Green Bay Packers running back Ryan Grant (25) gets past Kansas City Chiefs outside linebacker Justin Houston (50) during the second half of an NFL football game at Arrowhead Stadium in Kansas City, Mo., Sunday, Dec. 18, 2011. (AP Photo/Charlie Riedel)
Green Bay Packers running back Ryan Grant (25) gets past Kansas City Chiefs outside linebacker Justin Houston (50) during the second half of an NFL football game at Arrowhead Stadium in Kansas City, Mo., Sunday, Dec. 18, 2011. (AP Photo/Charlie Riedel)
Green Bay Packers coach Mike McCarthy talks with coaches in the booth during the first half of an NFL football game against the Kansas City Chiefs at Arrowhead Stadium in Kansas City, Mo., Sunday, Dec. 18, 2011. (AP Photo/Ed Zurga)
Green Bay Packers quarterback Aaron Rodgers (12) throws under pressure from Kansas City Chiefs defensive back Travis Daniels (34) during the second half of an NFL football game at Arrowhead Stadium in Kansas City, Mo., Sunday, Dec. 18, 2011. (AP Photo/Charlie Riedel)
KANSAS CITY, Mo. (AP) ? Mike McCarthy never put a whole lot of stock in a perfect season, except as a means of gaining home-field advantage and setting the Green Bay Packers up for another Super Bowl run.
Well, they still have a chance to earn home-field advantage.
The perfect season? That's history.
Kyle Orton threw for 299 yards to outduel Aaron Rodgers, and the Kansas City Chiefs rallied behind interim coach Romeo Crennel for a shocking 19-14 victory on Sunday that ended the Packers' 19-game winning streak. It was their first loss since Dec. 19, 2010, at New England.
"I personally always viewed the undefeated season as, really, just gravy," McCarthy said. "The goal was to get home-field advantage and win the Super Bowl. That's what we discussed.
"We were fortunate enough to be in the position to possibly achieve the undefeated season," he added, "but we still have the primary goal in front of us, and that's to get home-field advantage."
Green Bay, playing without leading receiver Greg Jennings and top rusher James Starks because of injuries, can wrap up the No. 1 seed in their final two games against Chicago and Detroit. But the Packers no longer have the pressure of becoming the second team in NFL history to win a Super Bowl with a perfect record, or extending the second-longest winning streak in league history.
"I think our goal ultimate goal is to win a Super Bowl. The next step is getting that number one seed in the playoffs," Rodgers said. "We've got a home playoff game ? we've got a bye secured."
Rodgers was 17 of 35 for 235 yards and a touchdown, and he also scampered 8 yards for another touchdown with 2:12 left in the game. But the Packers (13-1) were unable to recover the onside kick, and Kansas City picked up a couple of first downs to secure the victory.
"They had a good game plan," Rodgers said. "You have to give them credit."
Ryan Succop kicked four field goals for Kansas City (6-8), which had lost five of its last six games and fired coach Todd Haley last Monday. Jackie Battle added a short touchdown plunge with 4:53 left in the game, points that came in handy when Rodgers led one last scoring drive.
"Everybody had marked it off as a win for the Packers, but those guys in the locker room, they're football players," Crennel said. "They decided they were not going to lay down, they were not going to give up, so they went out and played a tremendous game."
Neither team looked all that tremendous in the first half.
Packers wide receiver Jordy Nelson was hit twice with offensive pass interference, Rodgers was harassed by the Chiefs' weak pass rush, and Green Bay wound up making five first downs.
One of them came when Kansas City's Jeremy Horne ran into Packers punter Tim Masthay, giving them 15 free yards. The Chiefs tried to give Green Bay another gift later on the drive when Mason Crosby missed a 59-yard field goal attempt but Kansas City had 12 men on the field.
With another chance from 54 yards, the normally reliable Crosby still pushed the kick right.
Rodgers finished the half 6 of 17 for 59 yards, with a handful of drops between wide receiver Donald Driver and tight end Jermichael Finley. In fact, things were going so badly for Green Bay that at one point it ran out of the wildcat despite having one of the best quarterbacks in the game.
The Chiefs were still clinging to a 6-0 lead when Rodgers finally hit down field, finding Finley over top the coverage for a 41-yard gain. Three plays later, the Packers' star quarterback hit Driver in the corner of the end zone for a 7-6 lead with 8:04 left in the third quarter.
