Though, it can't have been recently since APPARENTLY the two Twilight stars just spent the night together!
Unless, of course, the email is what caused the reunion!?!
Sources said:
“[Kristen] wasn’t happy…that Rob’s been dating other girls so soon after they split. She told him he was cheapening everything they’d had between them.”
WHOA! So she decides to send him an angry email?? Why not just call him up and tell him? Or… you know… move on… since you guys are broken up?
Just sayin'!!
Other sources, however, are reporting that all of these reunion rumors are "not true" which makes us wonder what is ACTUALLY happening!
These two are so up and down we can barely keep up!
FILE - In this April 30, 2013 file photo, Michael Skakel leaves the courtroom after the conclusion of trial regarding his legal representation at State Superior Court in Vernon, Conn. A Connecticut judge on Wednesday, Oct. 23, 2013, granted a new trial for Skakel, ruling his attorney failed to adequately represent him when he was convicted in 2002 of killing his neighbor in 1975. (AP Photo/The Greenwich Time, Jason Rearick, Pool, File)
FILE - In this April 30, 2013 file photo, Michael Skakel leaves the courtroom after the conclusion of trial regarding his legal representation at State Superior Court in Vernon, Conn. A Connecticut judge on Wednesday, Oct. 23, 2013, granted a new trial for Skakel, ruling his attorney failed to adequately represent him when he was convicted in 2002 of killing his neighbor in 1975. (AP Photo/The Greenwich Time, Jason Rearick, Pool, File)
HARTFORD, Conn. (AP) — Kennedy cousin Michael Skakel was granted a new trial on Wednesday by a Connecticut judge who ruled his attorney failed to adequately represent him when he was convicted in 2002 of killing his neighbor in 1975.
The ruling by Judge Thomas Bishop marked a dramatic reversal after years of unsuccessful appeals by Skakel, the 53-year-old nephew of Robert F. Kennedy's widow, Ethel Kennedy. Skakel is serving 20 years to life.
Bridgeport State's Attorney John Smriga said prosecutors will appeal the decision.
Skakel's current attorney, Hubert Santos, said he expects to file a motion for bail on Thursday. If a judge approves it, Skakel could then post bond and be released from prison.
"We're very, very thrilled," Santos said. "I always felt that Michael was innocent."
Skakel argued his trial attorney, Michael Sherman, was negligent in defending him when he was convicted in the golf club bludgeoning of Martha Moxley when they were 15 in wealthy Greenwich.
Prosecutors contended Sherman's efforts far exceeded standards and that the verdict was based on compelling evidence against Skakel.
John Moxley, the victim's brother, said the ruling took him and his family by surprise and they hope the state wins an appeal.
"Having been in the courtroom during the trial, there were a lot of things that Mickey Sherman did very cleverly," Moxley said about Skakel's trial lawyer. "But the evidence was against him. And when the evidence is against you, there's almost nothing you can do.
"I don't care if it was Perry Mason," Moxley said. "The state had the evidence. It was his own words and deeds that led to the conviction."
In his ruling, the judge wrote that defense in such a case requires attention to detail, an energetic investigation and a coherent plan of defense.
"Trial counsel's failures in each of these areas of representation were significant and, ultimately, fatal to a constitutionally adequate defense," Bishop wrote. "As a consequence of trial counsel's failures as stated, the state procured a judgment of conviction that lacks reliability."
Among other issues, the judge wrote that the defense could have focused more on Skakel's brother, Thomas, who was an early suspect in the case because he was the last person seen with Moxley. Had Sherman done so, "there is a reasonable probability that the outcome of the trial would have been different," the judge wrote.
During a state trial in April on the appeal, Skakel took the stand and blasted Sherman's handling of the case, portraying him as an overly confident lawyer having fun and basking in the limelight while making fundamental mistakes from poor jury picks to failing to track down key witnesses.
Santos argued that the prosecutors' case rested entirely on two witnesses of dubious credibility who came forward with stories of confessions after 20 years and the announcement of a reward. Skakel had an alibi, he said.
Santos contends Sherman was "too enamored with the media attention to focus on the defense." Sherman told criminal defense attorneys at a seminar in Las Vegas six months before the trial that one of his goals in representing Skakel was to have a "good time," Santos said.
Sherman has said he did all he could to prevent Skakel's conviction and denied he was distracted by media attention in the high-profile case.
Santos contends Sherman failed to obtain or present evidence against earlier suspects, failed to sufficiently challenge the state's star witness and other testimony and made risky jury picks including a police officer.
