NASA's Hubble sees asteroid spouting 6 comet-like tails
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7-Nov-2013
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Contact: Cheryl Gundy gundy@stsci.edu 410-338-4707 NASA/Goddard Space Flight Center
Astronomers viewing our solar system's asteroid belt with NASA's Hubble Space Telescope have seen for the first time an asteroid with six comet-like tails of dust radiating from it like spokes on a wheel.
Unlike all other known asteroids, which appear simply as tiny points of light, this asteroid, designated P/2013 P5, resembles a rotating lawn sprinkler. Astronomers are puzzled over the asteroid's unusual appearance.
"We were literally dumbfounded when we saw it," said lead investigator David Jewitt of the University of California at Los Angeles. "Even more amazing, its tail structures change dramatically in just 13 days as it belches out dust. That also caught us by surprise. It's hard to believe we're looking at an asteroid."
Jewitt leads a team whose research paper appears online in the Nov. 7 issue of the Astrophysical Journal Letters.
P/2013 P5 has been ejecting dust periodically for at least five months. Astronomers believe it is possible the asteroid's rotation rate increased to the point where its surface started flying apart. They do not believe the tails are the result of an impact with another asteroid because they have not seen a large quantity of dust blasted into space all at once.
Scientists using the Pan-STARRS survey telescope in Hawaii announced their discovery of the asteroid Aug. 27. P/2013 P5 appeared as an unusually fuzzy-looking object. The multiple tails were discovered when Hubble was used to take a more detailed image Sept. 10.
When Hubble looked at the asteroid again Sept. 23, its appearance had totally changed. It looked as if the entire structure had swung around.
"We were completely knocked out," Jewitt said.
Careful modeling by team member Jessica Agarwal of the Max Planck Institute for Solar System Research in Lindau, Germany, showed that the tails could have been formed by a series of impulsive dust-ejection events. She calculated that dust-ejection events occurred April 15, July 18, July 24, Aug. 8, Aug. 26 and Sept. 4. Radiation pressure from the sun stretched the dust into streamers.
Radiation pressure could have spun P/2013 P5 up. Jewitt said the spin rate could have increased enough that the asteroid's weak gravity no longer could hold it together. If that happened, dust could slide toward the asteroid's equator, shatter and fall off, and drift into space to make a tail. So far, only about 100 to 1,000 tons of dust, a small fraction of the P/2013 P5's main mass, has been lost. The asteroid's nucleus, which measures 1,400 feet wide, is thousands of times more massive than the observed amount of ejected dust.
Astronomers will continue observing P/2013 P5 to see whether the dust leaves the asteroid in the equatorial plane. If it does, this would be strong evidence for a rotational breakup. Astronomers will also try to measure the asteroid's true spin rate.
Jewitt's interpretation implies that rotational breakup must be a common phenomenon in the asteroid belt; it may even be the main way small asteroids die.
"In astronomy, where you find one, you eventually find a whole bunch more," Jewitt said. "This is just an amazing object to us, and almost certainly the first of many more to come."
Jewitt said it appears P/2013 P5 is a fragment of a larger asteroid that broke apart in a collision roughly 200 million years ago. There are many collision fragments in orbits similar to P/2013 P5's. Meteorites from these bodies show evidence of having been heated to as much as 1,500 degrees Fahrenheit. This means the asteroid likely is composed of metamorphic rocks and does not hold any ice as a comet does.
###
For images and more information about P/2013 P5, visit:
http://hubblesite.org/news/2013/52
For more information about NASA's Hubble Space Telescope, visit:
http://www.nasa.gov/hubble
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NASA's Hubble sees asteroid spouting 6 comet-like tails
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Cheryl Gundy gundy@stsci.edu 410-338-4707 NASA/Goddard Space Flight Center
Astronomers viewing our solar system's asteroid belt with NASA's Hubble Space Telescope have seen for the first time an asteroid with six comet-like tails of dust radiating from it like spokes on a wheel.
Unlike all other known asteroids, which appear simply as tiny points of light, this asteroid, designated P/2013 P5, resembles a rotating lawn sprinkler. Astronomers are puzzled over the asteroid's unusual appearance.
"We were literally dumbfounded when we saw it," said lead investigator David Jewitt of the University of California at Los Angeles. "Even more amazing, its tail structures change dramatically in just 13 days as it belches out dust. That also caught us by surprise. It's hard to believe we're looking at an asteroid."
Jewitt leads a team whose research paper appears online in the Nov. 7 issue of the Astrophysical Journal Letters.
P/2013 P5 has been ejecting dust periodically for at least five months. Astronomers believe it is possible the asteroid's rotation rate increased to the point where its surface started flying apart. They do not believe the tails are the result of an impact with another asteroid because they have not seen a large quantity of dust blasted into space all at once.
Scientists using the Pan-STARRS survey telescope in Hawaii announced their discovery of the asteroid Aug. 27. P/2013 P5 appeared as an unusually fuzzy-looking object. The multiple tails were discovered when Hubble was used to take a more detailed image Sept. 10.
When Hubble looked at the asteroid again Sept. 23, its appearance had totally changed. It looked as if the entire structure had swung around.
"We were completely knocked out," Jewitt said.
Careful modeling by team member Jessica Agarwal of the Max Planck Institute for Solar System Research in Lindau, Germany, showed that the tails could have been formed by a series of impulsive dust-ejection events. She calculated that dust-ejection events occurred April 15, July 18, July 24, Aug. 8, Aug. 26 and Sept. 4. Radiation pressure from the sun stretched the dust into streamers.
Radiation pressure could have spun P/2013 P5 up. Jewitt said the spin rate could have increased enough that the asteroid's weak gravity no longer could hold it together. If that happened, dust could slide toward the asteroid's equator, shatter and fall off, and drift into space to make a tail. So far, only about 100 to 1,000 tons of dust, a small fraction of the P/2013 P5's main mass, has been lost. The asteroid's nucleus, which measures 1,400 feet wide, is thousands of times more massive than the observed amount of ejected dust.
Astronomers will continue observing P/2013 P5 to see whether the dust leaves the asteroid in the equatorial plane. If it does, this would be strong evidence for a rotational breakup. Astronomers will also try to measure the asteroid's true spin rate.
Jewitt's interpretation implies that rotational breakup must be a common phenomenon in the asteroid belt; it may even be the main way small asteroids die.
"In astronomy, where you find one, you eventually find a whole bunch more," Jewitt said. "This is just an amazing object to us, and almost certainly the first of many more to come."
