Coldplay is looking to help support some youth charities in Los Angeles as the group is set to perform live at a special iHeartRadio concert next month.
The band will appear at Club Nokia on February 8, with proceeds benefiting A Place Called Home and Youth Mentoring Connection. The popular radio station teamed up with the two youth-based charities to help underprivileged youth and empower them with resources like adult mentors to help them reach their potential.
In addition to their charitable gesture, Coldplay will also be performing at this year's Grammy Awards ceremony alongside pop star Rihanna on Feb. 12.
LL Cool J to Host Grammys
For more information on how you can attend the iHeartRadio benefit concert, visit ticketmaster.com.
Mapping the destructive path from cigarette to emphysemaPublic release date: 18-Jan-2012 [ | E-mail | Share ]
Contact: Dipali Pathak pathak@bcm.edu 713-798-4710 Baylor College of Medicine
HOUSTON (Jan. 18, 2012) -- From the cherry red tip of a lighted cigarette through the respiratory tract to vital lung cells, the havoc created by tobacco smoke seems almost criminal, activating genes and portions of the immune system to create inflammation that results in life-shortening emphysema, said researchers led by those at Baylor College of Medicine and the Michael E. DeBakey Veterans Affairs Medical Center.
In a report online in the journal Science Translational Medicine, the scientists, including two from The University of Texas MD Anderson Cancer Center, described the track the toxic smoke takes through the tissues and how they accomplish their destructive work.
"It's like walking into a crime scene," said Dr. Farrah Kheradmand, professor of medicine and immunology at BCM and a senior author of the report. In their current work, the scientists took cells present in the "crime scene" apart, piece by piece to elucidate what occurred when, and how.
It is a complicated story that took more than four years for her, her co-senior author Dr. David Corry and members of their laboratories and colleagues in the Dan L. Duncan Cancer Center at BCM to unravel, she said. Corry is professor and chief of the section of immunology, allergy and rheumatology in the department of medicine at BCM and a member of the faculty at the Michael E. DeBakey VA Medical Center.
"Previously, emphysema was thought to be a non-specific injurious response to long-term smoke exposure," she said. "These studies show for the first time that emphysema is caused by a specific immune response induced by smoke."
"It is a combination of little genes affected by an epigenetic factor," she said. Epigenetics are factors that affect the way genes are expressed after DNA forms. Cigarette smoke is an environmental epigenetic factor.
"DNA is written in pen," said Kheradmand, using a metaphor. "Epigenetics is written in pencil. If you have enough genes affected by epigenetic factors strung together, it can tip you over into lung damage and emphysema. The inflammation that drives emphysema could also drive cancer development, a testable hypothesis that we have begun to pursue."
This study showed that the cigarette recruited antigen-presenting cells (cells that orchestrate the immune system's response to antigens) as co-conspirators in the lung-destroying crime, using specific genes that regulate proteins in their deadly role.
To uncover the cause of tobacco- induced emphysema, they studied mice exposed to conditions that closely simulated how humans smoke. These animals developed the lung disease in three to four months. Certain inflammatory cells and genes proving crucial to the process, she said.
For example, the cytokine interleukin-17 was critical. "When we removed IL-17 from the mice, they did not develop emphysema in the same time span," she said. "The number of a type of immune cell the gamma delta T-cell would increase dramatically in the crime scene of the lung, she said."
"But when we took them out, the inflammation worsened. The gamma delta T-cells went there to dampen the inflammation," she said. "When they become overwhelmed, the disease ensues."
They confirmed that a subset of antigen-presenting cells (cells that present antigen to activate the immune system) are the key to orchestrating the disease. They had first found these cells in studies of human lung tissue. Then, they duplicated that finding in mice.
Dr. Ming Shan, now a postdoctoral associate in Kheradmand's laboratory, then took the cells out of the lungs of the mice with disease and transferred into mice who had never been exposed to cigarette smoke. After three months, these mice showed inflammatory signs indicating that they were on the way to developing lung damage and emphysema.
When they analyzed "gene chips" to screen the disease-causing antigen-presenting cells recovered from lungs with emphysema, they uncovered the gene for osteopontin, which promotes initiation of the inflammatory cascade that damages lungs. Mice that lacked this gene were resistant to emphysema, said Kheradmand.