Kansas City answered when Orton hit his own tight end, Leonard Pope, for a career-long 38-yard catch. Jon Baldwin added a 17-yard grab to set up Succop's 46-yard, go-ahead field goal.
The Packers moved into field-goal range on their ensuing drive, but rather than have Crosby attempt a 56-yard kick in the same direction he had already missed, McCarthy elected to go for it on fourth-and-9. Rodgers' pass fell incomplete and the Chiefs took over.
They needed seven plays to cover 59 yards, but had to settle for another field goal and a 12-7 lead. It was the third time the Chiefs drove inside the 5 and had six total points to show for it.
They got seven on their next trip, though.
With first-and-goal at the 5, Thomas Jones managed to gain a yard and Le'Ron McClain bulled ahead for three more, setting up third down from just outside the goal line. Battle took the carry over the right side and powered into the end zone, giving the woeful Kansas City offense its highest-scoring game since the Chiefs beat San Diego in overtime in late October.
The Packers marched down field in the closing minutes, and Rodgers showed his moxie by scampering around the end for a touchdown that made it 19-14, but that was as close as they got.
Green Bay came into the game averaging nearly 36 points, but was held to its lowest total since beating the Chicago Bears 10-3 in Week 17 last year. The Packers needed to win that game to make the playoffs, and wound up riding the momentum to a Super Bowl victory over the Pittsburgh Steelers.
All that momentum finally came to an end against the most unlikely of scenarios.
"We set the tone on both sides of the ball," Chiefs linebacker Derrick Johnson said. "This is the great thing about football. You can't always look at the records, because you've got grown men out there who are all getting paid. You don't have to be better on paper.
"If you're better on that given Sunday, you'll get the win."
Notes: Succop has made 21 consecutive field goals. ... Palko was inactive for Kansas City. ... The Chiefs wound up having the ball for 36:11, while Green Bay had it for 23:49. ... Kansas City won despite going 1 for 5 in the red zone. ... Packers OL Derek Sherrod broke his leg in the fourth quarter. He was playing in place of Bryan Bulaga, who went down with a knee strain.
First comprehensive DNA study of mast cell leukemia uncovers clues that could improve therapyPublic release date: 16-Dec-2011 [ | E-mail | Share ]
Contact: Hema Bashyam bashyam@cshl.edu 516-367-6822 Cold Spring Harbor Laboratory
Sequencing a cancer patient's 'exome' reveals mutations critical for improving diagnostic power and targeted therapy
Cold Spring Harbor, N.Y. Cancer researchers at Cold Spring Harbor Laboratory (CSHL) have carried out the first comprehensive study of the changes seen in the DNA of a patient with mast cell leukemia (MCL), an extremely aggressive subtype of acute myeloid leukemia (AML) with a very poor prognosis.
Their genomic survey has helped identify two previously unknown mutations that could directly influence patient response to currently available therapeutic drugs.
The details uncovered by the study not only suggest a diagnostic improvement and an alternative treatment strategy for MCL, but could also serve as a springboard for novel diagnostic and therapeutic approaches for other cancers such as lymphoma.
"This is incredibly exciting because we've gone from knowing very little about the genetics of MCL to uncovering information that could directly benefit patients diagnosed with MCL," says Research Investigator Mona Spector, Ph.D., who led the team's efforts.
The study, which appears online in the journal Leukemia on December 16, is a collaboration between cancer researchers at CSHL and clinicians led by Steven L. Allen, MD, FACP, associate chief of hematology at North Shore-LIJ's Monter Cancer Center and associate investigator at The Feinstein Institute for Medical Research. "This collaboration between the North Shore-LIJ Health System and CSHL allows us to increase medical knowledge and make innovative discoveries that may lead to new treatments for patients who are living with MCL," says Allen.
Made possible in large part by funding from the Don Monti Memorial Research Foundation, "the goal of this collaboration was to sequence patient DNA to find information about individual cancers that could be used to improve or design patient-specific treatment strategies," explains CSHL Adjunct Professor and HHMI Investigator Scott Lowe, Ph.D.