Jewitt said it appears P/2013 P5 is a fragment of a larger asteroid that broke apart in a collision roughly 200 million years ago. There are many collision fragments in orbits similar to P/2013 P5's. Meteorites from these bodies show evidence of having been heated to as much as 1,500 degrees Fahrenheit. This means the asteroid likely is composed of metamorphic rocks and does not hold any ice as a comet does.
###
For images and more information about P/2013 P5, visit:
http://hubblesite.org/news/2013/52
For more information about NASA's Hubble Space Telescope, visit:
http://www.nasa.gov/hubble
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Share
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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.
Charts show percentages of students performing at or above proficiency in math and reading; 2c x 5 inches; 96.3 mm x 127 mm;
Charts show percentages of students performing at or above proficiency in math and reading; 2c x 5 inches; 96.3 mm x 127 mm;
Education Secretary Arne Duncan, left, stands with Washington Mayor Vincent Gray, as he speaks to reporters during a visit to Malcolm X Elementary School in Washington, Thursday, Nov. 7, 2013. Duncan announced that today's fourth and eighth graders are doing better than their predecessors in math and reading. Today’s fourth and eighth graders are doing better than their predecessors in math and reading, but despite record high scores it’s too soon to start celebrating. The vast majority of students still are not demonstrating solid academic achievement in either subject, according to the Nation’s Report Card, released Thursday. (AP Photo/Susan Walsh)
Education Secretary Arne Duncan arrives for a visit to Malcolm X Elementary School in Washington, Thursday, Nov. 7, 2013. Duncan announced that today's fourth and eighth graders are doing better than their predecessors in math and reading. Today’s fourth and eighth graders are doing better than their predecessors in math and reading, but despite record high scores it’s too soon to start celebrating. The vast majority of students still are not demonstrating solid academic achievement in either subject, according to the Nation’s Report Card, released Thursday (AP Photo/Susan Walsh)
WASHINGTON (AP) — Sometimes the best isn't good enough: Most American fourth- and eighth-graders still lack basic skills in math and reading despite record high scores on a national exam.
Yes, today's students are doing better than those who came before them. But the improvements have come at a snail's pace.
The 2013 Nation's Report Card released Thursday finds that the vast majority of the students still are not demonstrating solid academic performance in either math or reading. Stubborn gaps persist between the performances of white children and their Hispanic and African-American counterparts, who scored much lower.
Overall, just 42 percent of fourth-graders and 35 percent of eighth-graders scored at or above the proficient level in math. In reading, 35 percent of fourth graders and 36 percent of eighth graders hit that mark.
Still, as state and federal policies evolve in the post-No Child Left Behind era, the nation's school kids are doing better today on the test than they did in the early 1990s, when such tracking started, with more improvement in math than in reading. Students of all races have shown improvement over the years.
The results come from the National Assessment of Educational Progress, or NAEP, which is given every two years to a sample of fourth- and eighth-graders.
This year's results, compared to results in 2011, show average incremental gains of about one or two points on a 500-point scale in math and reading in both grades, although the one-point gain in fourth grade reading was not considered statistically significant.
"Every two years, the gains tend to be small, but over the long run, they stack up," said Jack Buckley, commissioner of the Education Department's National Center for Education Statistics.
Buckley said he was "heartened" by some of the results, "but there are also some areas where I'd hoped to see improvement where we didn't."
Today, President W. Bush's landmark education law No Child Left Behind, which sought to close achievement gaps among racial groups and have every student doing math and reading at grade level by 2014, has essentially been dismantled.
After Congress failed to update the law before it was due for renewal in 2007, President Barack Obama allowed states to get waivers from it if they showed they have their own plans to prepare students. Most states took him up on the offer.
Meanwhile, a majority of states are rolling out Common Core State Standards with the goal of better preparing the nation's students for college or a job. The states-led standards establish benchmarks for reading and math and replace goals that varied widely from state.
Academic scholars have long debated what effects the law and other state-led reforms have had on test scores.
This year, Tennessee and the District of Columbia, which have both launched high-profile efforts to strengthen education by improving teacher evaluations and by other measures, showed across-the-board growth on the test compared to 2011, likely stoking more debate. Only the Defense Department schools also saw gains in both grade levels and subjects.
In Hawaii, which has also seen a concentrated effort to improve teaching quality, scores also increased with the exception of fourth grade reading. In Iowa and Washington state, scores increased except in 8th-grade math.
Specifically pointing to Tennessee, Hawaii and D.C., Education Secretary Arne Duncan said on a conference call with reporters that many of the changes seen in these states were "very, very difficult and courageous" and appear to have had an impact.
Chris Minnich, executive director of the Council of Chief State School Officers, said the biggest problem revealed in the results is the large gap that exists between the performances of students of different races.
There was a 26-point gap, for example, between how white and African American 4th graders performed on the math section. In eighth grade reading, white students outperformed Hispanic students by 21 points.
"We still have a situation where you have kids that are left behind. They aren't given the same instruction. They aren't given the same expectations as other kids," Minnich said. He said it's time for "doubling down and making sure the gaps get smaller."
Duncan said too many African-American and Hispanic children start kindergarten a year or two behind and that early childhood programs are key to leveling the playing field. Duncan and Obama have lobbied for congressional passage of a preschool-for-all program.
This test specifically looked at the performance of American children, but the results from other recent assessments and studies have shown American children and adults scoring below peers in many other countries.
The exam was given this year to about 377,000 fourth graders and 342,000 eighth graders in public and private schools. However, state-specific numbers are only from public schools.
In math, students were asked to answer questions about topics such as geometry, algebra and measurement. In reading, students were told to read passages and recall details or interpret them.
Among the other results:
—More boys than girls scored at or above the proficient level for both grades in math. In reading, more girls than boys scored at or above that mark.
—Twenty-five out of the 52 states or jurisdictions measured had a higher average score in 2013 than in 2011 in at least one subject and grade.
—Five states had a lower score than two years ago in at least one subject and grade: Massachusetts, Montana, North Dakota, Oklahoma, and South Dakota.
—Hispanic students were the only racial or ethnic group that saw improvements in math scores in both fourth and eighth grades; Asian/Pacific Islanders students had the highest percentage of students performing at or above the proficient level in both math and reading.
What's 50-feet tall, 250-feet long and outfitted with decorative "fish fin" sails? Google's so-called mystery barge, apparently. Mum's still the word in Mountain View, but at the Port of San Francisco, details about the floating technology scow are starting to emerge. Documents obtained by the San ...