###
Others who took part in this work include Xiaoyi Yuan,Li-zhen Song, Luz Roberts, Nazanin Zarinkamar, Alexander Seryshev, Yiqun Zhang and Susan Hilsenbeck, all of BCM and Seon-Hee Chang and Chen Dong of MD Anderson.
Funding for this work came from a Veterans Affairs merit award and the National Institutes of Health.
For more information on basic science research at Baylor College of Medicine, please go to From the Lab.
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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.
Mapping the destructive path from cigarette to emphysemaPublic release date: 18-Jan-2012 [ | E-mail | Share ]
Contact: Dipali Pathak pathak@bcm.edu 713-798-4710 Baylor College of Medicine
HOUSTON (Jan. 18, 2012) -- From the cherry red tip of a lighted cigarette through the respiratory tract to vital lung cells, the havoc created by tobacco smoke seems almost criminal, activating genes and portions of the immune system to create inflammation that results in life-shortening emphysema, said researchers led by those at Baylor College of Medicine and the Michael E. DeBakey Veterans Affairs Medical Center.
In a report online in the journal Science Translational Medicine, the scientists, including two from The University of Texas MD Anderson Cancer Center, described the track the toxic smoke takes through the tissues and how they accomplish their destructive work.
"It's like walking into a crime scene," said Dr. Farrah Kheradmand, professor of medicine and immunology at BCM and a senior author of the report. In their current work, the scientists took cells present in the "crime scene" apart, piece by piece to elucidate what occurred when, and how.
It is a complicated story that took more than four years for her, her co-senior author Dr. David Corry and members of their laboratories and colleagues in the Dan L. Duncan Cancer Center at BCM to unravel, she said. Corry is professor and chief of the section of immunology, allergy and rheumatology in the department of medicine at BCM and a member of the faculty at the Michael E. DeBakey VA Medical Center.
"Previously, emphysema was thought to be a non-specific injurious response to long-term smoke exposure," she said. "These studies show for the first time that emphysema is caused by a specific immune response induced by smoke."
"It is a combination of little genes affected by an epigenetic factor," she said. Epigenetics are factors that affect the way genes are expressed after DNA forms. Cigarette smoke is an environmental epigenetic factor.
"DNA is written in pen," said Kheradmand, using a metaphor. "Epigenetics is written in pencil. If you have enough genes affected by epigenetic factors strung together, it can tip you over into lung damage and emphysema. The inflammation that drives emphysema could also drive cancer development, a testable hypothesis that we have begun to pursue."
This study showed that the cigarette recruited antigen-presenting cells (cells that orchestrate the immune system's response to antigens) as co-conspirators in the lung-destroying crime, using specific genes that regulate proteins in their deadly role.
To uncover the cause of tobacco- induced emphysema, they studied mice exposed to conditions that closely simulated how humans smoke. These animals developed the lung disease in three to four months. Certain inflammatory cells and genes proving crucial to the process, she said.
For example, the cytokine interleukin-17 was critical. "When we removed IL-17 from the mice, they did not develop emphysema in the same time span," she said. "The number of a type of immune cell the gamma delta T-cell would increase dramatically in the crime scene of the lung, she said."
"But when we took them out, the inflammation worsened. The gamma delta T-cells went there to dampen the inflammation," she said. "When they become overwhelmed, the disease ensues."
They confirmed that a subset of antigen-presenting cells (cells that present antigen to activate the immune system) are the key to orchestrating the disease. They had first found these cells in studies of human lung tissue. Then, they duplicated that finding in mice.
Dr. Ming Shan, now a postdoctoral associate in Kheradmand's laboratory, then took the cells out of the lungs of the mice with disease and transferred into mice who had never been exposed to cigarette smoke. After three months, these mice showed inflammatory signs indicating that they were on the way to developing lung damage and emphysema.
When they analyzed "gene chips" to screen the disease-causing antigen-presenting cells recovered from lungs with emphysema, they uncovered the gene for osteopontin, which promotes initiation of the inflammatory cascade that damages lungs. Mice that lacked this gene were resistant to emphysema, said Kheradmand.
