Wednesday, December 7, 2011

3 charged for murder plot against Swedish artist (AP)

STOCKHOLM ? Three men were charged Tuesday with plotting to stab to death a Swedish artist who has faced numerous threats from Muslim extremists for depicting the Prophet Muhammad as a dog.

The men, ages 24 to 26 and of Somali and Iraqi origin, were arrested in the city of Goteborg on the eve of the 10th anniversary of the Sept. 11 terrorist attacks in the United States.

According to the charges, the suspects were planning to use knives to kill Lars Vilks, whose 2007 drawing of Muhammad offended many Muslims and rekindled a debate over free speech and Islam that raged a year earlier when a Danish newspaper printed 12 caricatures of the prophet.

Images of Muhammad, even favorable ones, are considered blasphemous by many Muslims.

The evidence included wiretapped phone conversations between the suspects and a note pad belonging to one of them, prosecutor Agnetha Hilding Qvarnstrom said.

Calls to the suspects' defense lawyers were not immediately returned.

An art gallery celebrating the opening of an exhibition was evacuated in connection with the arrests, and police originally treated the case as a terror investigation. They later relabeled it as a murder plot.

Vilks, 65, had mentioned on his blog that he planned to visit the exhibition, but he did not attend the opening ceremony.

The three men carried knives when they were arrested near the central train station in Goteborg on Sept. 10, the charges said, adding they had scouted the art gallery and one of them had gone inside to ask for Vilks.

The Swedish artist has been at the center of several planned attacks.

A Pennsylvania woman earlier this year pleaded guilty in a plot to try to kill Vilks. Two brothers were convicted in Sweden of trying to burn down his house last year.

Also last year, a suicide bomber who blew himself up in Stockholm referred to Vilks and the presence of Swedish troops in Afghanistan in an audio recording sent to a Swedish news agency before the bombing. No one else died in the attack.

"I have had so many incidents like these now I have become accustomed to it," Vilks told The Associated Press on Tuesday. "But I have a bodyguard now so it is difficult to get to me."

The trial is expected to start later this month. Vilks said he will participate by telephone.

Source: http://us.rd.yahoo.com/dailynews/rss/europe/*http%3A//news.yahoo.com/s/ap/20111206/ap_on_re_eu/eu_sweden_murder_plot

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Tuesday, December 6, 2011

AT&T's LG Nitro HD goes up for sale, LTE-enabled Gingerbread pep for $250

In case you forget that AT&T's latest LTE-equipped smartphone hit shelves today, consider this a friendly reminder from your mobile obsessed friends here at Engadget. We're talking about the LG's Nitro HD, the 4.5-inch device we lovingly handled last week -- loaded with a skinned version of Android 2.3.5 Gingerbread, running atop its peppy 1.5 GHz Qualcomm APQ8060 dual-core processor. If you'll recall, it's notably packing a 1280 x 720p screen resolution with an ultra-crisp looking 329ppi, an 8 megapixel rear camera (1.3 MP up front) and a healthy 4GB of internal storage supplemented by an included 16GB microSD card (expandable to 32GB). Thankfully, bloatware on the Nitro is at an all time low, but we'd be remiss if we didn't mention that's it's been confirmed to be loaded with the ickyness of Carrier IQ. Sure, it's not as tasty as an Ice Cream Sandwich, but if your hungering for LTE-enabled 4G speeds on Ma Bell, at least you now have a third option. It can be yours now for $250 with a two-year renewal of service, and you'll find more info at the source link below.

AT&T's LG Nitro HD goes up for sale, LTE-enabled Gingerbread pep for $250 originally appeared on Engadget on Sun, 04 Dec 2011 21:34:00 EDT. Please see our terms for use of feeds.

Permalink The Verge, Mobile Burn  |  sourceAT&T  | Email this | Comments


Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/golMclDNaqs/

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China services data may bolster case for further easing (Reuters)

SHANGHAI (Reuters) ? China's services sector contracted in November, mirroring similar weakness in the country's giant manufacturing sector and underlining expectations that Beijing can ease monetary policy further to cushion the blows of the global economy.

China's official purchasing managers' index for its non-manufacturing sector fell to 49.7 in November from 57.7 in October, the China Federation of Logistics and Purchasing said on Saturday. The 50-mark divides expansion from contraction.