Toronto Mayor Rob Ford makes a statement to the media outside his office at Toronto's city hall after the release of a video on Thursday Nov. 7, 2013. A new video surfaced showing Ford in a rage, using threatening words including "kill" and "murder." Ford said he was “extremely, extremely inebriated" in the video, which appeared Thursday on the Toronto Star’s website. The context of the video is unknown and it's unclear who the target of Ford's wrath is. (AP Photo/The Canadian Press, Chris Young)
Toronto Mayor Rob Ford makes a statement to the media outside his office at Toronto's city hall after the release of a video on Thursday Nov. 7, 2013. A new video surfaced showing Ford in a rage, using threatening words including "kill" and "murder." Ford said he was “extremely, extremely inebriated" in the video, which appeared Thursday on the Toronto Star’s website. The context of the video is unknown and it's unclear who the target of Ford's wrath is. (AP Photo/The Canadian Press, Chris Young)
Toronto Mayor Rob Ford makes a statement to the media outside his office at Toronto's city hall after the release of a video on Thursday Nov. 7, 2013. A new video surfaced showing Ford in a rage, using threatening words including "kill" and "murder." Ford said he was “extremely, extremely inebriated" in the video, which appeared Thursday on the Toronto Star’s website. The context of the video is unknown and it's unclear who the target of Ford's wrath is. (AP Photo/The Canadian Press, Chris Young)
Toronto Mayor Rob Ford makes a statement to the media outside his office at Toronto's city hall after the release of a video on Thursday Nov. 7, 2013. A new video surfaced showing Ford in a rage, using threatening words including "kill" and "murder." Ford said he was “extremely, extremely inebriated" in the video, which appeared Thursday on the Toronto Star’s website. The context of the video is unknown and it's unclear who the target of Ford's wrath is. (AP Photo/The Canadian Press, Chris Young)
Toronto Mayor Rob Ford talks to a staff member at city hall Wednesday, Nov. 6, 2013 in Toronty. City councilors called on the deputy mayor to "orchestrate a dignified" departure for Ford, who was greeted by angry protesters on his first day of work after acknowledging he smoked crack. Ford took a back stairway to his office to avoid a crush of media and protestors. (AP Photo/The Canadian Press, Chris Young)
Toronto Mayor Rob Ford leaves Toronto's city hall Wednesday, Nov. 6, 2013 in Toronto. City councilors called on the deputy mayor to "orchestrate a dignified" departure for Ford, who was greeted by angry protesters on his first day of work after acknowledging he smoked crack. Ford took a back stairway to his office to avoid a crush of media and protestors. (AP Photo/The Canadian Press, Chris Young)
TORONTO (AP) — A new video that surfaced Thursday shows Toronto Mayor Rob Ford in a rambling rage, using threatening words including "kill" and "murder," as the saga that has gripped Canadians for months took yet another twist.
The mayor told reporters moments after the video was posted online that he was "extremely, extremely inebriated" in it and "embarrassed" by it. The context of the video is unknown and it's unclear who the target of Ford's wrath is. The video, which appeared at length on the Toronto Star's website and in clips on the Toronto Sun's website, prompted another round of calls for Ford to step down.
It's been a whirlwind of a week for Ford, who on Tuesday admitted to smoking crack in a "drunken stupor" about a year ago. Police said last week they had obtained a different, long-sought video that shows Ford smoking a crack pipe.
Police obtained that video in the course of a massive drug investigation into the mayor's friend and occasional driver.
Despite immense pressure from allies and critics, the mayor of North America's fourth largest city has refused to resign or take a leave of absence.
Ford said Thursday he made mistakes and "all I can do is reassure the people. I don't know what to say."
"When you are in that state ... I hope none of you have ever or will ever be in that state," Ford said.
"It's extremely embarrassing. The whole world is going to see it."
In the new video, a visibly agitated Ford paces around, waves his arms and rolls up his sleeves as he says he'll "make sure" the unknown person is dead.
Ford tells another person in the room, possibly the man filming the video, that he wants to "kill" someone in an expletive-laced rant. "Cause I'm going to kill that (expletive) guy," Ford says. "No holds barred brother. He dies or I die."
At one point he says "My brothers are, don't tell me we're liars, thieves, birds?" and then later refers to "80-year-old birds."
The Toronto Star that it purchased the video from "a source who filmed it from someone else's computer" and that "the person with the computer was there in the room."
City Councilor James Pasternak urged Ford to make a "dignified exit."
"The video is very disturbing," he said. "It's very upsetting, it's very sad."
City Councilor Giorgio Mammoliti, a Ford ally, urged the mayor to enter rehab and said in a statement he fears "that if the mayor does not get help now he will succumb to health issues related to addiction."
Ford lawyer Dennis Morris told The Associated Press the context of the video "is skeletal."
"What we have to do is find out when it was taken," he said. "Was it taken eight, 10 months ago or a short time ago? I'm going to try to find that out too. Maybe the Toronto Star knows better."
Asked if Ford told him about the tape, Morris said: "I can't comment, but I don't think we really know."
Earlier Thursday, Morris said he was in talks with the police for Ford to view the video that shows the mayor smoking crack, as city councilors stepped up their efforts to force him from office.
The mayor's travails were taking their toll on his supporters. Canada's finance minister became emotional when asked about Ford, a longtime friend.
Police are seeking to question Ford. Morris previously said Ford would be willing to go view the tape but would not answer questions.
Police have not charged Ford, saying the video didn't provide enough evidence against him. A police spokesman declined to comment.
Municipal law makes no provision for the mayor's forced removal from office unless he's convicted and jailed for a criminal offence.
City Councilor Denzil Minnan-Wong, a member of Ford's executive committee, said Thursday he plans to amend a motion he has filed that would ask Ford to take a leave of absence. The amendment takes the unprecedented step of asking the province of Ontario to pass legislation to remove the mayor if he does not agree to take a leave of absence. The measure could be voted on next Wednesday.
The province, however, has no plans to step in and amend the law to allow Ford to be forced from office, Ontario Municipal Affairs Minister Linda Jeffrey reaffirmed Thursday.
Premier Kathleen Wynne has said she's concerned that Ford's personal issues were making it difficult for the city to carry on normally. But she said it was up to police, the courts or the mayor to take action.
Ford acknowledged a drinking problem for the first time Sunday, saying on his radio show that he was "hammered" in public at a street festival in August and "out of control" drunk, carrying a half empty bottle of brandy around city hall after St. Patrick's Day last year. He then made his stunning confession to reporters Tuesday that he had smoked crack while drunk.
The mayor has called on police to release the tape, but police said they are prohibited from doing so because it is evidence before the courts. Police said the video will come out when Ford associate Alexander Lisi goes to trial on drug and extortion charges.
Toronto Police Chief Bill Blair has also said police have a second tape, but he has declined to discuss what's on it. Police spokesman Mark Pugash told the AP the video released Thursday is not the tape Blair talked about.