###
Others who took part in this work include Xiaoyi Yuan,Li-zhen Song, Luz Roberts, Nazanin Zarinkamar, Alexander Seryshev, Yiqun Zhang and Susan Hilsenbeck, all of BCM and Seon-Hee Chang and Chen Dong of MD Anderson.
Funding for this work came from a Veterans Affairs merit award and the National Institutes of Health.
For more information on basic science research at Baylor College of Medicine, please go to From the Lab.
[ | 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.
KUALA LUMPUR, Malaysia ? Oil advanced above $101 a barrel Wednesday in Asia, buoyed by positive economic data from the world's top two crude consumers, China and the U.S.
Benchmark crude for February delivery was up 57 cents at $101.28 a barrel at late afternoon Kuala Lumpur time in electronic trading on the New York Mercantile Exchange. The contract jumped $2.01 to finish at $100.71 on Tuesday.
China, the world's second largest economy, reported 8.9 percent growth in the fourth quarter, slower than the previous quarter but robust enough to indicate it would avoid an abrupt slowdown. Retail and factory production improved while oil demand was up 6.4 percent in 2011 from 2010, according to data cited by Barclays Capital.
In the U.S., government data showed manufacturing in New York expanded at the fastest pace in nine months.
"The positive economic news out of China and the U.S. have increased optimism about global economic conditions and helped ease concern of a slowdown in oil demand," said Victor Shum, an energy analyst with Purvin & Gertz in Singapore.
Tension between Iran and Saudi Arabia, as well as a move by France to accelerate the EU's implementation of an embargo on Iranian oil export also supported prices, he said.
Saudi Oil Minister Ali al-Naimi has said Saudi Arabia wants to stabilize prices at $100 a barrel this year and was ready to pump more oil if needed. That came as Iran warned Gulf nations not to make up any shortfall and that it may shut the Strait of Hormuz which is used to transport about a fifth of the world's oil.
In other energy trading, heating oil rose 0.8 cent to $3.05 per gallon and gasoline futures rose 1.4 cents to $2.79 per gallon. Natural gas fell 0.8 cent to $2.48 per 1,000 cubic feet.
The Stop Online Piracy Act (SOPA) and the Protect IP Act (PIPA) are two bills that sound like they have a mildly positive aim but, in reality, have serious potential to negatively change the internet as we know it. While the Obama administration has come out against SOPA, effectively shelving it indefinitely, the very similar PIPA bill is still alive and well. Both SOPA and PIPA put power in the hands of the entertainment industry to censor sites that allegedly "engage in, enable or facilitate" copyright infringement. This language is vague enough to target sites you use every day, like Facebook and Google, making these bills a serious problem. Here's what you need to know about the bills and what you can do about them.
Due to the recent opposition of the Obama administration and focus changing to PIPA, we decided to make an update to this post to make it a bit more relevant. While SOPA is likely dead, we're explaining both bills as they're very similar.
What Are SOPA and PIPA All ABout, and Why Should I Care?
The idea behind these bills sounds reasonable. They came about in order to try and snuff out piracy online, as the entertainment industry is obviously not excited that many people are downloading their products without payment or permission. The issue is, however, that it doesn't really matter whether you're in support of piracy, against it, or just don't care. The methods are ineffective. Here's what they are and why they're problematic.
SOPA and PIPA were initially designed to do two things. The first was to make it possible for companies to block the domain names of web sites that are simply capable of, or seem to encourage copyright infringement. This would have been bad for everyone because such a measure doesn't actually prevent piracy. The reason that blocking a domain name isn't effective is because any blocked site can still be accessed via its numeric IP address. For example, if lifehacker.com were blocked, you could still find it by visiting a number-based address. In fact, before the bills were even supposed to come to a vote, tools were created to automatically route domain names to their IP addresses to completely render this measure of SOPA and PIPA useless. As a result, the IP-blocking provisions have been removed from both bills.
The other, still-active measure present in the SOPA and PIPA bills would allow rights holders to cut of the source of funding of any potentially infringing web site. This means any other companies doing business with this site would have to stop. Whether that means advertising, links in search engines, or any other listings would have to be removed.