Prosecutors countered that Sherman spent thousands of hours preparing the defense, challenged the state on large and small legal issues, consulted experts and was assisted by some of the state's top lawyers. Sherman attacked the state's evidence, presented an alibi and pointed the finger at an earlier suspect, prosecutors said.
"This strategy failed not because of any fault of Sherman's, but because of the strength of the state's case," prosecutor Susann Gill wrote in court papers.
The state's case included three confessions and nearly a dozen incriminating statements by Skakel over the years, Gill said. She also said there was strong evidence of motive.
"His drug-addled mental state, coupled with the infuriating knowledge that his hated brother Tommy had a sexual liaison with Martha, and the fact that Martha spurned his advances, triggered the rage which led him to beat her to death with a golf club," Gill wrote.
Gill said what Sherman did with his personal time was irrelevant. She said the evidence cited by the defense was not significant and that Sherman had sound strategic reasons for his decisions.
Skakel, who maintains his innocence, was denied parole last year and was told he would not be eligible again to be considered for release for five years.
WASHINGTON (Reuters) - House of Representatives Republicans remain committed to seeking a delay in the provision in President Barack Obama's health care law that requires uninsured Americans to purchase health insurance coverage, House Majority Leader Eric Cantor said on Wednesday.
House of Representatives Speaker John Boehner, speaking with reporters, said Republicans would use their oversight powers, including holding hearings, to hold the Obama administration accountable over the health care law known as "Obamacare."
Induced pluripotent stem cells reveal differences between humans and great apes
PUBLIC RELEASE DATE:
23-Oct-2013
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Contact: Kat Kearney kkearney@salk.edu 619-296-8466 Salk Institute
Key differences in the regulation of jumping genes may have arisen relatively recently in evolution
LA JOLLA, CA---- Researchers at the Salk Institute for Biological Studies have, for the first time, taken chimpanzee and bonobo skin cells and turned them into induced pluripotent stem cells (iPSCs), a type of cell that has the ability to form any other cell or tissue in the body.
Mouse iPSCs were created in 2006 by Kazutoshi Takahashi and Shinya Yamanaka at Kyoto University in Japan, and human iPSCs soon followed----feats which earned Yamanaka the Nobel Prize in Physiology or Medicine last year. Now scientists regularly use iPSCs to model diseases using cells that would be otherwise difficult to obtain from a living person or animal. By adding a combination of four key factors, a skin cell can be made into an iPSC, which can then be coaxed into forming liver, lung and brain cells in a culture dish.
It's now possible to not only model disease using the cells, but also to compare iPSCs from humans to those of our closest living relatives----great apes, with which we share a majority of genes----for insight into what molecular and cellular features make us human.
"Comparing human, chimpanzee and bonobo cells can give us clues to understand biological processes, such as infection, diseases, brain evolution, adaptation or genetic diversity," says senior research associate Iigo Narvaiza, who led the study with senior staff scientist Carol Marchetto at the Salk Institute in La Jolla. "Until now, the sources for chimpanzee and bonobo cells were limited to postmortem tissue or blood. Now you could generate neurons, for example, from the three different species and compare them to test hypotheses."
In the new study, published online October 23 in the journal Nature, scientists found disparities in the regulation of jumping genes or transposons----DNA elements that can copy and paste themselves into spots throughout the genome----between humans and non-human primate cells. Jumping genes provide a means to rapidly shuffle DNA and might be shaping the evolution of our genomes, the scientists say.
Working in the lab of Salk's Fred Gage, the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Disease, Narvaiza, Marchetto and their colleagues identified genes that are differentially expressed between iPSCs from humans and both chimpanzees and bonobos.
To the group's surprise, two of those genes code for proteins that restrict a jumping gene called long interspersed element-1or L1, for short. Compared with non-human primate cells, human iPSCs expressed higher levels of these restrictors, called APOBEC3B and PIWIL2. "We weren't expecting that," Marchetto says. "Those genes caught our eyes, so they were the first targets we focused on."
L1 and a handful of other jumping genes are abundant throughout our genomes. Where these bits of DNA insert themselves is hard to predict, and they can produce variable effects. For example, they might completely disrupt genes, modulate them, or cause them to be processed into entirely new proteins.
Using L1 tagged with a fluorescent marker, the group observed higher numbers of fluorescent iPSCs from non-human primates compared with humans. In separate experiments, they produced iPSCs with too much or too little APOBEC3B and PIWIL2, finding----as expected----that an excess of the two proteins dampened the mobility and reduced the appearance of newly inserted DNA in the non-human primate cells.