The allegations about Ford smoking crack first emerged earlier this year when reporters from the Toronto Star and the U.S. website Gawker separately said they saw that video, but they did not obtain a copy.
___
Follow Rob Gillies on Twitter at —http://twitter.com/rgilliescanada
The Economist honors cancer immunotherapy pioneer James Allison
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Scott Merville smerville@mdanderson.org 713-792-0661 University of Texas M. D. Anderson Cancer Center
2013 Innovation Award for bioscience goes to MD Anderson scientist
HOUSTON For basic science research that opened a completely new approach for treating cancer, The Economist has named James Allison, Ph.D., professor and chair of Immunology at The University of Texas MD Anderson Cancer Center, as its 2013 Innovations Award winner in Bioscience.
Allison identified an immune checkpoint molecule that turns off T cells white blood cells that are the attack dogs of the immune system before they can mount a successful response to tumors that they are primed to destroy.
An antibody that blocks that immune checkpoint molecule, unleashing a T cell attack, became the first drug to ever extend survival for patients with late-stage melanoma. The U.S. Food and Drug Administration approved ipilumumab (Yervoy) for treatment of metastatic melanoma in 2011.
"The approval of ipilimumab in 2011 represents the culmination of years of research by Dr Allison into tumor immunotherapy," said Tom Standage, Digital Editor at The Economist and chairman of the panel of 30 judges. "We are delighted to recognize his pioneering achievement in the fight against cancer."
The Economist is a 170-year-old weekly news publication based in London with a circulation of 4.5 million worldwide. Its Innovation Awards recognize significant contributions in eight fields: Bioscience, Computing and Telecommunications, Consumer Products, Energy and Environment, Process and Services, Social and Economic, No Boundaries and Corporate.
"I'm honored to receive this award, which recognizes the increasing importance of immune therapy in the treatment of cancer due to the efforts of many scientists, clinicians and patients willing to participate in clinical trials," Allison said.
The adaptive immune system routinely identifies, destroys and remembers infections and abnormal cells. Yet cancer cells evade or suppress immune attack, largely frustrating efforts to develop vaccines and other immune therapies against tumors.
Drug treats immune system, not specific tumor
"Immune checkpoint blockade treats the immune system, not the tumor, so we expect this approach to work across many types of cancer," Allison said. In addition to melanoma, ipilumumab has been effective in clinical trials against prostate, kidney, lung and ovarian cancers.
Allison's basic science research on T cell biology uncovered the receptor on these cells used to recognize and bind to antigens abnormalities that mark defective cells or viruses and bacteria for attack.
He also found that T cells require a second molecular signal to launch a response after they've bound to an antigen. And he identified a molecule called CTLA-4 that acts as an off switch to inhibit activated T cells from attacking.
This led to development of ipilumumab to block CTLA-4. In clinical trials against stage 4 melanoma, the drug extinguished the disease in 20 percent of patients for up to 12 years and counting.
Since arriving at MD Anderson in November 2012, Allison founded and directs an immunotherapy platform to cultivate, support and test new development of immunology-based drugs and combinations. MD Anderson's Moon Shots program, designed to accelerate the conversion of scientific discoveries into clinical advances that reduce cancer deaths, taps the expertise of the immunotherapy platform.
Allison earned his doctorate from The University of Texas at Austin in 1978, joining MD Anderson's faculty after his postdoctoral fellowship. He left MD Anderson for the University of California, Berkeley and later moved to Memorial Sloan-Kettering Cancer Center in New York.
He is a member of the National Academy of Sciences, the Institute of Medicine of the National Academies and has won many honors for biomedical research, including the first AACR-CRI Lloyd J. Old Award in Cancer Immunology at the annual meeting of the American Association for Cancer Research in April 2013.
Allison will receive his award at a ceremony in London on Dec. 3.
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The Economist honors cancer immunotherapy pioneer James Allison
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Scott Merville smerville@mdanderson.org 713-792-0661 University of Texas M. D. Anderson Cancer Center
2013 Innovation Award for bioscience goes to MD Anderson scientist
HOUSTON For basic science research that opened a completely new approach for treating cancer, The Economist has named James Allison, Ph.D., professor and chair of Immunology at The University of Texas MD Anderson Cancer Center, as its 2013 Innovations Award winner in Bioscience.
Allison identified an immune checkpoint molecule that turns off T cells white blood cells that are the attack dogs of the immune system before they can mount a successful response to tumors that they are primed to destroy.
An antibody that blocks that immune checkpoint molecule, unleashing a T cell attack, became the first drug to ever extend survival for patients with late-stage melanoma. The U.S. Food and Drug Administration approved ipilumumab (Yervoy) for treatment of metastatic melanoma in 2011.
"The approval of ipilimumab in 2011 represents the culmination of years of research by Dr Allison into tumor immunotherapy," said Tom Standage, Digital Editor at The Economist and chairman of the panel of 30 judges. "We are delighted to recognize his pioneering achievement in the fight against cancer."
The Economist is a 170-year-old weekly news publication based in London with a circulation of 4.5 million worldwide. Its Innovation Awards recognize significant contributions in eight fields: Bioscience, Computing and Telecommunications, Consumer Products, Energy and Environment, Process and Services, Social and Economic, No Boundaries and Corporate.
"I'm honored to receive this award, which recognizes the increasing importance of immune therapy in the treatment of cancer due to the efforts of many scientists, clinicians and patients willing to participate in clinical trials," Allison said.
The adaptive immune system routinely identifies, destroys and remembers infections and abnormal cells. Yet cancer cells evade or suppress immune attack, largely frustrating efforts to develop vaccines and other immune therapies against tumors.
Drug treats immune system, not specific tumor
"Immune checkpoint blockade treats the immune system, not the tumor, so we expect this approach to work across many types of cancer," Allison said. In addition to melanoma, ipilumumab has been effective in clinical trials against prostate, kidney, lung and ovarian cancers.
Allison's basic science research on T cell biology uncovered the receptor on these cells used to recognize and bind to antigens abnormalities that mark defective cells or viruses and bacteria for attack.
He also found that T cells require a second molecular signal to launch a response after they've bound to an antigen. And he identified a molecule called CTLA-4 that acts as an off switch to inhibit activated T cells from attacking.
This led to development of ipilumumab to block CTLA-4. In clinical trials against stage 4 melanoma, the drug extinguished the disease in 20 percent of patients for up to 12 years and counting.
Since arriving at MD Anderson in November 2012, Allison founded and directs an immunotherapy platform to cultivate, support and test new development of immunology-based drugs and combinations. MD Anderson's Moon Shots program, designed to accelerate the conversion of scientific discoveries into clinical advances that reduce cancer deaths, taps the expertise of the immunotherapy platform.
