importantly, regulation by p75NTR enhanced insulin's effectiveness in normal lean mice on a normal diet," said Bernat Baeza-Raja, PhD, postdoctoral fellow and lead author of the study. "Because these mice already process glucose efficiently, the actions of p75NTR on glucose transport indicate a direct role of this protein in the regulation of glucose metabolism."
"Our studies of p75NTR's unanticipated role in regulating glucose metabolism suggest a new target for drug therapies," said Dr. Akassoglou. "Future work is needed to test whether this finding may translate into a potential treatment."
###
This study was a collaborative work between scientists at Gladstone, the University of California, San Diego (UCSD), the University of Michigan and the University of Houston. Other scientists who participated in this research at Gladstone include Natacha Le Moan, PhD, Christian Schachtrup, PhD, Dimitrios Davalos, PhD, and Eirini Vagena. Jerrold Olefsky, PhD, and Pingping Li, PhD, at UCSD were co-senior and co-first authors, respectively. Funding was provided by a variety of sources, including the National Institutes of Health, the University of California San Francisco Liver Center and Diabetes and Endocrinology Center and the R. A. Welch Foundation.
About the Gladstone Institutes
Gladstone is an independent and nonprofit biomedical-research organization dedicated to accelerating the pace of scientific discovery and innovation to prevent, treat and cure cardiovascular, viral and neurological diseases. Gladstone is affiliated with the University of California, San Francisco.
[ | 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.
As much as I love Samsung hardware, I've felt for a long while now that the Galaxy Note was 
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Public release date: 28-Mar-2012
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