These results suggested that L1 elements insert themselves less often throughout our genomes. Indeed, looking at genomes of humans and chimpanzees that had already been sequenced, the researchers found that the primates had more copies of L1 sequences than did humans.
The question that remains is, what would be the impact of differences in L1 regulation? "It could mean that we have gone, as humans, through one or more bottlenecks in evolution, that decrease the variability present in our genome," says Marchetto, though the hypothesis is admittedly hard to prove. It is known, however, that humans' genomes are less variable than chimpanzees'.
The new study provides proof of concept that the iPSC technology can be used to understand some of the evolutionary differences between humans and non-human primates, says Narvaiza. The group plans to make technology, and all the data, available to the broader research community----which is especially helpful now that great ape research is severely restricted in the United States and abroad----so that other scientists can learn about primates using non-invasive, ethically sound methods.
The team plans to differentiate the stem cells into other tissues, such as neurons, and comparing how the cells from different species behave. They will also use the iPSC technology to investigate how chimpanzees might differ from people in susceptibility to cancer, genetic diseases and viral infection.
###
Other researchers on the study were Ahmet Denli, Christopher Benner, Thomas Lazzarini, and Apu Paquola of the Salk Institute for Biological Studies; Jason Nathanson
and Gene Yeo of the University of California San Diego,
Department of Cellular and Molecular Medicine; Keval Desai of the University of California San Diego, Division of Biological Sciences; Roberto Herai and Alysson Muotri of the University of California San Diego, School of Medicine; Matthew Weitzman of the Department of Pathology and Laboratory Medicine at the University of Pennsylvania Perelman School of Medicine; and senior and corresponding author Fred H. Gage of the Salk Institute and Center for Academic Research and Training in Anthropogeny.
The work was supported by the National Institutes of Health, the G. Harold & Leila Y. Mathers Foundation and the Leona M. and Harry B. Helmsley Charitable Trust.
About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.
Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.
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Induced pluripotent stem cells reveal differences between humans and great apes
PUBLIC RELEASE DATE:
23-Oct-2013
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]
Share
Contact: Kat Kearney kkearney@salk.edu 619-296-8466 Salk Institute
Key differences in the regulation of jumping genes may have arisen relatively recently in evolution
LA JOLLA, CA---- Researchers at the Salk Institute for Biological Studies have, for the first time, taken chimpanzee and bonobo skin cells and turned them into induced pluripotent stem cells (iPSCs), a type of cell that has the ability to form any other cell or tissue in the body.
Mouse iPSCs were created in 2006 by Kazutoshi Takahashi and Shinya Yamanaka at Kyoto University in Japan, and human iPSCs soon followed----feats which earned Yamanaka the Nobel Prize in Physiology or Medicine last year. Now scientists regularly use iPSCs to model diseases using cells that would be otherwise difficult to obtain from a living person or animal. By adding a combination of four key factors, a skin cell can be made into an iPSC, which can then be coaxed into forming liver, lung and brain cells in a culture dish.
It's now possible to not only model disease using the cells, but also to compare iPSCs from humans to those of our closest living relatives----great apes, with which we share a majority of genes----for insight into what molecular and cellular features make us human.
"Comparing human, chimpanzee and bonobo cells can give us clues to understand biological processes, such as infection, diseases, brain evolution, adaptation or genetic diversity," says senior research associate Iigo Narvaiza, who led the study with senior staff scientist Carol Marchetto at the Salk Institute in La Jolla. "Until now, the sources for chimpanzee and bonobo cells were limited to postmortem tissue or blood. Now you could generate neurons, for example, from the three different species and compare them to test hypotheses."
In the new study, published online October 23 in the journal Nature, scientists found disparities in the regulation of jumping genes or transposons----DNA elements that can copy and paste themselves into spots throughout the genome----between humans and non-human primate cells. Jumping genes provide a means to rapidly shuffle DNA and might be shaping the evolution of our genomes, the scientists say.
Working in the lab of Salk's Fred Gage, the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Disease, Narvaiza, Marchetto and their colleagues identified genes that are differentially expressed between iPSCs from humans and both chimpanzees and bonobos.
To the group's surprise, two of those genes code for proteins that restrict a jumping gene called long interspersed element-1or L1, for short. Compared with non-human primate cells, human iPSCs expressed higher levels of these restrictors, called APOBEC3B and PIWIL2. "We weren't expecting that," Marchetto says. "Those genes caught our eyes, so they were the first targets we focused on."
L1 and a handful of other jumping genes are abundant throughout our genomes. Where these bits of DNA insert themselves is hard to predict, and they can produce variable effects. For example, they might completely disrupt genes, modulate them, or cause them to be processed into entirely new proteins.