Allison earned his doctorate from The University of Texas at Austin in 1978, joining MD Anderson's faculty after his postdoctoral fellowship. He left MD Anderson for the University of California, Berkeley and later moved to Memorial Sloan-Kettering Cancer Center in New York.
He is a member of the National Academy of Sciences, the Institute of Medicine of the National Academies and has won many honors for biomedical research, including the first AACR-CRI Lloyd J. Old Award in Cancer Immunology at the annual meeting of the American Association for Cancer Research in April 2013.
Allison will receive his award at a ceremony in London on Dec. 3.
###
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The NSA wields its legal authority to collect phone call data from American telecom providers, but the CIA apparently doesn't even need to apply pressure. The New York Times claims that the agency has a years-old voluntary agreement with AT&T that lets it obtain the call records of foreign suspects; ...
"I am sorry that they are finding themselves in this situation based on assurances they got from me," President Obama said Thursday, speaking about Americans who will lose their current health insurance plans.
In speeches before parts of the Affordable Care Act took effect, the president promised that people who were content with the plans they already had would be able to keep them. But that hasn't always been the case, as The Two-Way reported in October.
Obama spoke about the troubled rollout of the new health care system with NBC's Chuck Todd Thursday. Todd asked the president about the pledge he often repeated when critics of the Affordable Care Act said it would mean thousands of cancelled policies.
"I meant what I said," Obama answered. "And we worked hard to try to make sure that we implemented it properly. But obviously, we didn't do a good enough job. And I regret that."
In addition to his apology, the president pledged to help those who have complained that the new law is forcing them to sign up for a more expensive plan.
"We've got to work hard to make sure that they know we hear them," Obama said, "and that we're going to do everything we can to deal with folks who find themselves in a tough position as a consequence of this."
The appearance on NBC marks "a more apologetic tone" for the president on this issue, NPR's Ari Shapiro reports.
"Until now, the White House had taken a defensive response to people being forced to change health plans. The president insisted that people losing their plans would get better and, in some cases, cheaper ones," Ari says in a report for our Newscast unit.
"The White House is also still struggling to get the HealthCare.gov website up and running," Ari adds. "It's functioning better than before, but it's still not up to speed."
Dartmouth researcher finds novel genetic patterns that make us rethink biology and individuality
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Derik Hertel derik.hertel@dartmouth.edu 603-650-1203 The Geisel School of Medicine at Dartmouth
Professor of Genetics Scott Williams, PhD, of the Institute for Quantitative Biomedical Sciences (iQBS) at Dartmouth's Geisel School of Medicine, has made two novel discoveries: first, a person can have several DNA mutations in parts of their body, with their original DNA in the restresulting in several different genotypes in one individualand second, some of the same genetic mutations occur in unrelated people. We think of each person's DNA as unique, so if an individual can have more than one genotype, this may alter our very concept of what it means to be a human, and impact how we think about using forensic or criminal DNA analysis, paternity testing, prenatal testing, or genetic screening for breast cancer risk, for example. Williams' surprising results indicate that genetic mutations do not always happen purely at random, as scientists have previously thought. His work, done in collaboration with Professor of Genetics Jason Moore, PhD, and colleagues at Vanderbilt University, was published in PLOS Genetics journal on November 7, 2013.1
Genetic mutations can occur in the cells that are passed on from parent to child and may cause birth defects. Other genetic mutations occur after an egg is fertilized, throughout childhood or adult life, after people are exposed to sunlight, radiation, carcinogenic chemicals, viruses, or other items that can damage DNA. These later or "somatic" mutations do not affect sperm or egg cells, so they are not inherited from parents or passed down to children. Somatic mutations can cause cancer or other diseases, but do not always do so. However, if the mutated cell continues to divide, the person can develop tissue, or a part thereof, with a different DNA sequence from the rest of his or her body.
"We are in reality diverse beings in that a single person is genetically not a single entityto be philosophical in ways I do not yet understandwhat does it mean to be a person if we are variable within?" says Williams, the study's senior author, and founding Director of the Center for Integrative Biomedical Sciences in iQBS. "What makes you a person? Is it your memory? Your genes?" He continues, "We have always thought, 'your genome is your genome.' The data suggest that it is not completely true."
In the past, it was always thought that each person contains only one DNA sequence (genetic constitution). Only recently, with the computational power of advanced genetic analysis tools that examine all the genes in one individual, have scientists been able to systematically look for this somatic variation. "This study is an example of the type of biomedical research project that is made possible by bringing together interdisciplinary teams of scientists with expertise in the biological, computational and statistical sciences." says Jason Moore, Director of the iQBS, who is also Associate Director for Bioinformatics at the Cancer Center, Third Century Professor, and Professor of Community and Family Medicine at Geisel.
Having multiple genotypes from mutations within one's own body is somewhat analogous to chimerism, a condition in which one person has cells inside his or her body that originated from another person (i.e., following an organ or blood donation; or sometimes a mother and childor twinsexchange DNA during pregnancy. Also, occasionally a person finds out that, prior to birth, he or she had a twin who did not survive, whose genetic material is still contained within their own body).2 Chimerism has resulted in some famous DNA cases: one in which a mother had genetic testing that "proved" that she was unrelated to two of her three biological sons.3
Williams says that, although this was a small study, "there is a lot more going on than we thought, and the results are, in some ways, astoundingly weird."
Because somatic changes are thought to happen at random, scientists do not expect unrelated people to exhibit the same mutations. Williams and colleagues analyzed the same 10 tissue samples in two unrelated people. They found several identical mutations, and detected these repeated mutations only in kidney, liver and skeletal body tissues. Their research examined "mitochondrial DNA" (mtDNA)a part of DNA that is only inherited from the mother.4 Technically all women would share mtDNA from one common female ancestor, but mutations have resulted in differences. The importance of Williams' finding is that these tissue-specific, recurrent, common mutations in mtDNA among unrelated study subjectsonly detected in three body tissuesare "not likely being developed and maintained through purely random processes," according to Williams. They indicate "a completely different model . a decidedly non-random process that results in particular mutations, but only in specific tissues."
If our human DNA changes, or mutates, in patterns, rather than randomly; if such mutations "match" among unrelated people; or if genetic changes happen only in part of the body of one individual, what does this mean for our understanding of what it means to be human? How may it impact our medical care, cancer screening, or treatment of disease? We don't yet know, but ongoing research may help reveal the answers.
