FILE - In this file photograph taken Nov. 30, 2011, specialist Dermot Bermingham, left, and trader Edward Radziewcz work on the floor of the New York Stock Exchange. Stocks rose Friday, Dec. 2, 2011, around the world as markets unnerved by the eurozone's debt crisis welcomed German Chancellor Angela Merkel's call for changes to EU treaties to enforce fiscal discipline. (AP Photo/Richard Drew, File)
FILE - In this file photograph taken Nov. 30, 2011, specialist Dermot Bermingham, left, and trader Edward Radziewcz work on the floor of the New York Stock Exchange. Stocks rose Friday, Dec. 2, 2011, around the world as markets unnerved by the eurozone's debt crisis welcomed German Chancellor Angela Merkel's call for changes to EU treaties to enforce fiscal discipline. (AP Photo/Richard Drew, File)
NEW YORK (AP) ? Stocks rose in early trading Friday after a report showed improvement in the U.S. job market and Germany's chancellor talked tough about fiscal discipline in the European Union.
The Dow Jones industrial average rose 78 points, or 0.7 percent, to 12,098 in the first half-hour of trading. The Standard & Poor's 500 index rose 9, or 0.7 percent, to 1,253. The Nasdaq composite rose 19, or 0.7 percent, to 2,645.
The gains were broad. Bank stocks rose the most, followed by industrial companies. JPMorgan Chase & Co. rose 3.4 percent, the most among the 30 stocks in the Dow average. Only two Dow stocks fell, Hewlett-Packard Co. and Wal-Mart Stores Inc.
The government said the unemployment rate fell to 8.6 percent last month, its lowest level in 2? years. Economists had expected the rate to stay at 9 percent. But a key reason the unemployment rate fell so much was because roughly 315,000 people had given up looking for work and were no longer counted as unemployed.
European stock indexes and the euro rose after German Chancellor Angela Merkel made a speech demanding tougher fiscal discipline in the region. Germany's DAX index rose 1.1 percent; France's CAC-40 rose 1.4 percent. Merkel said the 17 nations that use the euro must quickly restore market confidence by making financial controls stricter. Bond yields for Spain and Italy fell, a sign that investors are becoming more confident in the ability of those countries to pay their debt.
The improvements in the U.S. job market are "another illustration that the US economy is, for now at least, shrugging off the global economic downturn and fears about the collapse of the euro-zone," Capital Economics Chief U.S. Economist Paul Ashworth said in a note to clients.
Merkel and French President Nicolas Sarkozy are meeting Monday to discuss treaty changes that can restore confidence in the euro's future. The talks will culminate in a Dec. 9 summit of EU leaders, where the proposals are expected to be debated and detailed.
In corporate news:
? Big Lots Inc. slumped 7 percent, the most in the S&P 500 index, after the retailer reported a 76 percent plunge in income because of lower margins and a loss related to a newly acquired Canadian business. The company buys overstocked items including food and housewares and sells them at a discount.
? Western Digital Corp. soared 12.2 percent, the most in the S&P, after the data storage provider raised its revenue estimate for the current quarter and said that recovery efforts at its facility in Thailand following massive flooding there were proceeding faster than had been expected.
JONESBORO, Ark. (AP) ? The parents of one of three West Memphis, Ark., boys found dead 18 years ago are asking that a documentary about the killings be excluded from Academy Award consideration.
Todd and Dana Moore made the request in a letter sent Nov. 22 to the Academy of Motion Picture Arts and Sciences' documentary division. In it, the Moores argue that "Paradise Lost 3: Purgatory" glorifies Damien Echols, Jason Baldwin and Jessie Misskelley, who were released from prison in August after their sentences were set aside and they pleaded guilty to lesser charges.
"Because of public pressure that exploded due to gross misrepresentations of fact in the two previous documentaries, Michael's killers were unjustly able to enter into a plea agreement, were released from prison and now pose additional threats to society," the letter reads.
"We implore the Academy not to reward our child's killers and the directors who have profited from one of the greatest frauds ever perpetrated under the guise of a documentary film."
The couple's 8-year-old son, Michael, along with Steve Branch and Christopher Byers were found naked and bludgeoned in a ditch on May 6, 1993.