In this study, the CSHL scientists used two approaches to identify genetic changes seen in an MCL patient who succumbed to the disease about three months after diagnosis. MCL is characterized by out-of-control proliferation of transformed mast cells the same immune system cells that are notorious for their release of histamine during an allergic response.
In one approach, the CSHL team used a method called array comparative genomic hybridization (aCGH) to identify copy number variationsgenomic alterations that result in an abnormal number of copies of one or more sections of DNAin the leukemic mast cells. In a second approach, the team sequenced the majority of the "exome," the "exons" which are the DNA sequences that encode for protein (only about 2% of the genome).
This enabled them to identify mutations that result in the difference of a single nucleotide, or chemical "rung" in the DNA "ladder," between the patient's normal and tumor cells. These mutations often result in the production of aberrant proteins and can cause a cell to grow uncontrollably.
Bioinformatic analysis of the gigabytes of sequencing data by CSHL Fellow Ivan Iossifov, Ph.D., revealed the differences between the two genomes. Although several of the mutations occur within genes that have been previously linked to cancer, Spector immediately zeroed in on the mutations in two genes, KIT and MS4A2.
"MCL patients are screened for a mutation in the KIT gene that occurs at a specific amino acid referred to as D816V. This mutation not only spurs uncontrolled mast cell proliferation but also causes resistance to imatinib, a drug that works against some forms of leukemia; so patients with this mutation would normally not be treated with this drug," explains Spector.
"Our analysis showed that this patient, who lacked D816V and therefore received the drug, actually had a different KIT mutation called V654A, which may also cause resistance to the drug. Had this information been known before, the patient might have been treated differently and been spared the drug's side-effects." Spector hopes that this information might now encourage physicians to screen MCL patients for both KIT mutations.
The second mutation of interest occurs within the MS4A2 gene, which encodes for a protein that is part of a receptor that sits on a mast cell's surface and is required for its survival. The mutation identified by Spector occurs within the region of the protein that is essential both for its presence on the cell's surface, and more importantly, for triggering intracellular signaling by the enzyme Syk kinase. So Spector suspects that the MS4A2 mutation might be an "activating" mutation that may constantly keep the Syk signal in an "on" state, thereby prolonging the mast cell's life and eventually leading to cancer.
"If we prove this to be the case, then our finding could be therapeutically exploited because there already is a drug that blocks Syk signaling that has shown efficacy in a clinical trial for lymphoma," says Spector. She also observes that their findings might have implications beyond MCL. "For example, Syk signaling is also important in another type of immune cell called B cells, so researchers studying B cell cancers might also want to now look for mutations in genes within this pathway to identify patients who might respond to the Syk inhibitor drug," she says.
###
The study was supported by funding from the Don Monti Memorial Research Foundation and The Ryan Gibson Foundation.
"Mast-cell leukemia exome sequencing reveals a mutation in the IgE mast-cell receptor b chain and KIT V654A," appears online ahead of print in Leukemia on December 16. The full citation is: MS Spector, I Iossifov, A Kritharis, C He, JE Kolitz, SW Lowe and SL Allen. The paper can be downloaded at: http://www.nature.com/leu/journal/vaop/ncurrent/full/leu2011354a.html
About Cold Spring Harbor Laboratory
Founded in 1890, Cold Spring Harbor Laboratory (CSHL) has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. CSHL is ranked number one in the world by Thomson Reuters for impact of its research in molecular biology and genetics. The Laboratory has been home to eight Nobel Prize winners. Today, CSHL's multidisciplinary scientific community is more than 350 scientists strong and its Meetings & Courses program hosts more than 11,000 scientists from around the world each year. Tens of thousands more benefit from the research, reviews, and ideas published in journals and books distributed internationally by CSHL Press. The Laboratory's education arm also includes a graduate school and programs for undergraduates as well as middle and high school students and teachers. CSHL is a private, not-for-profit institution on the north shore of Long Island. For more information, visit http://www.cshl.edu.
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First comprehensive DNA study of mast cell leukemia uncovers clues that could improve therapyPublic release date: 16-Dec-2011 [ | E-mail | Share ]
Contact: Hema Bashyam bashyam@cshl.edu 516-367-6822 Cold Spring Harbor Laboratory
Sequencing a cancer patient's 'exome' reveals mutations critical for improving diagnostic power and targeted therapy
Cold Spring Harbor, N.Y. Cancer researchers at Cold Spring Harbor Laboratory (CSHL) have carried out the first comprehensive study of the changes seen in the DNA of a patient with mast cell leukemia (MCL), an extremely aggressive subtype of acute myeloid leukemia (AML) with a very poor prognosis.