Christopher Amos, PhD, Director of the Center for Genomic Medicine and Associate Director for Population Sciences at the Cancer Center, says, "This paper identifies mutations that develop in multiple tissues, and provides novel insights that are relevant to aging. Mutations are noticed in several tissues in common across individuals, and the aging process is the most likely contributor. The theory would be that selected mutations confer a selective advantage to mitochondria, and these accumulate as we age." Amos, who is also a Professor of Community and Family Medicine at Geisel, says, "To confirm whether aging is to blame, we would need to study tissues from multiple individuals at different ages." Williams concurs, saying, "Clearly these do accumulate with age, but how and why is unknownand needs to be determined."
As more and better data become available from high-throughput genetic analyses and high-powered computers, researchers are identifying an increasing number of medical conditions that result from somatic mutations, including neurological, hematological, and immune-related disorders. Williams and colleagues are conducting further research to examine how diseases, other than cancer or even benign conditions, may result from somatic changes.5 Williams, Moore and Amos will employ iQBS's Discovery supercomputer for next-generation sequencing to process subjects' DNA data.6 Future analyses will include large, whole-genome sequencing of the data for the two individuals studied in the current report.
Williams explains, "We know that cancer is caused by mutations that cause a tumor. But in this work, we chose to study mutations in people without any cancer. Knowing how we accumulate mutations may make it easier to separate genetic signals that may cause cancer from those that accumulate normally without affecting disease. It may also allow us to see that many changes that we thought caused cancer do not in many situations, if we find the same mutations in normal tissues."
Just as our bodies' immune systems have evolved to fight disease, interestingly, they can also stave off the effects of some genetic mutations. Williams states that, "Most genetic changes don't cause disease, and if they did, we'd be in big trouble. Fortunately, it appears our systems filter a lot of that out."
Mark Israel, MD, Director of Norris Cotton Cancer Center and Professor of Pediatrics and Genetics at Geisel, says, "The fact that somatic mutation occurs in mitochondrial DNA apparently non-randomly provides a new working hypothesis for the rest of the genome. If this non-randomness is general, it may affect cancer risks in ways we could not have previously predicted. This can have real impact in understanding and changing disease susceptibility."
###
1 Williams, Scott, et al., Recurrent tissue-specific mtDNA mutations are common in humans. http://www.plosgenetics.org/doi/pgen.1003929.
2 Strain L, Dean JC, Hamilton MP, Bonthron D. A true hermaphrodite chimera resulting from embryo amalgamation after in vitro fertilization. N Engl J Med 1998;(338):166-9/
3 Norton AT and Zehner O. Project MUSE: Today's Research, Tomorrow's Inspiration. http://www.academia.edu/202539/Which_Half_Is_Mommy_Tetragametic_Chimerism_and_Trans-Subjectivity.
4 The Bradshaw Foundation [online learning resource with main areas of focus on archaeology, anthropology and genetic research]: Mitochondrial DNA: The EVE Gene. http://www.bradshawfoundation.com/journey/eve.htm.
5 Li, Chun and Williams, Scott M. Human somatic variation: It's not just for cancer anymore. Current Genetic Medicine Reporter (In Press).
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.
Dartmouth researcher finds novel genetic patterns that make us rethink biology and individuality
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Derik Hertel derik.hertel@dartmouth.edu 603-650-1203 The Geisel School of Medicine at Dartmouth
Professor of Genetics Scott Williams, PhD, of the Institute for Quantitative Biomedical Sciences (iQBS) at Dartmouth's Geisel School of Medicine, has made two novel discoveries: first, a person can have several DNA mutations in parts of their body, with their original DNA in the restresulting in several different genotypes in one individualand second, some of the same genetic mutations occur in unrelated people. We think of each person's DNA as unique, so if an individual can have more than one genotype, this may alter our very concept of what it means to be a human, and impact how we think about using forensic or criminal DNA analysis, paternity testing, prenatal testing, or genetic screening for breast cancer risk, for example. Williams' surprising results indicate that genetic mutations do not always happen purely at random, as scientists have previously thought. His work, done in collaboration with Professor of Genetics Jason Moore, PhD, and colleagues at Vanderbilt University, was published in PLOS Genetics journal on November 7, 2013.1
Genetic mutations can occur in the cells that are passed on from parent to child and may cause birth defects. Other genetic mutations occur after an egg is fertilized, throughout childhood or adult life, after people are exposed to sunlight, radiation, carcinogenic chemicals, viruses, or other items that can damage DNA. These later or "somatic" mutations do not affect sperm or egg cells, so they are not inherited from parents or passed down to children. Somatic mutations can cause cancer or other diseases, but do not always do so. However, if the mutated cell continues to divide, the person can develop tissue, or a part thereof, with a different DNA sequence from the rest of his or her body.
"We are in reality diverse beings in that a single person is genetically not a single entityto be philosophical in ways I do not yet understandwhat does it mean to be a person if we are variable within?" says Williams, the study's senior author, and founding Director of the Center for Integrative Biomedical Sciences in iQBS. "What makes you a person? Is it your memory? Your genes?" He continues, "We have always thought, 'your genome is your genome.' The data suggest that it is not completely true."
In the past, it was always thought that each person contains only one DNA sequence (genetic constitution). Only recently, with the computational power of advanced genetic analysis tools that examine all the genes in one individual, have scientists been able to systematically look for this somatic variation. "This study is an example of the type of biomedical research project that is made possible by bringing together interdisciplinary teams of scientists with expertise in the biological, computational and statistical sciences." says Jason Moore, Director of the iQBS, who is also Associate Director for Bioinformatics at the Cancer Center, Third Century Professor, and Professor of Community and Family Medicine at Geisel.
Having multiple genotypes from mutations within one's own body is somewhat analogous to chimerism, a condition in which one person has cells inside his or her body that originated from another person (i.e., following an organ or blood donation; or sometimes a mother and childor twinsexchange DNA during pregnancy. Also, occasionally a person finds out that, prior to birth, he or she had a twin who did not survive, whose genetic material is still contained within their own body).2 Chimerism has resulted in some famous DNA cases: one in which a mother had genetic testing that "proved" that she was unrelated to two of her three biological sons.3
Williams says that, although this was a small study, "there is a lot more going on than we thought, and the results are, in some ways, astoundingly weird."
Because somatic changes are thought to happen at random, scientists do not expect unrelated people to exhibit the same mutations. Williams and colleagues analyzed the same 10 tissue samples in two unrelated people. They found several identical mutations, and detected these repeated mutations only in kidney, liver and skeletal body tissues. Their research examined "mitochondrial DNA" (mtDNA)a part of DNA that is only inherited from the mother.4 Technically all women would share mtDNA from one common female ancestor, but mutations have resulted in differences. The importance of Williams' finding is that these tissue-specific, recurrent, common mutations in mtDNA among unrelated study subjectsonly detected in three body tissuesare "not likely being developed and maintained through purely random processes," according to Williams. They indicate "a completely different model . a decidedly non-random process that results in particular mutations, but only in specific tissues."