Director Joe Berlinger defended the film but also acknowledged that he understood the parents' grief.
"We feel tremendous sorrow for them," Berlinger told the Jonesboro Sun (http://bit.ly/sdbSAG) for a story in Wednesday's editions. "We understand why a film that comes to a different conclusion than they do would make them feel this way. We stand by our films. We fervently believe the West Memphis Three are innocent."
Echols, Baldwin and Misskelley, dubbed the West Memphis Three, entered their pleas under a legal provision that allowed them to maintain their innocence while acknowledging that prosecutors had enough evidence to convict them. Echols was sentenced to death for the killings.
An email sent to the academy after hours seeking comment wasn't immediately answered Wednesday. An attempt to leave an after-hours phone message was unsuccessful.
The Moores appeared briefly in the first documentary about the deaths, "Paradise Lost: The Child Murders at Robin Hood Hills," which aired on HBO in 1996. But they claimed Berlinger and Sinofsky "misled" and "manipulated" them.
"We appeared solely in the first film because the directors lied and told us their purpose was to protect children," the letter says.
When Berlinger and fellow director Bruce Sinofsky began the first film, they thought the three men were guilty of committing the killings, Berlinger said. Every effort was made to show that Todd and Dana believed the men were guilty, he added.
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Medical tests can reveal critical information about a person's health, but sometimes, the? test is lost and the doctor and patient never get the results, potentially delaying essential care. That was the case for one Maryland woman whose cancer went untreated for a year.
Look, the reality is that you can't drive your car into a Pay 'n' Spray every 15 minutes or so à la Grand Theft Auto, but what if you can simply change the vehicle's skin at the tap of a button? Toyota certainly likes the sound of that and has thus come up with the funky-looking Fun-Vii concept car. What's more, even the interior can be changed as well, and similarly it can be used as a display space for navigation or even racing simulation (assuming the latter's disabled while actually driving, of course). This is all good and well, but unlike many other concept exhibits we've seen, Toyota's mockup couldn't seat people -- we suspect the "car" only used a back projection from within, so we couldn't get to see what it'd feel like to play a Tron-like game inside the "car." Nevertheless, we look forward to day when this idea becomes a reality -- here's looking at you, flexible OLED! Video after the break.
>>the attorney's office has taken the lead in the
child sex abuse
investigation of the former
syracuse university
assistant basketball coach. fine was fired sunday night after a third man accused him of molestation. the latest come after the release of a recorded phone conversation said to be between one of the alleged vehicles and fine's wife. during the call they discussed the alleged abuse. the man said he experienced as a
ball boy
. darren rovell has more. they are taking over and looking for any possible victims they can bring charges on fine this time around. i want to play the tape between
bobby davis
and fine's wife. let's take a listen.
>>i don't know everything that went on. i know everything that went on with him. maybe canny are not aware of it, but he had issues. barney is also in denial. i think that they did the things he did.
>>the only one that he had ever dwn it to?
>>no. i think there might have been others, but --
>>this was obtained by
espn
and it happened in
2002
. is this why we saw fine be fired?
>>i think so. obviously we had multiple investigations.
espn
and the local paper and syracuse have been investigating for a long time. couldn't really wrap it up. this was enough for
syracuse university
to say they had just cause. someone like his wife and obviously
espn
put it out after they can id
bernie fine
's wife had said what she said about him. that was deemed just cause. the question now is, is he next?
>>that is the question. you have been tweeting on this. this is the next shoe to drop. you are talking
child abuse
here.
>>right. obviously i'm dealing with the business of sports and that has nothing to do with what's going on from how horrible the facts might be. jim might have not known about this, but it doesn't really matter. a lot of people think that his comments when this first came out where he essentially called the accusers liars and extortionists trying to get money from syracuse and
bernie fine
or whoever based on the
penn state
situation. that i think a lot of people think is a disgusting enough thing and just cause to fire him. it doesn't have to hold the same burden and standard that
penn state
thought it had where
joe paterno
and the coach didn't have enough or didn't do enough when he was presented with what he was. this is a question that will be up to them to decide. i think whether they think it's right for a long time and probably had as much power.