Their genomic survey has helped identify two previously unknown mutations that could directly influence patient response to currently available therapeutic drugs.
The details uncovered by the study not only suggest a diagnostic improvement and an alternative treatment strategy for MCL, but could also serve as a springboard for novel diagnostic and therapeutic approaches for other cancers such as lymphoma.
"This is incredibly exciting because we've gone from knowing very little about the genetics of MCL to uncovering information that could directly benefit patients diagnosed with MCL," says Research Investigator Mona Spector, Ph.D., who led the team's efforts.
The study, which appears online in the journal Leukemia on December 16, is a collaboration between cancer researchers at CSHL and clinicians led by Steven L. Allen, MD, FACP, associate chief of hematology at North Shore-LIJ's Monter Cancer Center and associate investigator at The Feinstein Institute for Medical Research. "This collaboration between the North Shore-LIJ Health System and CSHL allows us to increase medical knowledge and make innovative discoveries that may lead to new treatments for patients who are living with MCL," says Allen.
Made possible in large part by funding from the Don Monti Memorial Research Foundation, "the goal of this collaboration was to sequence patient DNA to find information about individual cancers that could be used to improve or design patient-specific treatment strategies," explains CSHL Adjunct Professor and HHMI Investigator Scott Lowe, Ph.D.
In this study, the CSHL scientists used two approaches to identify genetic changes seen in an MCL patient who succumbed to the disease about three months after diagnosis. MCL is characterized by out-of-control proliferation of transformed mast cells the same immune system cells that are notorious for their release of histamine during an allergic response.
In one approach, the CSHL team used a method called array comparative genomic hybridization (aCGH) to identify copy number variationsgenomic alterations that result in an abnormal number of copies of one or more sections of DNAin the leukemic mast cells. In a second approach, the team sequenced the majority of the "exome," the "exons" which are the DNA sequences that encode for protein (only about 2% of the genome).
This enabled them to identify mutations that result in the difference of a single nucleotide, or chemical "rung" in the DNA "ladder," between the patient's normal and tumor cells. These mutations often result in the production of aberrant proteins and can cause a cell to grow uncontrollably.
Bioinformatic analysis of the gigabytes of sequencing data by CSHL Fellow Ivan Iossifov, Ph.D., revealed the differences between the two genomes. Although several of the mutations occur within genes that have been previously linked to cancer, Spector immediately zeroed in on the mutations in two genes, KIT and MS4A2.
"MCL patients are screened for a mutation in the KIT gene that occurs at a specific amino acid referred to as D816V. This mutation not only spurs uncontrolled mast cell proliferation but also causes resistance to imatinib, a drug that works against some forms of leukemia; so patients with this mutation would normally not be treated with this drug," explains Spector.
"Our analysis showed that this patient, who lacked D816V and therefore received the drug, actually had a different KIT mutation called V654A, which may also cause resistance to the drug. Had this information been known before, the patient might have been treated differently and been spared the drug's side-effects." Spector hopes that this information might now encourage physicians to screen MCL patients for both KIT mutations.
The second mutation of interest occurs within the MS4A2 gene, which encodes for a protein that is part of a receptor that sits on a mast cell's surface and is required for its survival. The mutation identified by Spector occurs within the region of the protein that is essential both for its presence on the cell's surface, and more importantly, for triggering intracellular signaling by the enzyme Syk kinase. So Spector suspects that the MS4A2 mutation might be an "activating" mutation that may constantly keep the Syk signal in an "on" state, thereby prolonging the mast cell's life and eventually leading to cancer.
"If we prove this to be the case, then our finding could be therapeutically exploited because there already is a drug that blocks Syk signaling that has shown efficacy in a clinical trial for lymphoma," says Spector. She also observes that their findings might have implications beyond MCL. "For example, Syk signaling is also important in another type of immune cell called B cells, so researchers studying B cell cancers might also want to now look for mutations in genes within this pathway to identify patients who might respond to the Syk inhibitor drug," she says.