If our human DNA changes, or mutates, in patterns, rather than randomly; if such mutations "match" among unrelated people; or if genetic changes happen only in part of the body of one individual, what does this mean for our understanding of what it means to be human? How may it impact our medical care, cancer screening, or treatment of disease? We don't yet know, but ongoing research may help reveal the answers.
Christopher Amos, PhD, Director of the Center for Genomic Medicine and Associate Director for Population Sciences at the Cancer Center, says, "This paper identifies mutations that develop in multiple tissues, and provides novel insights that are relevant to aging. Mutations are noticed in several tissues in common across individuals, and the aging process is the most likely contributor. The theory would be that selected mutations confer a selective advantage to mitochondria, and these accumulate as we age." Amos, who is also a Professor of Community and Family Medicine at Geisel, says, "To confirm whether aging is to blame, we would need to study tissues from multiple individuals at different ages." Williams concurs, saying, "Clearly these do accumulate with age, but how and why is unknownand needs to be determined."
As more and better data become available from high-throughput genetic analyses and high-powered computers, researchers are identifying an increasing number of medical conditions that result from somatic mutations, including neurological, hematological, and immune-related disorders. Williams and colleagues are conducting further research to examine how diseases, other than cancer or even benign conditions, may result from somatic changes.5 Williams, Moore and Amos will employ iQBS's Discovery supercomputer for next-generation sequencing to process subjects' DNA data.6 Future analyses will include large, whole-genome sequencing of the data for the two individuals studied in the current report.
Williams explains, "We know that cancer is caused by mutations that cause a tumor. But in this work, we chose to study mutations in people without any cancer. Knowing how we accumulate mutations may make it easier to separate genetic signals that may cause cancer from those that accumulate normally without affecting disease. It may also allow us to see that many changes that we thought caused cancer do not in many situations, if we find the same mutations in normal tissues."
Just as our bodies' immune systems have evolved to fight disease, interestingly, they can also stave off the effects of some genetic mutations. Williams states that, "Most genetic changes don't cause disease, and if they did, we'd be in big trouble. Fortunately, it appears our systems filter a lot of that out."
Mark Israel, MD, Director of Norris Cotton Cancer Center and Professor of Pediatrics and Genetics at Geisel, says, "The fact that somatic mutation occurs in mitochondrial DNA apparently non-randomly provides a new working hypothesis for the rest of the genome. If this non-randomness is general, it may affect cancer risks in ways we could not have previously predicted. This can have real impact in understanding and changing disease susceptibility."
###
1 Williams, Scott, et al., Recurrent tissue-specific mtDNA mutations are common in humans. http://www.plosgenetics.org/doi/pgen.1003929.
2 Strain L, Dean JC, Hamilton MP, Bonthron D. A true hermaphrodite chimera resulting from embryo amalgamation after in vitro fertilization. N Engl J Med 1998;(338):166-9/
3 Norton AT and Zehner O. Project MUSE: Today's Research, Tomorrow's Inspiration. http://www.academia.edu/202539/Which_Half_Is_Mommy_Tetragametic_Chimerism_and_Trans-Subjectivity.
4 The Bradshaw Foundation [online learning resource with main areas of focus on archaeology, anthropology and genetic research]: Mitochondrial DNA: The EVE Gene. http://www.bradshawfoundation.com/journey/eve.htm.
5 Li, Chun and Williams, Scott M. Human somatic variation: It's not just for cancer anymore. Current Genetic Medicine Reporter (In Press).
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.
Now that anyone (well, anyone with an invitation) with a spare $1,500 can get their very own Google Glass, the folks in Mountain View have thoughtfully released a software update for the famous wearable. We're frankly surprised Glass owners weren't able to do this before, but you can now look up your calendar directly from the headset. Simply say "ok glass, google my agenda" or "ok glass, what am I doing next week?" to see what's up next on your busy schedule. Another new feature is the ability to customize a location as either "home" or "work" so you can easily ask directions for either of those places.
Interestingly, the update also removed a feature. After finding out that people were long-pressing their touchpads by mistake, the company has turned that functionality off. Instead, Google recommends tapping the touchpad three times to initiate a search. Other upgraded goodies include a new tutorial setup and a screencast shortcut. So if you're lucky enough to own one of these headsets, go on and download the update from the thing on your noggin. And while you're at it, maybe figure out a way to invite us onto that Google barge.
Nov 7 (Reuters) - Twitter Inc stock soared 92 percent in their first day of trading on Thursday on the New York Stock Exchange as investors snapped up shares in the microblogging site, pushing its market value to a heady $25 billion.
The shares opened at $45.10 a share, up from the initial public offering price of $26 set on Wednesday, then added to those gains, hitting a high of $50.
Sources said the flotation had drawn strong demand, with investors asking for 30 times the number of shares on offer as they bet on potential growth at the money-losing social media company.
The opening price valued the shares at about 22 times forecast 2014 sales, nearly double that multiple at social media rivals Facebook Inc and LinkedIn Corp.
Twitter executives including Chief Executive Dick Costolo and founder Jack Dorsey thronged to the floor of the New York Stock Exchange to witness the IPO. The Big Board snatched the offering away from Nasdaq after the normally tech-focused Nasdaq stumbled with the larger Facebook flotation last year.
"Facebook was so overhyped people felt like they couldn't miss out," said Kenneth Polcari, a senior floor official at O'Neil Securities Inc. "Twitter isn't like that, though you can feel the excitement."
British actor Patrick Stewart rang the opening bell at the exchange together with 9-year-old Vivienne Harr, who started a charity to end childhood slavery using the microblogging site.
"I guess I represent the poster boy for Twitter," Stewart said, adding that he had only been tweeting for about a year and wasn't buying Twitter stock today.
Twitter's building staff opened its offices in San Francisco extra early, at 5:30 a.m. on Thursday. By 7:30 a.m., hundreds of employees had flocked to their 9th floor cafeteria to watch Stewart ring the opening bell on TV.
The microblogging network priced its 70 million shares at above the targeted range of $23 to $25, which had been raised once before. The IPO values Twitter at $14.1 billion, with the potential to reach $14.4 billion if underwriters exercise an overallotment option.
If the full overallotment is exercised, as expected, Twitter could raise $2.1 billion, making it the second largest Internet offering in the United States behind Facebook Inc's $16 billion IPO last year and ahead of Google Inc's 2004 IPO, according to Thomson Reuters data.
Twitter boasts 230 million global users, including heads of state and celebrities, but it lost $65 million in its most recent quarter and questions remained about long-term prospects.
