It's "National UnFriend Day" according to comedian Jimmy Kimmel; the perfect opportunity to lose some folks from your bloated buddy list on Facebook. Too hard to decide how to pick and choose? Kimmel has devised a point system to help you out.
"If any of your so-called friends make it to 50 points, unfriend them," he said on his show. Here are some of the point ratings:
"If they change their profile picture more than once a month," 5 points.
"If they took their profile picture in the bathroom mirror using a cellphone," 5 points.
"If they've ever posted more than three photos of food, that's 5 points each."
"If they've ever posted the phrase, 'OMG, my friends are the best,'" 5 points.
The Official Jimmy Kimmel Live Channel / YouTube
But those aren't the among the worst of unfriendable infractions, at least for Kimmel. "If they've uploaded an embarrassing photo of you from junior high and tagged you in it, that's 15 points," he said.
And one of the ultimate offenses? "If they've used the phrase 'amazeballs,' that's 40 points."
You can see Kimmel's full bit on this by going to his YouTube channel. But hurry: National UnFriend Day is quickly evaporating, as is your chance to winnow your list. And judging by his point system, we'll all be down to zero friends by the end of the day.
Related stories:
Check out Technolog, Gadgetbox, Digital Life and In-Game on?Facebook,?and on Twitter, follow Suzanne Choney.
VIENNA (Reuters) ? Arab states and Israel plan to attend a rare round of talks next week on efforts to free the world of nuclear weapons but Iran has yet to say whether it will take part, diplomats said on Wednesday.
The November 21-22 forum, hosted by the International Atomic Energy Agency in Vienna, is seen as symbolically significant bid to bring regional foes together at the same venue, even though no concrete outcome is expected.
If conducted smoothly with relatively toned-down rhetoric on all sides, it could send a positive signal ahead of a planned international conference next year on ridding the Middle East of nuclear and other weapons of mass destruction.
"It is a good opportunity for everybody to sit and talk but
I don't think it is going to achieve a tangible result," a Western diplomat told Reuters.
An Arab envoy said he and others would probably mention Israel's assumed nuclear arsenal in their statements, but would not include anything "that would create polarization" in the meeting room.
"We expect to pinpoint the issues that could be an obstacle or impediment to establishing a nuclear free zone in the Middle East and possibly how to deal with them," the envoy said.
"Everybody knows that the Israeli nuclear capabilities are a big obstacle in this endeavor," the Arab diplomat said in comments that may irritate Israel.
Israel is widely believed to have the Middle East's only nuclear arsenal, and faces frequent Arab and Iranian condemnation.
Israel and the United States regard Iran as the region's main nuclear threat, accusing Tehran of trying to develop an atomic bomb in secret. An IAEA report last week added weight to those allegations which Iran denies.
Next week's discussions, convened by IAEA chief Yukiya Amano, will focus on the experiences of regions which have set up Nuclear-Weapons-Free Zones (NWFZ), including Africa and Latin America.
IAEA member states decided in 2000 to hold the meeting but it has taken this long for the parties involved to agree on the agenda and other issues.
All 151 IAEA member countries have been invited to the talks, to be chaired by senior Norwegian diplomat Jan Petersen, but Middle East envoys will take center stage.
NUCLEAR MEETING IN FINLAND
"The forum will consider the experience of five NWFZs and two regional verification arrangements and discuss the potential relevance of such experience to the creation of a NWFZ in the Middle East," the IAEA said in a statement.
Diplomats said Israel and Arab states had accepted the invitation but that there had as yet been no word from Iran, which in September said it saw no justification for such a meeting now and took a swipe at arch-enemy Israel.
Israel, the only Middle East country outside the nuclear Non-Proliferation Treaty (NPT), has never confirmed or denied having nuclear weapons under a policy of ambiguity to deter numerically superior foes.
It says it would only join the treaty if there is a comprehensive Middle East peace with its longtime Arab and Iranian adversaries. Israel would have to renounce nuclear weaponry if it signed the 1970 agreement.
Last month, the United Nations said Finland agreed to host a potentially divisive international meeting in 2012 to discuss ridding the Middle East of weapons of mass destruction.
The idea for that conference came from Egypt, which pushed for a meeting with all states in the Middle East to negotiate a treaty that would establish a nuclear arms-free zone.
Washington's commitment will be key to the success or failure of next year's talks, Western diplomats say, as it is the only state that can persuade Israel to attend.
