Tuesday, July 3, 2012

What Is the Fibonacci Sequence, and Why Is It Famous?

Features | More Science

The Math Dude: Quick & Dirty Tips to Make Math Simpler


Scientific American presents Math Dude by Quick & Dirty Tips. Scientific American and Quick & Dirty Tips are both Macmillan companies.

It?s not often someone suggests that knowing some math could make you the life of the party, but that?s exactly what I?m going to do. Yes, a properly timed delivery of a few fun facts about the famed Fibonacci sequence just might leave your friends clamoring for more?because it really is that cool. So, without further ado, let?s continue our exploration of sequences that we began a few articles ago by jumping right in and talking about Fibonacci?s famous sequence.

Review of Mathematical Sequences
As we?ve discussed, sequences in math are fairly simple things?they?re just lists of numbers arranged in some particular order. The number of sequences that can be written is infinite since any random list of numbers will do. But some types of sequences are decidedly non-random?one of which being the geometric sequence. In such a sequence, each element is obtained from the previous one by multiplying it by the same fixed number. For example: 2, 4, 8, 16, 32, is a geometric sequence where each successive element is obtained by multiplying the previous one by 2.


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Blake wins 200 meters, goes 2 for 2 vs Bolt

Sprinter Yohan Blake, far right, crosses the finish line ahead of world-record holder Usain Bolt, second from left, Nickel Ashmeade, center, Warren Weir, left, and Jason Young to win the 200m final at Jamaica's Olympic trials in Kingston, Jamaica, Sunday, July 1, 2012. Blake edged Bolt by 0.03 finishing in 19.80 seconds. (AP Photo/Collin Reid)

Sprinter Yohan Blake, far right, crosses the finish line ahead of world-record holder Usain Bolt, second from left, Nickel Ashmeade, center, Warren Weir, left, and Jason Young to win the 200m final at Jamaica's Olympic trials in Kingston, Jamaica, Sunday, July 1, 2012. Blake edged Bolt by 0.03 finishing in 19.80 seconds. (AP Photo/Collin Reid)

World-record holder Usain Bolt looks at the crowd while getting his right hamstring stretched out after loosing to fellow country man Yohan Blake in the 200m final at Jamaica's Olympic trials in Kingston, Jamaica, Sunday, July 1, 2012. Blake edged Bolt by 0.03 finishing in 19.80 seconds. (AP Photo/Collin Reid)

World-record holder Usain Bolt gets his right hamstring stretched out after loosing to fellow country man Yohan Blake in the 200m final at Jamaica's Olympic trials in Kingston, Jamaica, Sunday, July 1, 2012. Blake edged Bolt by 0.03 finishing in 19.80 seconds. (AP Photo/Collin Reid)

Sprinter Yohan Blake is about to put on a new shirt after winning the 200m final of the Jamaica's Olympic trials in Kingston, Jamaica, Sunday, July 1, 2012. Blake edged world-record holder Usain Bolt by 0.03 finishing in 19.80 seconds. (AP Photo/Collin Reid)

Sprinter Yohan Blake gestures to the crowd after winning the 200m final at Jamaica's Olympic trials in Kingston, Jamaica, Sunday, July 1, 2012. Blake edged world-record holder Usain Bolt by 0.03 finishing in 19.80 seconds. (AP Photo/Collin Reid)

(AP) ? No posing, no salutes, no fist pumping. First, Yohan Blake fell to both knees and rested his head on the track. A bit later, he simply paced in front of the jam-packed grandstand at National Stadium and stared into the crowd, letting all those fans soak in a nice, long look.

This, ladies and gentlemen, is the man to beat at the London Olympics.

In a result that no longer feels like a surprise, Blake beat Usain Bolt in the 200 meters at the Jamaican Olympic trials Sunday, finishing in 19.80 seconds to edge the world-record holder by 0.03.

When it was over, Bolt was the first one to approach his training partner and buddy and give him a big bear hug. Moments later, Bolt was down on the ground, getting his right hamstring stretched out, while Blake was going through his understated celebration. At one point, he raised one finger to his mouth, as if asking everyone to "shhhhh." But the fans didn't listen. They now have not one, but two, legitimate gold medal prospects for the men's sprints in London.

"Usain always gives me a lot of encouragement and tells me to keep coming to this race," Blake said about the 200.

Boy, did he.

The win came two days after Blake, the reigning world champion at 100 meters, beat Bolt in the 100 by running a personal-best 9.75.

That was a shocker, but there were explanations ? most notably the terrible starts Bolt got off to throughout the 100 heats and in the final, to say nothing of any doubt that might still linger over the false start that scratched him from worlds last year.

Bolt has always considered the 200, which better suits his lanky 6-foot-5 frame, his real work. And now, indeed, he has work to do there, as well.

As they approached the finish, Bolt was grimacing ? or was that the hint of a frustrated smile? ? as he looked to his left to see what very few thought possible earlier this week: Blake beating him to the line for the second time in three days.

"I can never be discouraged," Bolt said. "I'm never worried until my coach gets worried, and my coach isn't worried, so I'm OK."

Said Glen Mills, who coaches both runners: "Usain, he has the experience, the ability, he has been there already. He might be a little off at the moment, but I'm sure when the time of delivery comes around, he'll be on top of his game."

The clock is ticking. As of Sunday, there were 34 days until the start of the men's 100 heats at Olympic Stadium.

In the women's 200, Shelly-Ann Fraser-Pryce ran a personal best 22.10 seconds to also complete the 100-200 sweep. She'll be joined by Sherone Simpson and two-time defending Olympic champion Veronica Campbell-Brown.

Fraser-Pryce took the world by surprise four years ago when she won the 100 at Beijing. Her next act could be this 200, her second-best event, where she beat Simpson with lots of room to spare, a 0.27-second margin.

"I'm still learning, you know," Fraser-Pryce said.

Even at that, Fraser-Pryce and the rest of the Jamaicans have some ground to make up. At U.S. trials this weekend, Allyson Felix won the 200 final, also in a personal best of 21.69 seconds.

"I'm happy for Allyson," said Campbell-Brown, who finished third in 22.42. "That's a very good time for her. And the faster we run, the sweeter it will be at the Olympic Games, because anyone who wins that will have to run very, very fast."

While word of Felix's mark had been swirling around Jamaica for about 24 hours, details of Blake's victory were just working their way to the States, where Wallace Spearmon won the 200 in 19.82 seconds Sunday.

"Honestly, I figured they'd run about 19.5 or 19.6 today," Spearmon said. "You caught me off guard a little. Not a bad thing, but I didn't know."

Now, the guessing game figures to take on Olympics-sized proportions.

Blake, Bolt and Mills all conceded that Blake came into these trials in better shape than the man whose marks ? 9.58 and 19.19 ? sit atop the record book.

So, was Bolt genuinely just coasting through this weekend in front of all his home fans, making sure he made it, getting ready to defend his Olympic titles? Is his conditioning not up to snuff, and if so, is there time for him to get there? Or, might he be hurting, as it appeared when he was getting his leg worked on while lying on the track?

"I don't want to get into that," Bolt said. "I was just working (the leg) around for a few moments to get myself back together. I'm not far off. I can get it done."

Blake will be making his first trip to the Olympics, which can be a daunting prospect. After these pair of benchmark victories, he sounded ready for more work, not a celebration.

"It leaves me to get back into training," Blake said. "It's not over. I still have the Olympics to go."

On the other hand, if Bolt was feeling any sense that he had it made ? well, he no longer has to worry about that.

He said Sunday's race was lost in the curve ? the same curve Blake has been watching Bolt run for the past several months in practice, picking up tips, learning the nuances.

"I was very sad with my turn, it was awful, but I've been working more on the 100 meters," Bolt said. "I can't blame it on that, though. Just have to get my things together and get it done."

After Bolt's bad curve, he came into the straightaway with a deficit. Finally, over the last 50 meters, the Olympic champion started closing.

Like a racecar driver catching a glimpse of something lurking in his rearview mirror, Blake could see Bolt making up ground out of the corner of his eye.

The best ones know how to close things out.

"I felt him on my right-hand side. No need to panic," Blake said. "I just stayed focused."

___

Associated Press Writers Pat Graham in Eugene, Ore., and David McFadden in Kingston contributed to this report.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2012-07-01-ATH-Jamaica%20Trials/id-fb80b79347ca458ca3e8f54621a72b96

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Monday, July 2, 2012

Palestinians detain dozens in weapons crackdown

[ [ [['Connery is an experienced stuntman', 2]], 'http://yhoo.it/KeQd0p', '[Slideshow: See photos taken on the way down]', ' ', '630', ' ', ' ', ], [ [['Connery is an experienced stuntman', 7]], ' http://yhoo.it/KpUoHO', '[Slideshow: Death-defying daredevils]', ' ', '630', ' ', ' ', ], [ [['know that we have confidence in', 3]], 'http://yhoo.it/LqYjAX ', '[Related: The Secret Service guide to Cartagena]', ' ', '630', ' ', ' ', ], [ [['We picked up this other dog and', 5]], 'http://yhoo.it/JUSxvi', '[Related: 8 common dog fears, how to calm them]', ' ', '630', ' ', ' ', ], [ [['accused of running a fake hepatitis B', 5]], 'http://bit.ly/JnoJYN', '[Related: Did WH share raid details with filmmakers?]', ' ', '630', ' ', ' ', ], [ [['accused of running a fake hepatitis B', 3]], 'http://bit.ly/KoKiqJ', '[Factbox: AQAP, al-Qaeda in Yemen]', ' ', '630', ' ', ' ', ], [ [['have my contacts on or glasses', 3]], 'http://abcn.ws/KTE5AZ', '[Related: Should the murder charge be dropped?]', ' ', '630', ' ', ' ', ], [ [['have made this nation great as Sarah Palin', 5]], 'http://yhoo.it/JD7nlD', '[Related: Bristol Palin reality show debuts June 19]', ' ', '630', ' ', ' ', ], [ [['have made this nation great as Sarah Palin', 1]], 'http://bit.ly/JRPFRO', '[Related: McCain adviser who vetted Palin weighs in on VP race]', ' ', '630', ' ', ' ', ], [ [['A JetBlue flight from New York to Las Vegas', 3]], 'http://yhoo.it/GV9zpj', '[Related: View photos of the JetBlue plane in Amarillo]', ' ', '630', ' ', ' ', ], [ [['the 28-year-old neighborhood watchman who shot and killed', 15]], 'http://news.yahoo.com/photos/white-house-stays-out-of-teen-s-killing-slideshow/', 'Click image to see more photos', 'http://l.yimg.com/cv/ip/ap/default/120411/martinzimmermen.jpg', '630', ' ', 'AP', ], [ [['He was in shock and still strapped to his seat', 6]], 'http://news.yahoo.com/photos/navy-jet-crashes-in-virginia-slideshow/', 'Click image to see more photos', 'http://l.yimg.com/cv/ip/ap/default/120406/jet_ap.jpg', '630', ' ', 'AP', ], [ [['xxxxxxxxxxxx', 11]], 'http://news.yahoo.com/photos/russian-grannies-win-bid-to-sing-at-eurovision-1331223625-slideshow/', 'Click image to see more photos', 'http://l.yimg.com/a/p/us/news/editorial/1/56/156d92f2760dcd3e75bcd649a8b85fcf.jpeg', '500', ' ', 'AP', ] ]

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Source: http://news.yahoo.com/palestinians-detain-dozens-weapons-crackdown-062118303.html

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Potential treatment target identified in an animal model of pancreatic cancer

Potential treatment target identified in an animal model of pancreatic cancer [ Back to EurekAlert! ] Public release date: 1-Jul-2012
[ | E-mail | Share Share ]

Contact: Sue McGreevey
smcgreevey@partners.org
617-724-2764
Massachusetts General Hospital

Analyzing circulating tumor cells reveals signaling pathway that may be essential to spread of deadly tumor

Detailed analysis of genes expressed in circulating tumor cells (CTCs) -- cells that break off from solid tumors and travel through the bloodstream -- has identified a potential treatment target in metastatic pancreatic cancer. In a report that will appear in Nature and has received advance online publication, Massachusetts General Hospital (MGH) Cancer Center investigators describe finding increased expression of WNT2, a member of a known family of oncogenes, in CTCs from a mouse model of the deadly tumor and from human patients. The researchers were able to capture the CTCs - present in the bloodstream at extremely low levels - using a microchip-based device previously developed by members of the team.

"This proof of principle study is the first to show that, by studying both mouse and human pancreatic cancer cells captured with this device, we can dissect genes that are overexpressed in these cells and identify signaling pathways that allow them to survive in the bloodstream," says Daniel Haber, MD, PhD, director of the MGH Cancer Center and senior author of the Nature paper. "We also found that targeting a key step in these pathways can reduce metastatic potential, which is critically important for control of pancreatic cancer. This study would not have been possible without a way to isolate rare CTCs from both mouse models and human patients."

Using the second-generation version of the CTC-chip, developed in collaboration with the MGH Center for Engineering in Medicine, the researchers first captured CTCs from mice genetically programmed to develop pancreatic cancer, one of the most deadly tumors since it is rarely diagnosed before spreading. Analysis of RNA expression levels in pancreatic CTCs, in primary tumor cells, and in normal pancreatic tissue identified several genes with significantly increased expression in the CTCs. One of these, WNT2, belongs to a family of developmental genes often overexpressed in cancer, and while the gene's expression in pancreatic tumors was higher than in normal tissue, WNT2 expression was significantly more elevated in both CTCs and metastatic cells.

Closer analysis of cells from several individual animals confirmed that WNT2 was highly expressed in pancreatic cancer CTCs and in metastases, but WNT2-expressing cells were found to be rare in primary tumors. Testing the consequences of WNT2 expression indicated that cancer cells expressing the gene were more likely to generate metastases, probably because of an improved ability to survive after dislodging from the primary tumor and entering the bloodstream.

The researchers tested several agents known to inhibit the activity of molecules in the WNT2 pathway their results implied was associated with pancreatic cancer and found that inhibition of TGF-beta activated kinase 1 (TAK1) prevented metastasis-associated activities in cultured CTCs. Knocking down TAK1 expression with RNA interference also reduced the development of metastasis in mice injected with WNT2-expressing CTCs. A significant percentage of tested CTCs from patients with metastatic pancreatic cancer were found to express WNT-related genes, along with other components of the signaling pathway associated with pancreatic cancer in the mouse model.

"The picture in more complicated in humans, since multiple WNTs are upregulated," Haber says. "But the TAK1 inhibitor we tested appears to have an effect on diverse WNT pathways involved in the survival of pancreatic CTCs. We previously reported that TAK1 inhibition has promise for treating a genetically defined subset of colon cancers, and these findings now extend the relevance of the TAK1 pathway to suppression of blood-borne metastasis in pancreatic cancer. Considerable more work will be needed to fully understand the critical pathways involved, but it is our hope that TAK1 inhibitors will ultimately be developed for clinical testing."

###

Haber is the Kurt Isselbacher/Peter Schwartz Professor of Oncology at Harvard Medical School and a Howard Hughes Medical Institute investigator. Co-lead authors of the Nature report are Min Yu, PhD, and David Ting, MD, PhD, MGH Cancer Center. Additional co-authors include Shyamala Maheswaran, PhD, Ben Wittner, PhD, Sridhar Ramaswamy, MD, Nabeel Bardeesy, PhD, and Lecia Sequist, MD, MGH Cancer Center; and Shannon Stott, PhD, and Mehmet Toner, PhD, MGH Center for Engineering in Medicine. The study was supported by grants from Stand Up to Cancer, the Howard Hughes Medical Institute, the National Institute of Biomedical Imaging and Bioengineering, the National Institutes of Health, the Pancreatic Cancer Action Network and the Warshaw Institute for Pancreatic Cancer Research.

Massachusetts General Hospital (www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.


[ Back to EurekAlert! ] [ | E-mail | Share 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.


Potential treatment target identified in an animal model of pancreatic cancer [ Back to EurekAlert! ] Public release date: 1-Jul-2012
[ | E-mail | Share Share ]

Contact: Sue McGreevey
smcgreevey@partners.org
617-724-2764
Massachusetts General Hospital

Analyzing circulating tumor cells reveals signaling pathway that may be essential to spread of deadly tumor

Detailed analysis of genes expressed in circulating tumor cells (CTCs) -- cells that break off from solid tumors and travel through the bloodstream -- has identified a potential treatment target in metastatic pancreatic cancer. In a report that will appear in Nature and has received advance online publication, Massachusetts General Hospital (MGH) Cancer Center investigators describe finding increased expression of WNT2, a member of a known family of oncogenes, in CTCs from a mouse model of the deadly tumor and from human patients. The researchers were able to capture the CTCs - present in the bloodstream at extremely low levels - using a microchip-based device previously developed by members of the team.

"This proof of principle study is the first to show that, by studying both mouse and human pancreatic cancer cells captured with this device, we can dissect genes that are overexpressed in these cells and identify signaling pathways that allow them to survive in the bloodstream," says Daniel Haber, MD, PhD, director of the MGH Cancer Center and senior author of the Nature paper. "We also found that targeting a key step in these pathways can reduce metastatic potential, which is critically important for control of pancreatic cancer. This study would not have been possible without a way to isolate rare CTCs from both mouse models and human patients."

Using the second-generation version of the CTC-chip, developed in collaboration with the MGH Center for Engineering in Medicine, the researchers first captured CTCs from mice genetically programmed to develop pancreatic cancer, one of the most deadly tumors since it is rarely diagnosed before spreading. Analysis of RNA expression levels in pancreatic CTCs, in primary tumor cells, and in normal pancreatic tissue identified several genes with significantly increased expression in the CTCs. One of these, WNT2, belongs to a family of developmental genes often overexpressed in cancer, and while the gene's expression in pancreatic tumors was higher than in normal tissue, WNT2 expression was significantly more elevated in both CTCs and metastatic cells.

Closer analysis of cells from several individual animals confirmed that WNT2 was highly expressed in pancreatic cancer CTCs and in metastases, but WNT2-expressing cells were found to be rare in primary tumors. Testing the consequences of WNT2 expression indicated that cancer cells expressing the gene were more likely to generate metastases, probably because of an improved ability to survive after dislodging from the primary tumor and entering the bloodstream.

The researchers tested several agents known to inhibit the activity of molecules in the WNT2 pathway their results implied was associated with pancreatic cancer and found that inhibition of TGF-beta activated kinase 1 (TAK1) prevented metastasis-associated activities in cultured CTCs. Knocking down TAK1 expression with RNA interference also reduced the development of metastasis in mice injected with WNT2-expressing CTCs. A significant percentage of tested CTCs from patients with metastatic pancreatic cancer were found to express WNT-related genes, along with other components of the signaling pathway associated with pancreatic cancer in the mouse model.

"The picture in more complicated in humans, since multiple WNTs are upregulated," Haber says. "But the TAK1 inhibitor we tested appears to have an effect on diverse WNT pathways involved in the survival of pancreatic CTCs. We previously reported that TAK1 inhibition has promise for treating a genetically defined subset of colon cancers, and these findings now extend the relevance of the TAK1 pathway to suppression of blood-borne metastasis in pancreatic cancer. Considerable more work will be needed to fully understand the critical pathways involved, but it is our hope that TAK1 inhibitors will ultimately be developed for clinical testing."

###

Haber is the Kurt Isselbacher/Peter Schwartz Professor of Oncology at Harvard Medical School and a Howard Hughes Medical Institute investigator. Co-lead authors of the Nature report are Min Yu, PhD, and David Ting, MD, PhD, MGH Cancer Center. Additional co-authors include Shyamala Maheswaran, PhD, Ben Wittner, PhD, Sridhar Ramaswamy, MD, Nabeel Bardeesy, PhD, and Lecia Sequist, MD, MGH Cancer Center; and Shannon Stott, PhD, and Mehmet Toner, PhD, MGH Center for Engineering in Medicine. The study was supported by grants from Stand Up to Cancer, the Howard Hughes Medical Institute, the National Institute of Biomedical Imaging and Bioengineering, the National Institutes of Health, the Pancreatic Cancer Action Network and the Warshaw Institute for Pancreatic Cancer Research.

Massachusetts General Hospital (www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.


[ Back to EurekAlert! ] [ | E-mail | Share 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.


Source: http://www.eurekalert.org/pub_releases/2012-07/mgh-ptt062912.php

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Barclays chairman quits after rate-rigging scandal

By Steve Slater

LONDON (Reuters) - Barclays Plc Chairman Marcus Agius quit on Monday, saying "the buck stops with me" after an interest rate rigging scandal dealt "a devastating blow" to the bank's reputation.

Agius, chairman for 5-1/2 years, is the first major scalp from the scandal, which is likely to draw in more banks and potentially the regulatory authorities, but his resignation did not take the heat off Chief Executive Bob Diamond, who is under pressure to go, too.

"The buck in Barclays stops with Bob Diamond, and it is Bob Diamond who must accept responsibility," said John Mann, a Labor politician who is part of a panel of lawmakers who will grill Diamond on Wednesday and Agius on Thursday.

"He (Diamond) must resign. He's got to go. There is no role for people like him if banking is to be trusted again in this country and if British banking is to restore its tarnished reputation in the world, which of course is of great importance to our economy," Mann said on Sky News.

Diamond and Agius have also faced calls from some shareholders to resign after Barclays was last week fined $453 million by British and U.S. regulators for submitting inaccurate submissions on the Libor interest rate.

"I still think it is going to be hard for Bob Diamond to keep his job. I don't think he has built up enough shareholder goodwill in the past to be able to ride this one out," said a top 25 investor in the bank, who asked not to be named.

Barclays has admitted that some of its traders attempted to manipulate the setting of the London interbank offered rate (Libor), which is used worldwide as a benchmark for setting prices on about $350 trillion of derivatives and other financial products.

"Last week's events - evidencing as they do unacceptable standards of behavior within the bank - have dealt a devastating blow to Barclays reputation ... The buck stops with me, and I must acknowledge responsibility by standing aside," Agius said in a statement.

When Diamond and Agius appear before the parliamentary committee this week they are likely to be quizzed on what the Bank of England (BoE) and other regulators knew.

Details released in documents last week could prove embarrassing to the BoE, after sources said a key conversation held in October 2008 cited in the documents was between Diamond and BoE Deputy Governor Paul Tucker.

Some people at Barclays mistakenly believed the bank had been granted permission to submit artificially low Libor estimates after that conversation, the documents released last week showed.

More than a dozen other banks are being investigated in the long-running global probe by authorities in North America, Europe and Japan, including Citigroup, HSBC, UBS and Royal Bank of Scotland. Analysts and bankers expect more big fines.

ROOT & BRANCH REVIEW

Barclays has admitted it submitted artificially low estimates of its borrowing costs from late 2007 to May 2009 because it thought rivals were doing the same and higher submissions would make it appear to be in trouble.

Between November 2007 and October 2008 some Barclays employees raised concerns with the British Bankers' Association - the UK banking lobby group that is also responsible for setting Libor - the Financial Services Authority, the BoE and the Federal Reserve Bank of New York regarding its concern that Libor rates were being set too low, U.S. Department of Justice documents said.

It said the employees did not provide "full and accurate information" to the authorities.

Barclays said it would launch an audit of its business practices, led by Michael Rake, its senior independent director, who will move up to deputy chairman.

"I am truly sorry that our customers, clients, employees and shareholders have been let down," Agius said.

The audit will undertake "a root and branch review of all of the past practices that have been revealed as flawed" and assess implications for its practices and culture. Diamond said its recommendations would be implemented in full.

Agius said Barclays had been "well served by an excellent executive team" under him, first led by John Varley and now by Diamond.

Agius became chairman at the start of 2007 after more than 30 years as an investment banker and then chairman at Lazard.

He is also BBA chairman, but that position is always drawn from one of the banks, so he is set to leave that position too.

(Additional reporting by Tim Castle and Sinead Cruise; editing by Anna Willard and Will Waterman)

Source: http://finance.yahoo.com/news/barclays-chair-quits-devastating-libor-061637797.html

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Chinese megacity limits new car sales

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Source: http://news.yahoo.com/chinese-megacity-limits-car-sales-134446603.html

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Samsung appeals Galaxy Nexus ban, of course

Samsung appeals Galaxy Nexus ban, of course

In a completely expected move, Samsung today filed to appeal the preliminary Galaxy Nexus ban granted to Apple last week, moving to stay the injunction. Among other claims, Samsung is arguing that the ban is "inconsistent with the Federal Circuit's directive that market share losses must be substantial," and, as Foss Patents puts it, "attributable to the 'infringing feature,' not just the presence of the infringing product on the market." This, of course, mirrors Samsung's appeal for the Galaxy Tab 10.1, which also had its US sales halted last week. The Federal Circuit could very well decide to stay, putting the devices back on store shelves, but until then, we imagine Sammy will be looking longingly at Posner's courtroom.

Samsung appeals Galaxy Nexus ban, of course originally appeared on Engadget on Sun, 01 Jul 2012 18:26:00 EDT. Please see our terms for use of feeds.

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Source: http://feeds.engadget.com/~r/weblogsinc/engadget/~3/X7p4wUu5N-Q/

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