It also lacks the ubiquity of Facebook or the "stickiness" factor that keeps people checking the No. 1 social network on a daily basis.
A Reuters-Ipsos poll last month showed that 36 percent of people who signed up for a Twitter account say they do not use it.
FILE - In this Oct. 20, 2013 file photo, Chicago Bears quarterback Josh McCown talks with head coach Marc Trestman during an NFL football game against the Washington Redskins in Landover, Md. During the game, McCown led the Bears to a 24-point second half when pressed into service to replace injured Jay Cutler, but he had no preparation time in that one. Now, after a couple weeks to get ready to face the Green Bay Packers on Monday, Nov. 4, McCown expects to be ready to produce against a defense that has always given Cutler fits. (AP Photo/Alex Brandon File)
FILE - In this Oct. 20, 2013 file photo, Chicago Bears quarterback Josh McCown talks with head coach Marc Trestman during an NFL football game against the Washington Redskins in Landover, Md. During the game, McCown led the Bears to a 24-point second half when pressed into service to replace injured Jay Cutler, but he had no preparation time in that one. Now, after a couple weeks to get ready to face the Green Bay Packers on Monday, Nov. 4, McCown expects to be ready to produce against a defense that has always given Cutler fits. (AP Photo/Alex Brandon File)
Chicago Bears quarterback Josh McCown (12) talks to Jay Cutler during the first half of an NFL football game against the Green Bay Packers Monday, Nov. 4, 2013, in Green Bay, Wis. (AP Photo/Mike Roemer)
Chicago Bears quarterback Josh McCown throws past Green Bay Packers' Datone Jones during the second half of an NFL football game Monday, Nov. 4, 2013, in Green Bay, Wis. (AP Photo/Jeffrey Phelps)
LAKE FOREST, Ill. (AP) — Bears quarterback Jay Cutler will start against the Detroit Lions on Sunday after missing one game with a groin muscle tear.
Coach Marc Trestman confirmed Cutler's return Thursday following practice, saying doctors have given Cutler the clearance to play. Trestman said Cutler will not be restricted in any way due to the injury.
Cutler suffered the injury against the Washington Redskins Oct. 20 when he was sacked during the 45-41 loss. The Bears had a bye the following week, then Josh McCown started and played all of Monday night's 27-20 win at Green Bay.
Cutler has completed 146 of 225 passes for 1,658 yards and 12 touchdowns with seven interceptions. McCown completed 36 of 61 for 476 yards and did not turn the ball over as Cutler's replacement.
Episode VII may still be in the throes of pre-production, but Lucasfilm has confirmed that the Star Wars saga will continue on December 18th, 2015, with shooting officially set to start in spring 2014 and leaving just 771 days left to speculate. ...
TU Muenchen hosts international symposium on 'informal urbanism'
PUBLIC RELEASE DATE:
7-Nov-2013
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Contact: Barbara Wankerl barbara.wankerl@tum.de 49-892-892-2562 Technische Universitaet Muenchen
UN Habitat Hub to be launched at Munich meeting Nov. 20-23, 2013
In developing countries millions of new residents stream into megacities
often building "informal" neighborhoods where new generations will be
born. Official responses have typically been like efforts to hold back the
tide. With the expected influx of another two billion low-income migrants
by 2050, this challenge is being reframed, with a focus on exploring more
constructive approaches that channel the energy, creativity, and
resourcefulness of the new city dwellers.
Researchers at the forefront of this worldwide movement are converging on Munich from November 20 to 23 for a symposium hosted by the Technische Universitt Mnchen (TUM). The interdisciplinary symposium "Metropolis Nonformal Anticipation" assumes that collaboration, not prevention, offers the only path toward sustainable living in the megacities of the future.
The second such meeting of the minds arranged under the auspices of the TUM Institute for Advanced Study, this symposium also marks a new beginning: the official launch of a United Nations Habitat Hub on Informal Urbanism.
Journalists interested in covering the event need to register and should also contact the TUM Corporate Communications Center (presse@tum.de).
###
Symposium program and further information: http://www.tum-ias.de/metropolis-nonformal-symposium/
Contact:
Juliane Schneegans
Scientific Assistant, Landscape Architecture and Public Space
Technische Universitt Mnchen
T: +49 (0)8161 71 4166
E: juliane.schneegans@wzw.tum.de
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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.
TU Muenchen hosts international symposium on 'informal urbanism'
PUBLIC RELEASE DATE:
7-Nov-2013
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]
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Contact: Barbara Wankerl barbara.wankerl@tum.de 49-892-892-2562 Technische Universitaet Muenchen
UN Habitat Hub to be launched at Munich meeting Nov. 20-23, 2013
In developing countries millions of new residents stream into megacities
often building "informal" neighborhoods where new generations will be
born. Official responses have typically been like efforts to hold back the
tide. With the expected influx of another two billion low-income migrants
by 2050, this challenge is being reframed, with a focus on exploring more
constructive approaches that channel the energy, creativity, and
resourcefulness of the new city dwellers.
Researchers at the forefront of this worldwide movement are converging on Munich from November 20 to 23 for a symposium hosted by the Technische Universitt Mnchen (TUM). The interdisciplinary symposium "Metropolis Nonformal Anticipation" assumes that collaboration, not prevention, offers the only path toward sustainable living in the megacities of the future.
The second such meeting of the minds arranged under the auspices of the TUM Institute for Advanced Study, this symposium also marks a new beginning: the official launch of a United Nations Habitat Hub on Informal Urbanism.
Journalists interested in covering the event need to register and should also contact the TUM Corporate Communications Center (presse@tum.de).
###
Symposium program and further information: http://www.tum-ias.de/metropolis-nonformal-symposium/
Contact:
Juliane Schneegans
Scientific Assistant, Landscape Architecture and Public Space
Technische Universitt Mnchen
T: +49 (0)8161 71 4166
E: juliane.schneegans@wzw.tum.de
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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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What's 50-feet tall, 250-feet long and outfitted with decorative "fish fin" sails? Google's so-called mystery barge, apparently. Mum's still the word in Mountain View, but at the Port of San Francisco, details about the floating technology scow are starting to emerge. Documents obtained by the San ...
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The NSA wields its legal authority to collect phone call data from American telecom providers, but the CIA apparently doesn't even need to apply pressure. The New York Times claims that the agency has a years-old voluntary agreement with AT&T that lets it obtain the call records of foreign suspects; ...
Source: 
Episode VII may still be in the throes of pre-production, but Lucasfilm has confirmed that the Star Wars saga will continue on December 18th, 2015, with shooting officially set to start in spring 2014 and leaving just 771 days left to speculate. ...
Source: