AAA??May. 11, 2013?1:12 PM ET America's Cup expected to go on after fatal wreck By PAUL ELIASBy PAUL ELIAS, Associated Press??
Stephen Barclay, center, CEO America's Cup Event Authority, speaks at a news conference, Friday, May 10, 2013, in San Francisco. At left is Iain Murray, Regatta Director and CEO, America's Cup Race Management and at right is Captain Matt Bliven of the United States Coast Guard. British Sailor Andrew Simpson died Thursday when Artemis Racing's AC72 catamaran, an America's Cup entry from Sweden, capsized during training in San Francisco Bay, trapping him underwater.(AP Photo/George Nikitin)
Stephen Barclay, center, CEO America's Cup Event Authority, speaks at a news conference, Friday, May 10, 2013, in San Francisco. At left is Iain Murray, Regatta Director and CEO, America's Cup Race Management and at right is Captain Matt Bliven of the United States Coast Guard. British Sailor Andrew Simpson died Thursday when Artemis Racing's AC72 catamaran, an America's Cup entry from Sweden, capsized during training in San Francisco Bay, trapping him underwater.(AP Photo/George Nikitin)
FILE - In this Aug. 21, 2008, file photo, gold medalist Andrew Simpson,of Britain, smiles during the medal ceremony for the Star class sailing competition of the 2008 Beijing Olympics in Qingdao, China, about 720 kilometers southeast of Beijing. Simpson died the Thursday, May 9, 2013, when Artemis Racing's AC72 catamaran, an America's Cup entry from Sweden, capsized during training in San Francisco Bay, trapping him underwater. (AP Photo/Herbert Knosowski, File)
Artemis Racing's 72-foot-long catamaran floats upside down at a Treasure Island dock on Friday, May 10, 2013, in San Francisco. Sailor Andrew "Bart" Simpson died the day before when the high-tech catamaran capsized during America's Cup training trapping him underwater. San Francisco's financial district is in the background, (AP Photo/Noah Berger)
SAN FRANCISCO (AP) ? The head of the America's Cup planning effort says he expects sailing's most prestigious event to go forward after the death of a sailor on a training run in the San Francisco Bay.
In an interview Saturday morning, Stephen Barclay said he would await the results of an internal examination of Thursday's accident before making the formal decision.
Andrew "Bart" Simpson was killed when he was trapped under the wreckage of the Artemis Racing sailboat that capsized during a training run. Barclay said investigators are expected to announce a probable cause of the wreck early next week.
The three teams vying to challenge Oracle Racing for sailing's most prestigious trophy are scheduled to begin racing in July.
KABUL, Afghanistan -- Senior American and Afghan officials held talks Saturday to try to iron out the details of a key pact signed a year ago that defines the future of the United States' commitment to Afghanistan.
The Strategic Partnership Agreement outlines a set of principles and general commitments for relations between Washington and Kabul after 2014, when foreign combat troops are to withdraw from Afghanistan. But there is lingering uncertainty over whether either party will be willing or able to stick to the provisions of the pact, which includes several loopholes for both nations.
The meeting Saturday in Kabul between U.S. Deputy Secretary of State William Burns and Afghan Foreign Minister Zalmai Rasoul is the second round of negotiations over how to implement the agreement, which was signed in May 2012 by President Barak Obama and Afghan President Hamid Karzai.
The deal spells out Washington's commitment to Afghanistan over the next 10 years as well as its expectations of Kabul, including free and fair presidential elections next year, pledges to fight corruption, improve efficiency and protect human rights, including women's rights.
Sticking points may include the amount of funds the U.S. provides to Afghan security forces. The two countries are also still squabbling over a separate agreement that would protect from prosecution a residual force of as many as 10,000 U.S. troops who would stay behind after the final withdrawal.
In remarks before Saturday's talks, Burns promised that Washington would stick by Afghanistan and its nascent national security forces after 2014 and the end to the international combat mission.
But the deal allows either country to opt out with a one year's notice, which means that Karzai's successor in next year's presidential elections could scuttle the agreement.