>>you mentioned the school chancellor and the tape was never provided to the school. it took place six years ago when they did their investigation. we will see what happens next. thank you very much, darren. coming up, a critical
Scientists identify defect in brain cell channel that may cause autism-like syndromePublic release date: 27-Nov-2011 [ | E-mail | Share ]
Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center
STANFORD, Calif. Neuroscientists at Stanford University School of Medicine have homed in on potential differences in autistic people's brain cells by studying brainlike spheres grown in an elaborate process from skin cells.
The scientists studied cells from patients with Timothy syndrome, a rare genetic condition that is associated with one of the most penetrant forms of autism: In other words, most people with the Timothy syndrome mutation have autism as a symptom, among other problems.
Autism is a spectrum of developmental disorders of impaired social and verbal interaction. Currently, no medication exists to treat its underlying causes, according to the U.S. National Library of Medicine. Understanding what goes awry in autistic brain development could improve prospects for treating the condition.
In this study, the scientists suggest that the autism in Timothy syndrome patients is caused by a gene mutation that makes calcium channels in neuron membranes defective, interfering with how those neurons communicate and develop. The flow of calcium into neurons enables them to fire, and the way that the calcium flow is regulated is a pivotal factor in how our brains function.
The researchers also found brain cells grown from individuals with Timothy syndrome resulted in fewer of the kind of cells that connect both halves of the brain, as well as an overproduction of two of the brain's chemical messengers, dopamine and norepinephrine. Furthermore, they found they could reverse these effects by chemically blocking the faulty channels.
Postdoctoral scholar Sergiu Pasca, MD, and Ricardo Dolmetsch, PhD, associate professor of neurobiology, led the study, which will be published online Nov. 27 in Nature Medicine. Dolmetsch, a biophysicist, redirected his research to study autism after his son was diagnosed with Timothy syndrome. It's unclear what leads to autism, but its incidence is increasing, he said.
The gaps in our understanding of the causes of psychiatric disorders such as autism have made them difficult to treat. Perhaps the biggest obstacle to research into autism and other psychiatric and neurological diseases is that scientists can't get living brain cell samples from people with these conditions, for obvious reasons. Dolmetsch and his colleagues figured out a solution to this dilemma, using a novel approach involving what are known as induced pluripotent stem cells, or iPS cells.
"We developed a way of taking skin cells from humans with Timothy syndrome and converting them into stem cells, then converting those stem cells into neurons," said Dolmetsch.
The scientists grew these iPS cells as free-floating clumps in a nutrient-rich solution, later transferring the clumps to tissue culture plates. Here, some of them formed three-dimensional, brainlike spheres whose cells later migrated outward and matured into neurons. These neurons formed three distinct layers, a good first approximation of living tissue in the brain. By visualizing these neurons under a microscope and quantifying their gene expression, the scientists were able to characterize at the cellular level abnormalities that may be associated with autism.
The neurons grown from Timothy-syndrome iPS cells showed larger-than-normal spikes in calcium levels, suggesting the calcium channels lost their ability to shut off. This set off dramatic changes in neuronal signaling, reconfiguring how genes were expressed.
The cerebral cortex, the outer layer of the brain, has six distinct layers. In Timothy syndrome cell cultures, the proportion of neurons of specific layers differed from that in normal brains additional biological evidence for the disorder. The neurons grown from the Timothy syndrome cells were less characteristic of lower-level neurons, which include neurons that bridge the left and right halves of the brain via the bundle of fibers known as the corpus callosum. This reinforces the view that autism results from defects in brain connectivity.
Pasca and Dolmetsch had an "aha" moment when they realized the neurons grown from Timothy syndrome cells were making too much of the enzyme most critical for producing dopamine and norepinephrine, which play an important role in sensory processing and social behavior. The realization may offer important clues about what causes the problems seen in autism.
To determine whether the enzyme upsurge was reversible, the scientists treated the neurons with a chemical that blocks the defective calcium channels, called roscovitine. They saw a nearly 70 percent reduction in the proportion of cells producing the enzyme, confirming the defective calcium channel was the culprit in producing too much dopamine and norepinephrine. Such reversibility suggests that certain cellular abnormalities in autism may be treatable.