A private-sector PMI on non-manufacturers from HSBC is due for release at 9:30 p.m. EST on Monday and may paint a similar picture of weakness in services as the euro-zone debt crisis weighs on the global economy. The HSBC gauge in October was running at 54.1, the strongest growth in four months.

PMI data in the past week has shown that both domestic and export orders are weakening, helping explain the central bank's decision last Wednesday to cut reserve requirements for commercial lenders for the first time in three years.

The move to free up cash was a signal that the central bank was shifting toward loosening monetary policy to support the economy, which is widely expected to grow next year at less than 9 percent for the first time in a decade, economists said.

Indeed, former central bank adviser Fan Gang said in the Securities Times newspaper on Saturday that there was room for further cuts in reserve requirements provided inflation continued to fall.

"There is plenty of room for adjusting banks' reserve requirements ratios," he said.

The official manufacturing PMI on Thursday showed prices fell in November and Premier Wen Jiabao said on November 9 that prices had fallen since October.

Consumer inflation dropped in October to 5.5 percent, backtracking from a three-year high of 6.5 percent in July.

The official services PMI suggested the sector was weak due to softer consumption patterns and a slowdown in the construction industry.

"The retail, food and beverage industry-based consumer services were in an off-season, showing a more significant decline," Cai Jin, a vice president with the CFLP, said in a statement.

The sub-index of new orders in services PMI declined to 47.2 in November, indicating they were actually falling, from 52.5 in October. Input prices for the Chinese services sector eased to 54.4 from 55.7 in October, showing inflationary pressures eased.

The services PMI index aims to give a snapshot of conditions in the services sector, which accounts for less than 45 percent of China's economy, much less than in developed countries.

Last Thursday, the official manufacturing PMI fell to 49 in November from October's 50.4, pointing to the first contraction in activity in nearly three years, or since the global financial crisis.

The HSBC manufacturing PMI dropped to a 32-month low of 47.7 in November from October's 51.

"The November PMI final reading points to a sharp deterioration in business conditions across the Chinese manufacturing sector," said Qu Hongbin, China economist at

HSBC.

Globally, the picture was similar.

A global PMI produced by JPMorgan, with research and supply management organizations, fell to 49.6, suggesting a contraction in global manufacturing.

Chinese officials have expressed growing alarm at the slide in the global economy as Europe struggles to produce a decisive solution to its debt crisis.

Vice Finance Minister Zhu Guangyao said last week that the world economy faced a worse crisis now than during 2008 and that stimulating growth should be a priority.

Vice Premier Wang Qishan in November said a chronic global recession was certain.

Although analysts say China is shifting policy to support growth, China's Ministry of Housing and Urban-Rural Development suggested there would be no let up in policy controls on the property market.

The ministry told local governments not to relax home purchase restrictions, the China Business Journal said on Saturday, adding that the restrictions would continue despite their scheduled expiry in at least 11 cities by year-end.

The paper quoted an unnamed government official with the ministry as saying China's current property controls of restrictive home buying would not change.

On Friday, China's central bank said Chinese home prices were at a turning point. Home prices fell in October from September for the first time this year, official data showed, but a private survey has indicated that November could mark a third consecutive monthly fall.

(Reporting by Melanie Lee; Writing by Kevin Yao and Neil Fullick; Editing by Mark Bendeich)

Source: http://us.rd.yahoo.com/dailynews/rss/economy/*http%3A//news.yahoo.com/s/nm/20111204/bs_nm/us_china_economy

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Sunday, December 4, 2011

Campaigns turning more to Web to link with voters (AP)

NEW YORK ? As they peruse the Internet, voters in New Hampshire and Iowa are probably seeing ads for Mitt Romney and President Barack Obama alongside those for shoes and holiday gifts. The ads will then follow those voters around the Web, popping up on news sites, Google searches and on social networking sites like Facebook.

Online advertising, once used primarily as a way to reach young and heavily wired consumers, has emerged as an essential communications tool in the 2012 presidential contest. While few expect Web ads to supplant television commercials anytime soon, strategists say online ads may be the most nimble, efficient and cost-effective way to reach voters.

"Online advertising cuts through because of its ability to target. It's unparalleled in any other medium," said Romney's digital director, Zac Moffatt. "TV may be more effective for driving a big message, but per usage, the Internet is more powerful. We are probably one presidential cycle from everyone believing that."