Karzai's election in 2009 was marred by widespread allegations of corruption, vote tampering and election fraud. He denied the charges but the acrimonious aftermath tainted his relationship with the West, which was the most vocal of his critics.
The pact emphasizes a free, fair and transparent election in 2014. Karzai however has been relentless in his criticism of U.S. involvement in Afghanistan's political process, alleging Washington was maneuvering secretly to strengthen his political opposition even though he cannot run for a third term.
Burns denied that Washington was backing any candidate to replace Karzai.
"We are supporting the process and not any particular candidate," he said, adding the elections next year should be "transparent, credible and inclusive."
Burns also repeated Washington's support for the opening of an office for the Taliban in Qatar to provide a venue where Karzai's High Peace Council could meet Taliban representatives to try to find a peaceful end to the 12-year war.
The Taliban have met representatives of about 30 countries, participated in international forums in Tokyo and France, and held backdoor talks with Afghanistan's opposition politicians. But they have steadfastly refused to meet Karzai's representatives including the High Peace Council, calling his government a "puppet."
Karzai recently accused the United States of trying to bring his political opponents and the Taliban together, an allegation the U.S. denied and Burns tried also to dispel in his opening remarks.
"We reaffirm our support for the office in Doha for the purpose of negotiation between the High Peace Council and the Taliban," Burns said.
The U.S. diplomat added that on the security front, Washington is on track to transfer full control of Afghanistan's security to Afghan forces by the end of the year.
There are 350,000 Afghan National Security Forces deployed throughout the country, although there has been criticism that the training, which was rarely more than two months, was inadequate and Karzai has often complained of a lack of military equipment to outfit his forces. NATO officials nonetheless say that this spring, when the weather allows more military activity, is the first of the 12-year war in which Afghan forces have done the majority of the fighting.
The next meeting is scheduled for Washington in October. Rasoul at the last meeting said he expected a conclusion of the talks within eight to 10 months but US is not giving a time frame.
As negotiations lumber along, Afghan analysts said it is difficult to foresee the results of an agreement signed almost one year ago.
"So far we haven't seen any practical steps forward from the Strategic Partnership Agreement," said analyst and former Parliamentarian Abbas Nuyan. "Maybe there are some but if there are we are not aware of it."
"The most important factors ... are security in the country, tensions between Afghanistan and its neighbors, upcoming elections and the fight against corruption, which is a serious issue not just for us but for the international community," Nuyan said.
___
Associated Press Writer Kathy Gannon contributed to this report.
INDIANAPOLIS (AP) ? Roy Hibbert had 24 points and 12 rebounds and Paul George had 14 points, eight rebounds and eight assist to lead the Pacers past New York 82-71 Saturday night in Game of the Eastern Conference semifinals.
The Pacers are up 2-1, with Game 4 of the best-of-seven series Tuesday in Indy.
Carmelo Anthony scored 21 points to lead the Knicks, who led only once in the game for a total of 76 seconds. New York spent the final 45 minutes trying to play catch-up but never did.
Amare Stoudemire looked rusty after returning from a two-month absence, going 3 of 8 from the field and finishing with seven points. J.R. Smith scored nine points after missing the morning shootaround because of a 102-degree fever.
Indiana took control with a 14-3 run that gave it a 58-44 third-quarter lead, and the Knicks never got closer than eight
The big questions heading into the game were whether Smith would play, whether Stoudemire would be effective and whether Indiana could get back to its brand of basketball.
Smith gave it a go, but his shooting problems continued as he went 4 of 12 from the field and walked straight to the locker room when he was replaced with 7:45 left in the game. He returned to the game a few minutes later.
Stoudemire, meanwhile, hit a buzzer-beating 3-pointer in eight minutes and grabbed two rebounds.
The biggest difference between Games 2 and 3 was how the Pacers played.
Four days after being embarrassed in a 26-point loss at New York, the Pacers got tough. New York shot just 35.2 percent from the field and made only three 3s, Anthony got into foul trouble by picking up three in a 2:18 span during the third quarter and, of course, Indiana finished with a 53-40 rebounding advantage.
The result: Instead of struggling over the final 18 minutes, the Pacers thrived.