###
The study was supported by funding from the Don Monti Memorial Research Foundation and The Ryan Gibson Foundation.
"Mast-cell leukemia exome sequencing reveals a mutation in the IgE mast-cell receptor b chain and KIT V654A," appears online ahead of print in Leukemia on December 16. The full citation is: MS Spector, I Iossifov, A Kritharis, C He, JE Kolitz, SW Lowe and SL Allen. The paper can be downloaded at: http://www.nature.com/leu/journal/vaop/ncurrent/full/leu2011354a.html
About Cold Spring Harbor Laboratory
Founded in 1890, Cold Spring Harbor Laboratory (CSHL) has shaped contemporary biomedical research and education with programs in cancer, neuroscience, plant biology and quantitative biology. CSHL is ranked number one in the world by Thomson Reuters for impact of its research in molecular biology and genetics. The Laboratory has been home to eight Nobel Prize winners. Today, CSHL's multidisciplinary scientific community is more than 350 scientists strong and its Meetings & Courses program hosts more than 11,000 scientists from around the world each year. Tens of thousands more benefit from the research, reviews, and ideas published in journals and books distributed internationally by CSHL Press. The Laboratory's education arm also includes a graduate school and programs for undergraduates as well as middle and high school students and teachers. CSHL is a private, not-for-profit institution on the north shore of Long Island. For more information, visit http://www.cshl.edu.
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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.
FORT MEADE, Maryland (Reuters) ? An American Army intelligence analyst accused of giving hundreds of thousands of classified U.S. documents to WikiLeaks for public disclosure made his first court appearance on Friday to face charges including aiding the enemy, which could send him to prison for life.
Private First Class Bradley Manning, charged with supplying WikiLeaks with massive dumps of classified U.S. documents, sat quietly in the courtroom at Fort Meade, Maryland, wearing military fatigues, dark-rimmed glasses and a short haircut.
He answered with a quick, "yes sir" as investigating officer Lieutenant Paul Almanza asked him whether he understood the charges against him.
After questioning Almanza, Manning attorney David Coombs announced that the defense was filing a motion for the investigating officer to recuse himself because of his work at the Department of Justice.
The Justice Department is conducting an investigation of WikiLeaks founder Julian Assange. If Justice "had its way," Coombs argued, it would get a plea from Manning that would help it "go after Assange."
Security was tight as media and some protesters gathered at the base, which also serves as the home of the intelligence-gathering National Security Agency.
WikiLeaks eventually posted online hundreds of thousands of sensitive diplomatic cables that exposed the candid views of U.S. officials and their allies.
It also released about half a million classified U.S. files on the Iraq and Afghan wars -- actions that Washington said jeopardized national security.
Secretary of State Hillary Clinton on Thursday called the WikiLeaks dump a "a very unfortunate and damaging action ... that put at risk individuals and relationships."
Prosecutors aim to show there is sufficient evidence to bring Manning to trial at a general court martial on 22 criminal charges.
If convicted of all counts, Manning would face a maximum punishment of life imprisonment, reduction in rank to the lowest enlisted pay grade, forfeiture of all pay and allowances and a dishonorable discharge, the Army said in a statement.
The most serious charge, aiding the enemy, is a capital crime that carries the death penalty, but the Army has indicated it does not plan to seek that punishment.
For much of the time since his detention beginning in May 2010 in Iraq, Manning was held on a charge of improperly obtaining a classified gunsight video that showed a 2007 helicopter attack that killed a dozen people in Iraq, including two Reuters journalists. The video was released publicly by WikiLeaks.
The additional charges were brought against Manning last spring.
DEFENDERS SEE A HERO
The proceedings begin one day before Manning, a Crescent, Oklahoma, native, celebrates his 24th birthday.
Members of the Bradley Manning Support Network were planning demonstrations on Friday outside Fort Meade and a march outside the base on Saturday, joined by protesters from the Occupy movement's encampments in Washington and on Wall Street, the organizations said.
Daniel Ellsberg, who released the controversial history of the Vietnam War known as the Pentagon Papers in 1971, is expected to address the protesters on Saturday along with former military veterans and diplomats, Manning supporters said in an email.