Web ads can take many forms, from small display boxes to clickable videos to 15- or 30-second commercials known as "pre-rolls" a viewer sees before the start of a news clip or YouTube video.

Targeting is key. While campaigns invest heavily in television ads to reach a mass audience, Web ads are geared specifically to people based on their ZIP code, demographics and, most importantly, their Internet browsing history.

That means someone who has visited the Obama campaign website will likely start seeing his ads on a number of different Web pages. And those who use Google to search for information on the Republican candidates might notice a Romney campaign pre-roll the next time they watch a TV show online.

Campaigns also buy ads on websites that cater to the different demographic groups the campaigns are hoping to reach.

"When someone expresses interest in politics online, it's an incredibly good time for the campaigns to talk to them," said Andrew Roos, a Google account leader who works with Democratic campaigns on Web ad strategy. "You want to grab people when they are paying attention and ask them to take another action, like send money or attend an offline event. It's an old-school organization principle that has been working its way online."

Campaigns were slow to adapt to online advertising even as the corporate world flocked to the Web with product ads years ago. Internet ad revenue climbed to nearly $7.9 billion in the third quarter of 2011, up 22 percent from the same time last year, according to the Internet Advertising Bureau, which tracks online ad spending.

Corporations now spend from 18 to 28 percent of their advertising budget online, while campaigns historically have spent no more than 5 percent.

Chris Talbot, a freelance campaign digital strategist, noted that big companies can devote considerable time, money and research to figuring out what works online and what doesn't. Campaigns don't have that luxury.

"There is no `next quarter' in politics, so campaigns usually revert to a template of what's worked in the past," he said.

In 2008, Obama and Republican presidential rival John McCain both did limited online campaign advertising. Web ads grew more prevalent in the 2010 midterm elections, when 85 of the top-spending House races and 600 interest groups bought display ads on Google.

To be sure, plenty of Internet users say they aren't thrilled with the proliferation of online ads, particularly those that follow them from site to site.

A USA Today/Gallup poll taken in late 2010 found 9 out of 10 respondents said they pay little attention to online ads. Two-thirds said they don't believe advertisers should be able to target them based on their past Web searches.

"The only way it works is on a mass scale. Most people ignore ads on the Web," said Aaron Shapiro, head of the digital marking firm HUGE.

Web ads' biggest advantage, many strategists say, is accountability.

"Online ads are very metric driven ? you can figure out how many impressions you got, how many people clicked, how many people signed up for an email address. All of that is calculated in real time," Google's Roos said. "It's much more efficient than direct mail and TV."

The Romney campaign's Moffatt said Web ads became part of the media strategy when officials there realized how much their own viewing habits had changed.

"Strategists here acknowledge they really don't watch live TV," Moffatt said.

___

Associated Press researcher Rhonda Shafner contributed to this report.

___

Follow Beth Fouhy on Twitter at http://www.twitter.com/bfouhy

Source: http://us.rd.yahoo.com/dailynews/rss/politics/*http%3A//news.yahoo.com/s/ap/20111203/ap_on_el_pr/us_online_campaign_ads

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Saturday, December 3, 2011

Josh Krajcik Steps Outside Comfort Zone for "Dirty Diana"


Josh Krajcik performed "Dirty Diana" on The X Factor last night. At least we think he did. With all the staging and sound mixing and choreography, it was legitimately difficult to hear the singer throughout this rendition.

Which is too bad because we adore Josh. Remember last week's cover of "Wild Horses?" Great stuff.

"That was the first time I’ve seen you step out of your comfort zone. But you landed on your feet," LA Reid told the only over-30 crooner remaining in the competition.

Do you concur? Watch Krajcik's latest now:

Source: http://www.thehollywoodgossip.com/2011/12/josh-krajcik-steps-outside-comfort-zone-for-dirty-diana/

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DigiTimes: Acer eyes ultrabook price drop for next year, bigger cuts coming in 2013

Having recently affirmed its commitment to the netbook, Acer is now reportedly looking to boost its ultrabook sales, with the help of a handsome price cut. Citing company president Jim Wong, DigiTimes reports that Acer will slash the price of its ultrabook offerings by as much as 20 percent next year, dropping them from around $1,000 to between $800 and $900. The cut, expected to go into effect during Q2 2012, will be followed by a subsequent reduction to $500 in 2013, when Acer expects more vendors to enter the market. The hope is that the manufacturer will be able to reclaim some of the ground it's lost to competitors in recent months, though it remains to be seen whether or not the strategy pays dividends.