Dolmetsch warned, however, that roscovitine is not currently approved for use in humans and has never been tested in children. While it is currently in clinical trials for lung cancer, it reportedly causes nausea and other side effects. "The reported side effects are probably due to the fact that, in addition to targeting the channel that is mutated in autism, roscovitine also inhibits kinases that are required for cell proliferation," he said. "We think that roscovitine is a good starting point, but probably has to be optimized before it would be useful for autism."
In the meantime, the study represents a major achievement with its success in developing a technique to recreate how the neurons of individuals with Timothy syndrome develop in a lab setting. It's the first time it's been possible to study the disorder in human cells rather than mouse cells, so it represents a better clinical model, Dolmetsch said.
"These results could lead to a very powerful research tool," he said. "It's human psychiatric disease in a petri dish."
###
Researchers from UCLA contributed to the study. Other authors from Stanford were postdoctoral scholars Thomas Portmann, PhD, Masayuki Yazawa, PhD, and Oleksandr Shcheglovitov, PhD; clinical researcher Anca Pasca, MD; neurology researcher Branden Cord MD, PhD; associate professor of neurosurgery Theo Palmer, PhD; Sachiko Chikahisa, PhD, and research professor of psychiatry and behavioral sciences Nishino Seiji, MD, PhD, both of the Sleep and Circadian Neurobiology Laboratory; clinical assistant professor of medical genetics Jonathan Bernstein, MD, PhD; and associate professor of psychiatry and behavioral sciences Joachim Hallmayer, MD.
Financial support was provided by the National Institutes of Health, Simons Foundation Grant, International Brain Research Organization, the Tashia and John Morgridge Endowed Fellowship, Japan Society of the Promotion for Science, American Heart Association Western States, the Swiss National Science Foundation, the California Institute for Regenerative Medicine and several individual donors. Information about the Department of Neurobiology, in which the study was conducted, is available at http://neurobiology.stanford.edu/.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
PRINT MEDIA CONTACT: Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu)
BROADCAST MEDIA CONTACT: M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)
[ | 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.
Scientists identify defect in brain cell channel that may cause autism-like syndromePublic release date: 27-Nov-2011 [ | E-mail | Share ]
Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center
STANFORD, Calif. Neuroscientists at Stanford University School of Medicine have homed in on potential differences in autistic people's brain cells by studying brainlike spheres grown in an elaborate process from skin cells.
The scientists studied cells from patients with Timothy syndrome, a rare genetic condition that is associated with one of the most penetrant forms of autism: In other words, most people with the Timothy syndrome mutation have autism as a symptom, among other problems.
Autism is a spectrum of developmental disorders of impaired social and verbal interaction. Currently, no medication exists to treat its underlying causes, according to the U.S. National Library of Medicine. Understanding what goes awry in autistic brain development could improve prospects for treating the condition.
In this study, the scientists suggest that the autism in Timothy syndrome patients is caused by a gene mutation that makes calcium channels in neuron membranes defective, interfering with how those neurons communicate and develop. The flow of calcium into neurons enables them to fire, and the way that the calcium flow is regulated is a pivotal factor in how our brains function.
The researchers also found brain cells grown from individuals with Timothy syndrome resulted in fewer of the kind of cells that connect both halves of the brain, as well as an overproduction of two of the brain's chemical messengers, dopamine and norepinephrine. Furthermore, they found they could reverse these effects by chemically blocking the faulty channels.
Postdoctoral scholar Sergiu Pasca, MD, and Ricardo Dolmetsch, PhD, associate professor of neurobiology, led the study, which will be published online Nov. 27 in Nature Medicine. Dolmetsch, a biophysicist, redirected his research to study autism after his son was diagnosed with Timothy syndrome. It's unclear what leads to autism, but its incidence is increasing, he said.
The gaps in our understanding of the causes of psychiatric disorders such as autism have made them difficult to treat. Perhaps the biggest obstacle to research into autism and other psychiatric and neurological diseases is that scientists can't get living brain cell samples from people with these conditions, for obvious reasons. Dolmetsch and his colleagues figured out a solution to this dilemma, using a novel approach involving what are known as induced pluripotent stem cells, or iPS cells.
"We developed a way of taking skin cells from humans with Timothy syndrome and converting them into stem cells, then converting those stem cells into neurons," said Dolmetsch.