There is, however, an important difference between SOPA and PIPA. SOPA targeted any site that contributed to copyright infringement, even if it was simply facilitating the act by providing a tool that could be used for illegal purposes (regardless of intention). PIPA, on the other hand, requires the targeted site to have no significant use beyond copyright infringement. Basically, PIPA can only be used to censor a site if it's more likely to be a source of illegal content than not. This is still problematic because a tool designed to accept user-generated content is, to some extent, at the whims of its users. If infringing content is found, rights holders already have the Digital Millenium Copyright Act (DMCA) to help them request the legal removal of that content. They also have the ability to sue infringers for damages, as we've previously seen with the Recording Industry Association of America (RIAA) when they, for example, sued a 12-year-old for downloading music. SOPA and PIPA provide a means to censor the tool that provided a means for the infringing content to exist on the internet rather than the content itself. This puts a lot of power in the hands of rights holders and has significant potential for abuse.
This is, of course, our interpretation of these bills. Because we love the internet and oppose censorship, we have an obvious bias. While we believe the right thing to do is to oppose these bills, you should make an informed decision on your own. For more information, please read the exact content of both the SOPA and PIPA bills.
What Can I Do About SOPA and PIPA?
Currently Twitter, Google, Reddit, Kickstarter, Tumblr, Mozilla, Yahoo, AOL, eBay, Zynga, Facebook, and several other sites have spoken out in opposition of SOPA and PIPA. In fact, many sites are censoring their logos (e.g. Google) or completely taking down their sites (e.g. Wikipedia) in protest on January 18th, 2012. There is incredible opposition to these bills because they don't just affect users like you, or small startups, but even very large companies with a large stake in the great things the internet and modern technology have to offer. If you'd like to join in your protest, there are a few things you can do.
First, call your congressperson on the phone. This is especially important if you live in a state with SOPA and/or PIPA supports or sponsors. Nonetheless, if your congresspeople do not support these bills you should still contact them to voice your support for their position.
Second, get the word out. Post this article, the American Censorship Day web site, or any other information about SOPA/PIPA on your social media accounts. Send emails to friends and family. If you oppose the bill, help others to understand why you believe they should oppose and encourage them to read more so they can make an informed choice.
Let's End the Fight and Start a Discussion
Finally, if you know a supporter or person in favor of SOPA and/or PIPA, have an open discussion. Myself and many others believe that the root of this problem stems from a lack of communication on both sides. Despite what my articles may suggest, I'm not a supporter of piracy. I do believe there is a compromise that both sides can reach with enough discussion, education, and understanding. It's important to remember that both the supporters and opposers of SOPA and PIPA have legitimate concerns. This should not be a fight but rather a cooperative discussion to find a solution. Whichever side you're on, please encourage a conversation that will move us towards change that is good for everyone rather than extreme measures that won't help anyone.
On Tuesday alone, the Republican presidential candidate branded Mitt Romney a liberal, said Newt Gingrich's policy positions have been "all over the place" and laughed that Ron Paul has been running for president "since 1938."
The more acerbic tone comes as the South Carolina primary looms on Saturday and with polls showing Santorum trailing Romney and other rivals.
In the effort to claw his way to the front of the pack, Santorum coupled his scathing critiques of his rivals on the campaign trail with a new TV ad that compares Romney to President Barack Obama.
"Obama supported the Wall Street bailouts. So did Romney. Obama gave us radical Obamacare that was based on Romneycare," the ad's narrator says. "Obama's a liberal on social issues. Romney once bragged he's even more liberal than Ted Kennedy on social issues."
The ad then asks: "Why would we ever vote for someone who is just like Obama?"
Santorum urged South Carolina conservatives to coalesce around one of their own.
"He's got a lot of money, but he doesn't have the convictions, the authenticity nor the record that is necessary to win this election," Santorum said.
He also said Gingrich wasn't the best conservative option.
"Newt is bold, but he is all over the place," Santorum said. "Attacking capitalism, supporting capitalism. Against global warming, for global warming."
Santorum, often sarcastic as a campaigner, offered this explanation for how Paul, 76, had bested him in the nation's first primary: "Congressman Paul had been running in New Hampshire for president since 1938."