Manning defenders see him as a hero. Some view the release of the cables, with their frank discussion of corruption in some countries, as having contributed to the Arab Spring protests in the Middle East.
"He stands accused of doing the right thing," said Zack Pesavento, who was at Fort Meade on Friday morning.
Manning was caught after he bragged about his activities to former hacker Adrian Lamo, who turned him in to authorities, Lamo told Reuters.
Lamo said Manning, who worked as an intelligence analyst for the 10th Mountain Division's 2nd Brigade in Iraq, told him he would come into work with music on a recordable CD labeled "something like 'Lady Gaga.'" He would then erase the music and download data from the military's Secret Internet Protocol Router Network, known as SIPRNet.
Manning said he "listened and lip-synced to Lady Gaga's song 'Telephone' while exfiltrating possibly the largest data spillage in (A)merican history," according to a transcript of his Internet chats with Lamo, the details of which were confirmed by Lamo to Reuters and which were published by Wired Magazine.
In his Internet chats with Lamo, Manning appears to acknowledged giving materials to Assange. He wrote to Lamo: "I'm a high profile source ... and I've developed a relationship with Assange."
Assange is in Britain fighting extradition to Sweden over accusations of rape and sexual assault made by two female former WikiLeaks volunteers in August 2010. Britain's Supreme Court said on Friday it granted permission for Assange to appeal his case.
(Additional reporting by Phil Stewart; Editing by Xavier Briand)
SAN FRANCISCO?? Seeding clouds with saltwater spray in select regions of the globe could reduce the strength of some hurricanes and possibly prevent others from forming, a new study suggests.
The basic idea is to brighten marine clouds above the tropical Atlantic Ocean by pumping tiny salt particles into them. Brighter clouds reflect more sunlight into space, so the geoengineering effort could lower ocean temperatures and thus throw a wrench into the engine that sends hurricanes churning toward the Caribbean and the southeastern United States every summer, researchers said.
"The sea surface temperatures will respond, and that could reduce the category of the storm," said study co-author Alan Gadian of the University of Leeds in the United Kingdom, who presented the work here Dec. 8 at the annual meeting of the American Geophysical Union (AGU).
Brightening the clouds
Cloud seeding is a fairly established practice, but the intent is usually to spur or suppress precipitation. China employed the technique in 2008, for example, in an attempt to prevent rain from marring the opening and closing ceremonies of the Beijing Olympics.
Cloud seeding also may have potential to slow the pace of global warming, according to Gadian and his colleagues.
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The researchers have argued that injecting tiny sea-spray particles into marine stratocumulus clouds near the equator could help cool down the Earth. If they're the right size, the particles would increase the clouds' reflectivity and more sunlight would bounce off them and back into space.
The effects could be particularly profound at the poles, which most scientists say are getting hit hardest by climate change.
"If you want to cool the poles, you cool the equator regions," Gadian told OurAmazingPlanet."Because the atmosphere and oceans, the whole role of them is to take heat from the equator to the poles."
Reducing the power of hurricanes
Because hurricanes draw their strength from warm ocean waters, many scientists have predicted that the storms will become more powerful as the planet continues to heat up.
But cloud-brightening could conceivably help tackle this problem, too, by reducing ocean temperatures in the regions where hurricanes are born. In the new study, the team ? led by John Latham of the University Corporation for Atmospheric Research in Boulder, Colo. ? looked into this possibility using computer simulations.
The researchers found that seeding marine stratocumulus clouds in the tropical and subtropical Atlantic could potentially have a big impact. [ Photos: Hurricanes From Above ]
The intensity of some hurricanes could be reduced by a full category, for example, Gadian said. (Meteorologists classify hurricanes into five categories based on their wind speeds and other characteristics, with Category 1 being the weakest and Category 5 the strongest.)
Further, the reduced sea surface temperatures would likely prevent some hurricanes from forming at all, researchers said.
A trial run?
The team's studies highlight the potential of cloud-brightening as a tool to help stave off the worst effects of climate change, researchers said. But the extent of that potential is hard to gauge, because cloud-brightening hasn't been tested in the real world yet.
The researchers want to change that. They hope to stage a cloud-brightening experiment in the near future, using ships to inject sea-spray particles into clouds over a stretch of ocean measuring 62-miles square.
The goal of this next step wouldn't be to cool sea surface temperatures appreciably. Rather, researchers want to make sure they have a firm grasp on the technology ? how big the particles should be, how best to inject them, how the clouds respond and so forth.
"A field experiment could potentially provide really important information for understanding aerosol indirect effects, one of the largest sources of uncertainty in future climate warming," said team member Robert Wood of the University of Washington, who spoke about the proposed experiment during a talk here at the AGU meeting Dec. 8.
"It's an experiment that actually has a lot of potential for understanding geoengineering," Wood added.
The researchers stressed that cloud-brightening is not a solution to the problem of global warming, which is not going to go away as long as we keep pumping greenhouse gases into the atmosphere.
"It's not going to solve the problem," Gadian said. "It might buy you a little time."
You can follow SPACE.com senior writer Mike Wall on Twitter:@michaeldwall. Follow SPACE.com for the latest in space science and exploration news on Twitter @Spacedotcomand on Facebook.
? 2011 OurAmazingPlanet. All rights reserved. More from OurAmazingPlanet.
WASHINGTON ? A small comet survived what astronomers figured would be a sure death when it danced uncomfortably close to the broiling sun.
Comet Lovejoy, which was only discovered a couple of weeks ago, was supposed to melt Thursday night when it came close to where temperatures hit several million degrees. Astronomers had tracked 2,000 other sun-grazing comets make the same suicidal trip. None had ever survived.
But astronomers watching live with NASA telescopes first saw the sun's corona wiggle as Lovejoy went close to the sun. They were then shocked when a bright spot emerged on the sun's other side. Lovejoy lived.
"I was delighted when I saw it go into the sun and I was astounded when I saw something re-emerge," said U.S. Navy solar researcher Karl Battams.
Lovejoy didn't exactly come out of its hellish adventure unscathed. Only 10 percent of the comet ? which was probably millions of tons ? survived the encounter, said W. Dean Pesnell, project scientist for NASA's Solar Dynamics Observatory, which tracked Lovejoy's death-defying plunge.
And the comet lost something pretty important: its tail.
"It looks like the tail broke off and is stuck" in the sun's magnetic field, Pesnell said.
Comets circle the sun and sometimes get too close. Lovejoy came within 75,000 miles of the sun's surface, Battams said. For a small object often described as a dirty snowball comprised of ice and dust, that brush with the sun should have been fatal.
Astronomers say it probably didn't melt completely because the comet was larger than they thought.
The frozen comet was evaporating as it made the trip toward the sun, "just like you're sweating on a hot day," Pesnell said.
"It's like an ice cube going by a barbecue grill," he said.
Pesnell said the comet, although only discovered at the end of November by an Australian observer, probably is related to a comet that came by Earth on the way to the sun in 1106.
As Comet Lovejoy makes its big circle through the solar system, it will be another 800 or 900 years before it nears the sun again, astronomers say.
___
Online:
NASA's Solar Dynamics Observatory: http://1.usa.gov/upZJgS
U.S. Naval Research Lab's Sun-grazing comet website (video, photos at bottom): http://bit.ly/sfAAN5
The judges are not ready to crown Melanie Amaro X Factor champion just yet.
Following one of Chris Rene's two performances last night, Nicole Scherzinger and Paula Abdul jokingly argued about whether or not he looks like $1 million on stage... or $5 million the grand prize that will be awarded to next week's winner.
Does Rene have the best voice in the competition? No. But his spirit "transcends across the universe," according to Scherzinger. That, or he's just very good looking, right, ladies? Watch Chris cover "Fly" and "No One" now:
MEXICO CITY ? Mexico's government has publicly apologized for failing to protect the rights of an indigenous woman raped by soldiers in 2002.
Interior Secretary Alejandro Poire offered what he called "the most sincere of apologies" to Valentina Rosendo on Thursday.
Rosendo is a Me'phaa Indian who took her case to the Inter-American Court of Human Rights after failing to get justice in Mexico.
She was washing clothes in a river in southern Guerrero state when eight soldiers approached her and asked her about a suspect. When she said she didn't know anything, two soldiers beat and raped her.
The Costa Rica-based court last year ordered Mexico to apologize and have civilian authorities investigate. Federal prosecutors are now in charge of the probe.
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