New York closed the deficit to 44-41 midway through the third quarter. That's when things fell apart.
After Tyson Chandler was called for his third foul, he picked up a technical that allowed the Pacers to score three points on the possession. West followed that with a 19-foot jumper and after Chandler went 1-of-2 from the free throw line, Indiana seized control by going on a 9-0 run that made it 58-44.
Stoudemire's buzzer-beater to end the quarter got the Knicks within 62-51 and New York eventually got as close as 65-57 with 9:10 left. But Indiana answered with seven straight points and never let the Knicks challenge seriously again.
Notes: The Pacers are 4-0 at home with an average victory margin of 16.5 points. ... New York is now 0-3 at Bankers Life Fieldhouse this season. ... Saturday's loss marked the first time New York lost in this year's playoffs while holding a team to fewer than 90 points. The Knicks are now 5-1. ... Movie director Spike Lee showed up inside Bankers Life Fieldhouse for Game 3 in a Knicks jersey and orange hat
Ryan Gosling might be taking some time off from acting, but the Internet isn't taking any time off from him. The latest, greatest Baby Goose meme has hit the web, and it's about to make your day a whole lot brighter.
Has Jack Bauer been missing the days when he pulled an all-nighter to save the world? Numerous web sites are reporting that "24" is going to return to FOX as a limited series.
Deadline noted that no deals are in place for the real-time drama's return, but said that the network is looking to add it to a list of limited-event series. The show ended an eight-season run in 2010, and discussions about how to bring it to the big screen as a feature were ultimately dropped over what appeared to be budget issues.
The pieces could already be in place: Star Kiefer Sutherland's new drama "Touch" has been canceled after two seasons (and E! reports that he's set to rejoin the series, which would seem to be a requirement). Meanwhile, producer Howard Gordon (who has Emmy-winning "Homeland" and in-the-works "Tyrant" and "Legends" series on his plate) was pitching the reboot, which would start over with a brand new story arc.
To add to the discussion, ex-"24" executive producer David Fury (now over at "Tyrant") tweeted that he's also signed back on: "Yep, I'm pulling double duty along w/TYRANT," he said. "Woo & Hoo!" Later, answering some of his followers, he indicated the new show would offer 12 two-hour episodes (rather than 24 individual hours as in the series), each presented like a mini-movie.
There has been no confirm of any deal being in place, however, so fans of the show will have to continue living in suspense -- a familiar place to be. As the network told E! News, "We aren't confirming anything until Monday at our upfront presentation."
2nd?Place ($1,000):? Maxwell Lykins ? University of Wisconsin, Madison
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U.S. High School Awards
1st?Place ($1,000): Florian Riederer ? North Andover, MA
2nd?Place ($500):? Marwa Sayed ? Boston University Academy, MA
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Iowa High School Awards
1st?Place ($1,000):? Noreen Gentry, Decorah
2nd?Place ($500):? Hannah Gaffney, Mancester
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Elkader Central Award
Robin Rochleau ? $300
Thanks to all of our students and their faculty mentors that participated in this year?s competition! We are getting ready for another big year at AEP. Our essay project is going global? more information to come in the following months!
Contact: Rachel Steinhardt Rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research
Researchers elucidate how precise chemical modifications across the genome turn genes on and off during early human development -- and how those mechanisms are disrupted in cancer
May 9, 2013, New York, NY and San Diego, CA A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis in the current issue of the journal Cell of how genes are turned on and off to direct early human development. Led by Bing Ren of the Ludwig Institute for Cancer Research, Joseph Ecker of The Salk Institute for Biological Studies and James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences.
After an egg has been fertilized, it divides repeatedly to give rise to every cell in the human bodyfrom the patrolling immune cell to the pulsing neuron. Each functionally distinct generation of cells subsequently differentiates itself from its predecessors in the developing embryo by expressing only a selection of its full complement of genes, while actively suppressing others. "By applying large-scale genomics technologies," explains Bing Ren, PhD, Ludwig Institute member and a professor in the Department of Cellular and Molecular Medicine at the UC San Diego School of Medicine, "we could explore how genes across the genome are turned on and off as embryonic cells and their descendant lineages choose their fates, determining which parts of the body they would generate."
One way cells regulate their genes is by DNA methylation, in which a molecule known as a methyl group is tacked onto cytosineone of the four DNA bases that write the genetic code. Another is through scores of unique chemical modifications to proteins known as histones, which form the scaffolding around which DNA winds in the nucleus of the cell. One such silencing modification, called H3K27me3, involves the highly specific addition of three methyl groups to a type of histone named H3. "People have generally not thought of these two 'epigenetic' modifications as being very different in terms of their function," says Ren.
The current study puts an end to that notion. The researchers found in their analysis of those modifications across the genomereferred to, collectively, as the epigenomethat master genes that govern the regulation of early embryonic development tend largely to be switched off by H3K27me3 histone methylation. Meanwhile, those that orchestrate the later stages of cellular differentiation, when cells become increasingly committed to specific functions, are primarily silenced by DNA methylation.
"You can sort of glean the logic of animal development in this difference," says Ren. "Histone methylation is relatively easy to reverse. But reversing DNA methylation is a complex process, one that requires more resources and is much more likely to result in potentially deleterious mutations. So it makes sense that histone methylation is largely used to silence master genes that may be needed at multiple points during development, while DNA methylation is mostly used to switch off genes at later stages, when cells have already been tailored to specific functions, and those genes are less likely to be needed again."
The researchers also found that the human genome is peppered with more than 1,200 large regions that are consistently devoid of DNA methylation throughout development. It turns out that many of the genes considered master regulators of development are located in these regions, which the researchers call DNA methylation valleys (DMVs). Further, the team found that the DMVs are abnormally methylated in colon cancer cells. While it has long been known that aberrant DNA methylation plays an important role in various cancers, these results suggest that changes to the cell's DNA methylation machinery itself may be a major step in the evolution of tumors.
Further, the researchers catalogued the regulation of DNA sequences known as enhancers, which, when activated, boost the expression of genes. They identified more than 103,000 possible enhancers and charted their activation and silencing in six cell types. Researchers will in all likelihood continue to sift through the data generated by this study for years to come, putting the epigenetic phenomena into biological context to investigate a variety of cellular functions and diseases.
"These data are going to be very useful to the scientific community in understanding the logic of early human development," says Ren. "But I think our main contribution is the creation of a major information resource for biomedical research. Many complex diseases have their roots in early human development."
Laboratories led by Michael Zhang, at the University of Texas, Dallas, and Wei Wang, at the University of California, La Jolla, contributed extensively to the computational analysis of data generated by the epigenetic mapping.
###
The study was supported by the Ludwig Institute for Cancer Research, the NIH Epigenome Roadmap Project (U01 ES017166), NSFC 91019016, NIH R01 HG001696 (M.Q.Z.), NIH P01 GM081629 (J.A.T.), CIRM RN2-00905-1 (B.R.), the NIH/National Heart, Lung and Blood Institute and the American Heart Association (12POST12050080).
About The Ludwig Institute for Cancer Research
The Ludwig Institute for Cancer Research is an international non-profit organization committed to improving the understanding and control of cancer through integrated laboratory and clinical discovery. Leveraging its worldwide network of investigators and the ability to sponsor and conduct its own clinical trials, Ludwig is actively engaged in translating its discoveries into applications for patient benefit. Since its establishment in 1971, the Ludwig Institute has expended more than $1.5 billion on cancer research.
For further information please contact Rachel Steinhardt, rsteinhardt@licr.org or +1-212-450-1582.
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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.
Contact: Rachel Steinhardt Rsteinhardt@licr.org 212-450-1582 Ludwig Institute for Cancer Research
Researchers elucidate how precise chemical modifications across the genome turn genes on and off during early human development -- and how those mechanisms are disrupted in cancer
May 9, 2013, New York, NY and San Diego, CA A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis in the current issue of the journal Cell of how genes are turned on and off to direct early human development. Led by Bing Ren of the Ludwig Institute for Cancer Research, Joseph Ecker of The Salk Institute for Biological Studies and James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences.