HONG KONG ? British and Hong Kong leaders unveiled steps on Monday aimed at developing London into an international trading center for China's currency.
British Treasury chief George Osborne said in Hong Kong that his trip to Asia this week, which also includes stops in Beijing and Tokyo, furthers dialogue with Chinese authorities and Chinese and British banks "on establishing London as a new hub for the renminbi market as a complement to Hong Kong."
The Hong Kong Monetary Authority and the UK Treasury said a new private sector forum will work on tightening cooperation between Hong Kong and London, particularly on settlement systems, market liquidity and the development of renminbi financial products.
European and Chinese banks including HSBC Plc, Standard Chartered Plc, Bank of China Ltd., Deutsche Bank AG and Barclays Plc will take part in the forum, which will meet twice a year starting in May.
Osborne said he welcomed a recent announcement by the Hong Kong Monetary Authority to extend operating hours of its renminbi payments system that would make it easier for payments to be settled in London.
The moves follow an agreement in September by British and Chinese officials to back London's development as a renminbi trading hub.
Beijing is promoting the international use of the renminbi, also known as the yuan. It's also promoting Hong Kong, a semiautonomous Chinese territory with its own financial system and currency, as an offshore trading center for the yuan.
Last year, yuan-denominated bank deposits in Hong Kong doubled to 630 billion renminbi ($100 billion) as savers sought higher returns from the yuan, which has been strengthening 4-5 percent a year.
A market for yuan-denominated bonds has sprung up in Hong Kong, with foreign issuers including McDonald's, Caterpillar and the Asian Development Bank.
Beijing would like to see the currency become an alternative to the dollar, although tight capital controls limit its circulation overseas.
"It's clear that there's scope for substantial expansion of the renminbi market in coming years," said Osborne, who was speaking at a financial conference.
He said that in June 2011, China's share of world trade was 11 percent but the yuan's share of global foreign exchange trading last year was only 0.9 percent.
China has begun allowing companies to use yuan to settle international transactions. It has also signed currency swap deals recently with Pakistan, Thailand, South Korea and some other countries. Such deals would reduce costs for Chinese traders and might also increase the appeal of Chinese goods for foreign buyers with yuan to spend.
I'm happy to drive to get nominated for best picture and director....
but no albert brooks for supporting actor....???
jonah hill overrated.
who is Jim Broadbent?
glad to see gary oldman and carey mulligan get the nomination....
and senna....!!!
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Public release date: 18-Jan-2012
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The Stop Online Piracy Act (SOPA) and the Protect IP Act (PIPA) are two bills that sound like they have a mildly positive aim but, in reality, have serious potential to negatively change the internet as we know it. While the Obama administration has come out against SOPA, effectively shelving it indefinitely, the very similar PIPA bill is still alive and well. Both SOPA and PIPA put power in the hands of the entertainment industry to censor sites that allegedly "engage in, enable or facilitate" copyright infringement. This language is vague enough to target sites you use every day, like Facebook and Google, making these bills a serious problem. Here's what you need to know about the bills and what you can do about them. 
SOPA and PIPA were initially designed to do two things. The first was to make it possible for companies to block the domain names of web sites that are simply capable of, or seem to encourage copyright infringement. This would have been bad for everyone because such a measure doesn't actually prevent piracy. The reason that blocking a domain name isn't effective is because any blocked site can still be accessed via its numeric IP address. For example, if lifehacker.com were blocked, you could still find it by visiting a number-based address. In fact, before the bills were even supposed to come to a vote, tools were created to automatically route domain names to their IP addresses to completely render this measure of SOPA and PIPA useless. As a result, the IP-blocking provisions have been removed from both bills.
Currently Twitter, Google, Reddit, Kickstarter, Tumblr, Mozilla, Yahoo, AOL, eBay, Zynga, Facebook, and several other sites have spoken out in opposition of SOPA and PIPA. In fact, many sites are censoring their logos (e.g. Google) or completely taking down their sites (e.g. Wikipedia) in protest on January 18th, 2012. There is incredible opposition to these bills because they don't just affect users like you, or small startups, but even very large companies with a large stake in the great things the internet and modern technology have to offer. If you'd like to join in your protest, there are a few things you can do.