Using L1 tagged with a fluorescent marker, the group observed higher numbers of fluorescent iPSCs from non-human primates compared with humans. In separate experiments, they produced iPSCs with too much or too little APOBEC3B and PIWIL2, finding----as expected----that an excess of the two proteins dampened the mobility and reduced the appearance of newly inserted DNA in the non-human primate cells.
These results suggested that L1 elements insert themselves less often throughout our genomes. Indeed, looking at genomes of humans and chimpanzees that had already been sequenced, the researchers found that the primates had more copies of L1 sequences than did humans.
The question that remains is, what would be the impact of differences in L1 regulation? "It could mean that we have gone, as humans, through one or more bottlenecks in evolution, that decrease the variability present in our genome," says Marchetto, though the hypothesis is admittedly hard to prove. It is known, however, that humans' genomes are less variable than chimpanzees'.
The new study provides proof of concept that the iPSC technology can be used to understand some of the evolutionary differences between humans and non-human primates, says Narvaiza. The group plans to make technology, and all the data, available to the broader research community----which is especially helpful now that great ape research is severely restricted in the United States and abroad----so that other scientists can learn about primates using non-invasive, ethically sound methods.
The team plans to differentiate the stem cells into other tissues, such as neurons, and comparing how the cells from different species behave. They will also use the iPSC technology to investigate how chimpanzees might differ from people in susceptibility to cancer, genetic diseases and viral infection.
###
Other researchers on the study were Ahmet Denli, Christopher Benner, Thomas Lazzarini, and Apu Paquola of the Salk Institute for Biological Studies; Jason Nathanson
and Gene Yeo of the University of California San Diego,
Department of Cellular and Molecular Medicine; Keval Desai of the University of California San Diego, Division of Biological Sciences; Roberto Herai and Alysson Muotri of the University of California San Diego, School of Medicine; Matthew Weitzman of the Department of Pathology and Laboratory Medicine at the University of Pennsylvania Perelman School of Medicine; and senior and corresponding author Fred H. Gage of the Salk Institute and Center for Academic Research and Training in Anthropogeny.
The work was supported by the National Institutes of Health, the G. Harold & Leila Y. Mathers Foundation and the Leona M. and Harry B. Helmsley Charitable Trust.
About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world's preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused both on discovery and on mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer's, diabetes and infectious diseases by studying neuroscience, genetics, cell and plant biology, and related disciplines.
Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.
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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.
SAN FRANCISCO (AP) — Activist investor Carl Icahn may be putting more pressure on Apple CEO Tim Cook to get more aggressive about boosting the iPhone maker's stock price.
Icahn posted on his Twitter account Wednesday that he had sent Cook a letter in the afternoon. He said he would share the letter Thursday on a new website called "Shareholders' Square Table."
The missive follows up on a Sept. 30 dinner with Cook that Icahn hosted at his New York apartment. During that get-together, Icahn said he lobbied Cook to spend $150 billion buying back Apple Inc.'s own stock. That's more than double the amount that the Cupertino, Calif., company has committed to spend.
Icahn, whose wealth is estimated at $20 billion by Forbes magazine, has said his fund has invested about $2 billion in Apple. At that amount, Icahn would own less than a 1 percent stake in Apple.
Icahn, 77, has a long history of buying significant stakes in companies with a slumping stock price and then pressing the corporate leaders to pursue plans that he thinks would make the shares more valuable.
While Apple's market value of about $477 billion is more than any other publicly traded company, its stock prices has fallen about 25 percent from a peak 13 months ago. Investors have been worried about tougher competition facing Apple in the smartphone and table market, as well as the lack of a breakthrough product since the death of its chief visionary, Steve Jobs, two years ago. Those worries didn't dissipate with unveiling of Apple's latest iPads on Tuesday.
Apple's stock rose $5.09 Wednesday to close at $524.96.
Icahn believes Apple could lift its stock by taking advantage of low interest rates to borrow money to finance its proposed stock buybacks. The buybacks would fuel demand for Apple's stock and increase the company's earnings per share by reducing the amount of stock. Higher earnings per share usually lift a company's stock price.
Neither Apple nor Icahn responded to requests for comment on Wednesday.
In some instances, Icahn has threatened to try to oust corporate boards that don't follow his wishes. Icahn hasn't yet said whether he might pursue a shake-up at Apple if the company rebuffs him.
Icahn sent his letter to Cook the day after disclosing he had sold more than half his stake in one of his biggest successes, an investment in Internet movie service Netflix Inc.
In that instance, Icahn did little but give Netflix CEO Reed Hastings a vote of confidence at a time when the company had fallen out of favor. After accumulating a nearly 10 percent stake in Netflix while the stock was trading below $60 last year, Icahn reaped a pre-tax gain of nearly $800 million by selling 3 million shares at prices ranging from $304.23 to $341.44 earlier this month.
Icahn still owns nearly 2.7 million Netflix shares, leaving him with a 4.5 percent stake in the Los Gatos, Calif., company.
HARTFORD, Conn. (AP) — Kennedy cousin Michael Skakel was granted a new trial on Wednesday by a Connecticut judge who ruled his attorney failed to adequately represent him when he was convicted in 2002 of killing his neighbor in 1975.
The ruling by Judge Thomas Bishop marked a dramatic reversal after years of unsuccessful appeals by Skakel, the 53-year-old nephew of Robert F. Kennedy's widow, Ethel Kennedy. Skakel is serving 20 years to life.
Bridgeport State's Attorney John Smriga said prosecutors will appeal the decision.
Skakel's current attorney, Hubert Santos, said he expects to file a motion for bail on Thursday. If a judge approves it, Skakel could then post bond and be released from prison.
"We're very, very thrilled," Santos said. "I always felt that Michael was innocent."
Skakel argued his trial attorney, Michael Sherman, was negligent in defending him when he was convicted in the golf club bludgeoning of Martha Moxley when they were 15 in wealthy Greenwich.
Prosecutors contended Sherman's efforts far exceeded standards and that the verdict was based on compelling evidence against Skakel.
John Moxley, the victim's brother, said the ruling took him and his family by surprise and they hope the state wins an appeal.
"Having been in the courtroom during the trial, there were a lot of things that Mickey Sherman did very cleverly," Moxley said about Skakel's trial lawyer. "But the evidence was against him. And when the evidence is against you, there's almost nothing you can do.
"I don't care if it was Perry Mason," Moxley said. "The state had the evidence. It was his own words and deeds that led to the conviction."
In his ruling, the judge wrote that defense in such a case requires attention to detail, an energetic investigation and a coherent plan of defense.
"Trial counsel's failures in each of these areas of representation were significant and, ultimately, fatal to a constitutionally adequate defense," Bishop wrote. "As a consequence of trial counsel's failures as stated, the state procured a judgment of conviction that lacks reliability."
Among other issues, the judge wrote that the defense could have focused more on Skakel's brother, Thomas, who was an early suspect in the case because he was the last person seen with Moxley. Had Sherman done so, "there is a reasonable probability that the outcome of the trial would have been different," the judge wrote.
During a state trial in April on the appeal, Skakel took the stand and blasted Sherman's handling of the case, portraying him as an overly confident lawyer having fun and basking in the limelight while making fundamental mistakes from poor jury picks to failing to track down key witnesses.
Santos argued that the prosecutors' case rested entirely on two witnesses of dubious credibility who came forward with stories of confessions after 20 years and the announcement of a reward. Skakel had an alibi, he said.
Santos contends Sherman was "too enamored with the media attention to focus on the defense." Sherman told criminal defense attorneys at a seminar in Las Vegas six months before the trial that one of his goals in representing Skakel was to have a "good time," Santos said.
Sherman has said he did all he could to prevent Skakel's conviction and denied he was distracted by media attention in the high-profile case.
Santos contends Sherman failed to obtain or present evidence against earlier suspects, failed to sufficiently challenge the state's star witness and other testimony and made risky jury picks including a police officer.
Prosecutors countered that Sherman spent thousands of hours preparing the defense, challenged the state on large and small legal issues, consulted experts and was assisted by some of the state's top lawyers. Sherman attacked the state's evidence, presented an alibi and pointed the finger at an earlier suspect, prosecutors said.
"This strategy failed not because of any fault of Sherman's, but because of the strength of the state's case," prosecutor Susann Gill wrote in court papers.
The state's case included three confessions and nearly a dozen incriminating statements by Skakel over the years, Gill said. She also said there was strong evidence of motive.
"His drug-addled mental state, coupled with the infuriating knowledge that his hated brother Tommy had a sexual liaison with Martha, and the fact that Martha spurned his advances, triggered the rage which led him to beat her to death with a golf club," Gill wrote.
Gill said what Sherman did with his personal time was irrelevant. She said the evidence cited by the defense was not significant and that Sherman had sound strategic reasons for his decisions.
Skakel, who maintains his innocence, was denied parole last year and was told he would not be eligible again to be considered for release for five years.
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