The scientists grew these iPS cells as free-floating clumps in a nutrient-rich solution, later transferring the clumps to tissue culture plates. Here, some of them formed three-dimensional, brainlike spheres whose cells later migrated outward and matured into neurons. These neurons formed three distinct layers, a good first approximation of living tissue in the brain. By visualizing these neurons under a microscope and quantifying their gene expression, the scientists were able to characterize at the cellular level abnormalities that may be associated with autism.
The neurons grown from Timothy-syndrome iPS cells showed larger-than-normal spikes in calcium levels, suggesting the calcium channels lost their ability to shut off. This set off dramatic changes in neuronal signaling, reconfiguring how genes were expressed.
The cerebral cortex, the outer layer of the brain, has six distinct layers. In Timothy syndrome cell cultures, the proportion of neurons of specific layers differed from that in normal brains additional biological evidence for the disorder. The neurons grown from the Timothy syndrome cells were less characteristic of lower-level neurons, which include neurons that bridge the left and right halves of the brain via the bundle of fibers known as the corpus callosum. This reinforces the view that autism results from defects in brain connectivity.
Pasca and Dolmetsch had an "aha" moment when they realized the neurons grown from Timothy syndrome cells were making too much of the enzyme most critical for producing dopamine and norepinephrine, which play an important role in sensory processing and social behavior. The realization may offer important clues about what causes the problems seen in autism.
To determine whether the enzyme upsurge was reversible, the scientists treated the neurons with a chemical that blocks the defective calcium channels, called roscovitine. They saw a nearly 70 percent reduction in the proportion of cells producing the enzyme, confirming the defective calcium channel was the culprit in producing too much dopamine and norepinephrine. Such reversibility suggests that certain cellular abnormalities in autism may be treatable.
Dolmetsch warned, however, that roscovitine is not currently approved for use in humans and has never been tested in children. While it is currently in clinical trials for lung cancer, it reportedly causes nausea and other side effects. "The reported side effects are probably due to the fact that, in addition to targeting the channel that is mutated in autism, roscovitine also inhibits kinases that are required for cell proliferation," he said. "We think that roscovitine is a good starting point, but probably has to be optimized before it would be useful for autism."
In the meantime, the study represents a major achievement with its success in developing a technique to recreate how the neurons of individuals with Timothy syndrome develop in a lab setting. It's the first time it's been possible to study the disorder in human cells rather than mouse cells, so it represents a better clinical model, Dolmetsch said.
"These results could lead to a very powerful research tool," he said. "It's human psychiatric disease in a petri dish."
###
Researchers from UCLA contributed to the study. Other authors from Stanford were postdoctoral scholars Thomas Portmann, PhD, Masayuki Yazawa, PhD, and Oleksandr Shcheglovitov, PhD; clinical researcher Anca Pasca, MD; neurology researcher Branden Cord MD, PhD; associate professor of neurosurgery Theo Palmer, PhD; Sachiko Chikahisa, PhD, and research professor of psychiatry and behavioral sciences Nishino Seiji, MD, PhD, both of the Sleep and Circadian Neurobiology Laboratory; clinical assistant professor of medical genetics Jonathan Bernstein, MD, PhD; and associate professor of psychiatry and behavioral sciences Joachim Hallmayer, MD.
Financial support was provided by the National Institutes of Health, Simons Foundation Grant, International Brain Research Organization, the Tashia and John Morgridge Endowed Fellowship, Japan Society of the Promotion for Science, American Heart Association Western States, the Swiss National Science Foundation, the California Institute for Regenerative Medicine and several individual donors. Information about the Department of Neurobiology, in which the study was conducted, is available at http://neurobiology.stanford.edu/.
The Stanford University School of Medicine consistently ranks among the nation's top medical schools, integrating research, medical education, patient care and community service. For more news about the school, please visit http://mednews.stanford.edu. The medical school is part of Stanford Medicine, which includes Stanford Hospital & Clinics and Lucile Packard Children's Hospital. For information about all three, please visit http://stanfordmedicine.org/about/news.html.
PRINT MEDIA CONTACT: Bruce Goldman at (650) 725-2106 (goldmanb@stanford.edu)
BROADCAST MEDIA CONTACT: M.A. Malone at (650) 723-6912 (mamalone@stanford.edu)
[ | 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.
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Public release date: 27-Nov-2011
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