After an egg has been fertilized, it divides repeatedly to give rise to every cell in the human bodyfrom the patrolling immune cell to the pulsing neuron. Each functionally distinct generation of cells subsequently differentiates itself from its predecessors in the developing embryo by expressing only a selection of its full complement of genes, while actively suppressing others. "By applying large-scale genomics technologies," explains Bing Ren, PhD, Ludwig Institute member and a professor in the Department of Cellular and Molecular Medicine at the UC San Diego School of Medicine, "we could explore how genes across the genome are turned on and off as embryonic cells and their descendant lineages choose their fates, determining which parts of the body they would generate."
One way cells regulate their genes is by DNA methylation, in which a molecule known as a methyl group is tacked onto cytosineone of the four DNA bases that write the genetic code. Another is through scores of unique chemical modifications to proteins known as histones, which form the scaffolding around which DNA winds in the nucleus of the cell. One such silencing modification, called H3K27me3, involves the highly specific addition of three methyl groups to a type of histone named H3. "People have generally not thought of these two 'epigenetic' modifications as being very different in terms of their function," says Ren.
The current study puts an end to that notion. The researchers found in their analysis of those modifications across the genomereferred to, collectively, as the epigenomethat master genes that govern the regulation of early embryonic development tend largely to be switched off by H3K27me3 histone methylation. Meanwhile, those that orchestrate the later stages of cellular differentiation, when cells become increasingly committed to specific functions, are primarily silenced by DNA methylation.
"You can sort of glean the logic of animal development in this difference," says Ren. "Histone methylation is relatively easy to reverse. But reversing DNA methylation is a complex process, one that requires more resources and is much more likely to result in potentially deleterious mutations. So it makes sense that histone methylation is largely used to silence master genes that may be needed at multiple points during development, while DNA methylation is mostly used to switch off genes at later stages, when cells have already been tailored to specific functions, and those genes are less likely to be needed again."
The researchers also found that the human genome is peppered with more than 1,200 large regions that are consistently devoid of DNA methylation throughout development. It turns out that many of the genes considered master regulators of development are located in these regions, which the researchers call DNA methylation valleys (DMVs). Further, the team found that the DMVs are abnormally methylated in colon cancer cells. While it has long been known that aberrant DNA methylation plays an important role in various cancers, these results suggest that changes to the cell's DNA methylation machinery itself may be a major step in the evolution of tumors.
Further, the researchers catalogued the regulation of DNA sequences known as enhancers, which, when activated, boost the expression of genes. They identified more than 103,000 possible enhancers and charted their activation and silencing in six cell types. Researchers will in all likelihood continue to sift through the data generated by this study for years to come, putting the epigenetic phenomena into biological context to investigate a variety of cellular functions and diseases.
"These data are going to be very useful to the scientific community in understanding the logic of early human development," says Ren. "But I think our main contribution is the creation of a major information resource for biomedical research. Many complex diseases have their roots in early human development."
Laboratories led by Michael Zhang, at the University of Texas, Dallas, and Wei Wang, at the University of California, La Jolla, contributed extensively to the computational analysis of data generated by the epigenetic mapping.
###
The study was supported by the Ludwig Institute for Cancer Research, the NIH Epigenome Roadmap Project (U01 ES017166), NSFC 91019016, NIH R01 HG001696 (M.Q.Z.), NIH P01 GM081629 (J.A.T.), CIRM RN2-00905-1 (B.R.), the NIH/National Heart, Lung and Blood Institute and the American Heart Association (12POST12050080).
About The Ludwig Institute for Cancer Research
The Ludwig Institute for Cancer Research is an international non-profit organization committed to improving the understanding and control of cancer through integrated laboratory and clinical discovery. Leveraging its worldwide network of investigators and the ability to sponsor and conduct its own clinical trials, Ludwig is actively engaged in translating its discoveries into applications for patient benefit. Since its establishment in 1971, the Ludwig Institute has expended more than $1.5 billion on cancer research.
For further information please contact Rachel Steinhardt, rsteinhardt@licr.org or +1-212-450-1582.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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Public release date: 9-May-2013
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