DigiTimes: Acer eyes ultrabook price drop for next year, bigger cuts coming in 2013 originally appeared on Engadget on Thu, 01 Dec 2011 19:11:00 EDT. Please see our terms for use of feeds.

Permalink   |  sourceDigiTimes  | Email this | Comments

Source: http://www.engadget.com/2011/12/01/digitimes-acer-eyes-ultrabook-price-drop-for-next-year-bigger/

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Friday, December 2, 2011

How-To: Manually flash the OTA to your Galaxy Nexus

Galaxy Nexus

With the OTA slowly rolling out today for the Galaxy Nexus, it's always nice to have a way to manually apply it.  Things have changed a bit from how it used to be done, but Alex, Phil, and myself have been fooling around and have a method figured out to give yourself the OTA with no waiting.  Fair warning -- this requires an OEM unlocked phone, fastboot drivers, and a few command line commands.

Download the OTA package direct from Google.  Then, download the latest ClockWorkMod recovery here.  Store both these files on your computer desktop.

If you haven't already, OEM unlock your Galaxy Nexus bootloader.  Here's a handy guide for Windows 7.  Note that this erases everything on your phone. (So hopefully you've done this already.)

  • Copy the OTA package above to the /sdcard folder on your Galaxy Nexus
  • Drop the ClockWorkMod file in the same folder you have fastboot in on your computer.  Rename it to cwm.img to make things easy.
  • Reboot your Galaxy Nexus to bootloader mode (hold volume up and volume down, then press power).
  • Plug your phone into your computer, and open a command prompt or terminal.  Navigate to the folder with fastboot and the cwm.img inside it.
  • At the command line, type the following: fastboot-windows.exe boot cwm.img (or just fastboot.exe if that's what you've got)
  • Use the ClockWorkMod recovery menu to flash a zip file from the SD card, and choose the OTA zip file you downloaded earlier.

When finished, reboot as normal and enjoy the OTA.  See why everyone loves fastboot?  This made no permanant change to your recovery, and without it we'd have to wait for the OTA to push to us all.  Alex reports that the volume bug is fixed in his unit when booted up and running, and all went smoothly.  If you feel uncomfortable doing this -- or if you're in the U.S. or other area not affected by 900MHz shenanigans -- just sit tight and wait for the OTA.  And if you have any questions, jump in the forums for help.



Source: http://feedproxy.google.com/~r/androidcentral/~3/BxE2g-4-D5s/story01.htm

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Accused California hair salon gunman pleads not guilty (Reuters)

LOS ANGELES (Reuters) ? A man accused of killing eight people during a shooting spree at a Southern California hair salon in October pleaded not guilty on Tuesday to murder and attempted murder charges.

Scott Evans Dekraai, 42, entered his plea during a brief appearance in Orange County Superior Court at which a judge also set a preliminary hearing for April in the high-profile case.

Prosecutors are seeking the death penalty against Dekraai, who is charged with eight counts of first-degree murder and one count of attempted murder in the worst mass killing in Orange County history.

The former tug boat mate is accused of opening fire at the Salon Meritage in the coastal community of Seal Beach last month, killing his former wife and seven other people and critically injuring a 73-year-old woman.

Deputy Public Defender Scott Sanders told Orange County Superior Court Judge Erick Larsh that he may seek a postponement of the preliminary hearing if he can't adequately prepare in time for the complicated death penalty case.

A judge will determine following that hearing if Dekraai should be bound over for trial.

"We will be ready. We want the case to proceed as quickly as possible so that these families can get justice and some closure to their pain," Orange County District Attorney's spokeswoman Susan Kang Schroeder said.

At the start of the hearing Larsh rejected a request by the defense to bar cameras from the courtroom. Sanders had argued that allowing televised coverage of the proceedings could hurt Dekraai's chances at a getting a fair trial.

Prosecutors say Dekraai was seeking revenge against ex-wife Michelle Fournier in a bitter custody dispute over their 8-year-old son when he walked into Salon Meritage carrying three handguns and opened fire.

Killed were Fournier, 48, salon owner Randy Fannin, 62, and six other people.

Harriet Stretz, 73, who was in a chair having her hair styled by her daughter, Laura Lee Elody, at the time of the shooting, survived her wounds. Elody, 46, was among the dead.

Dekraai was arrested just blocks from the bloody scene in Seal Beach, a bucolic beachside community about 20 miles southeast of Los Angeles that had experienced only four homicides in the past decade.

(Editing by Jerry Norton and Cynthia Johnston)

Source: http://us.rd.yahoo.com/dailynews/rss/us/*http%3A//news.yahoo.com/s/nm/20111129/us_nm/us_shooting_hairsalon

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Monday, November 28, 2011

Scientists identify defect in brain cell channel that may cause autism-like syndrome

Scientists identify defect in brain cell channel that may cause autism-like syndrome [ Back to EurekAlert! ] Public release date: 27-Nov-2011
[ | E-mail | Share 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)


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Scientists identify defect in brain cell channel that may cause autism-like syndrome [ Back to EurekAlert! ] Public release date: 27-Nov-2011
[ | E-mail | Share 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)


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Source: http://www.eurekalert.org/pub_releases/2011-11/sumc-sid112311.php

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Letters: Debt 'supercommittee' let down country

If I went to my boss and told him I couldn't get a job done, I am sure he would find someone who could. I would expect this ("Panel's inability to cut debt deal reflects divide").

  • Capitol : House Speaker John Boehner, right, and Senate Majority Leader Harry Reid.

    By Mark Wilson, Getty Images

    Capitol : House Speaker John Boehner, right, and Senate Majority Leader Harry Reid.

By Mark Wilson, Getty Images

Capitol : House Speaker John Boehner, right, and Senate Majority Leader Harry Reid.

The 12 senators and representatives on the "supercommittee" should tender their resignations because they have failed this country. Instead, because there are no term limits, they will probably be re-elected.

Thanks for nothing, Congress.

Willson Blake; Savannah, Ga.

Political gain trumps progress

My challenge to both House Speaker John Boehner (" 'I did everything possible' ") and Majority Leader Harry Reid ("Democrats backed balanced plan") is to introduce, as legislation, the parts of the proposals they supposedly supported in the supercommittee negotiating room.

However, they won't because they favor political gain over any benefit for our country. Proof we no longer elect statesmen and women who put the interest of the country over political or special interests.

Larry Nielsen; Benton Harbor, Mich.

Letters to the editor

USA TODAY receives about 300 letters each day. Most arrive via e-mail, but we also receive submissions by postal mail and fax. We publish about 35 letters each week.

We often select comments that respond directly to USA TODAY articles or opinion pieces. Letters that are concise and make one or two good points have the best chance of being selected, as do letters that reflect the vibrant debate around the nation on a particular subject.

We aim to make the letters platform a place where readers, not just writers representing institutions or interest groups, have their say.

Time to Occupy Congress

A good first step in cutting the federal deficit would be to start with Congress itself. Once again, this privileged club of incompetent adolescents has demonstrated it lacks the ability to organize even a one car-funeral or a two team tournament.

Occupy Wall Street activists should focus on Congress. Occupy Congress. Demand term limits. Outlaw lobbyists. End government by bribery. Reduce the salaries and princely perks of everyone in Congress and their staff because they certainly do not earn their current paychecks.

Philip J. Brunskill; Mayville, N.Y.

Elect true leaders to office

The demagoguery and finger-pointing coupled with the very sincere self-righteous indignation expressed by members of Congress from both parties is beyond disheartening.

However, the American people have only themselves to blame for the current situation. We voted these non-leader/non-decision-makers into office. Perhaps it's time to vote them all out, Democrat or Republican. We need real leadership and courage.

Frederick Creamer; Lancaster, Pa.

Problem of partisanship

This failure to act by these committee members is no surprise to most Americans. The members of the committee are not Americans; they are just Democrats (stubborn donkeys) and Republicans (flat-footed elephants).

We shouldn't have expected them to put the best interest of America first!

Joanne Sheppard; Long Beach, Calif.

For more information about reprints & permissions, visit our FAQ's. To report corrections and clarifications, contact Standards Editor Brent Jones. For publication consideration in the newspaper, send comments to letters@usatoday.com. Include name, phone number, city and state for verification. To view our corrections, go to corrections.usatoday.com. We've updated the Conversation Guidelines. Changes include a brief review of the moderation process and an explanation on how to use the "Report Abuse" button. Read more.

Source: http://rssfeeds.usatoday.com/~r/News-Opinion/~3/gf4DNuKqX5E/1

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