The Arab envoy and others said setting up this kind of zone in the Middle East would not happen any time soon.
"It is very distant. It is a very complicated issue. There is a lot of mistrust among the parties," the envoy told Reuters.
The stumbling, two-decade-old war on hazardous air pollutants ? declared on Nov. 15, 1990, the day President George H. W. Bush signed the Clean Air Act amendments into law ? has stalled on bureaucratic dawdling, industry resistance, legal maneuvering, limited resources and politics. Untainted air for all Americans ? promised by Bush ? has proved elusive.
Our friends across the pond have had a month's head start getting to know Sony Ericsson'sXperia arc S inside and out. Now, it appears that refreshed flagship's gearing up to hit stateside as early as this week in unlocked fashion. Shown as having an estimated November 15th ship date on Sony's site, the 4.2-inch Gingerbread handset brings its Mobile Bravia Engine display, 1.4GHz Qualcomm processor and 8 megapixel shooter to North American mitts for $499 in four distinct shades. If carrier subsidization is your preferred method of purchase, you'll have to hold off for a bit as official US plans have yet to be announced. But why wait? Your early access mobile bragging rights await you at the source.
We've mentioned using bread tags as quick cord labels before, but if you don't have 10 loaves of bread lying around, you can easily make your own using just a hole punch and a milk jug.
The process is extremely simple: just cut your empty milk jug into a few small squares, punch a hole in the middle, and cut a small slit to imitate the look of a bread clip. Then, just write the name of each cable on the top of the tag, and affix them to your mess of cables behind your desk. Hit the link to read more.
How to: Make DIY 'Bread Clips' to Organize Your Cables and Power Cords | Curbly
You can contact Whitson Gordon, the author of this post, at whitson@lifehacker.com. You can also find him on Twitter, Facebook, and lurking around our #tips page. ?
MOSCOW (Reuters) ? Three astronauts will take off Monday returning a full crew to the International Space Station (ISS) after the crash of a Russian cargo spaceship disrupted operations and undermined faith in the Russian space program.
The launch at 11:14 p.m. EST is the first since NASA ended its 30-year shuttle program in July, heralding a gap of several years when the 16-nations investing in the $100-billion space station will rely solely on Russia to ferry crews.
Any problem with the launch could leave the space station empty for the first time in more than a decade when the current three-man crew returns to Earth later this month.
Monday's mission was delayed from September over safety fears after a Russian Progress craft taking supplies to astronauts broke up in the atmosphere in one of the worst Russian space disasters in decades.
For veteran NASA astronaut Daniel Burbank, it is the first voyage on board a Soyuz spacecraft from Russia's Baikonur launchpad in Kazakhstan, while cosmonauts Anatoly Ivanishin and Anton Shkaplerov are making their maiden space voyage.
But the crew shrugged off safety concerns before lift off.
"We don't have any black thoughts. We have faith in our equipment," Shkaplerov said, quoted by Russian news agencies.
After a cramped two-day journey aboard the Soyuz TMA-22 capsule, the crew will dock with the space station on November 16, overlapping briefly with station commander Mike Fossum of NASA, Japan's Satoshi Furukawa and Russia's Sergei Volkov.
Russia's space agency chief said the August 24 rocket failure was an "isolated" glitch caused by a fuel pipe blockage.
But it added to a string of failures that marred this year's celebration of the 50 years since Yuri Gagarin's pioneering orbit and pointed to deeper troubles with Russia's space industry.
Moscow hopes a smooth mission will begin to restore its reputation after more trouble this week when a launch touted as post-Soviet Russia's interplanetary debut went awry.
Russia has likely lost the $165-million Phobos-Grunt probe, which is stuck in orbit and may drop to Earth after it failed to set a course toward Mars' moon after launch Wednesday.
Botched launches have also lost Russia a high-tech military orbiter, a costly telecommunication satellite and set back plans for a global navigation system to rival the U.S. GPS.
While NASA suffered the tragic loss of crews on its Columbia and Challenger shuttles in 2003 and 1986, Russia last suffered such an accident in 1971 when three cosmonauts died on their way back to Earth on the Soyuz-11 mission.
This year the United States turned over all crewed flight responsibilities to Russia, at a cost of about $350 million a year, until commercial firms can offer space-taxi rides.
NASA is seeking $850 million to help U.S.-based private companies develop human orbital transport capabilities with the goal of breaking Russia's monopoly on ferrying astronauts to the space station before the end of 2016.
(Writing by Alissa de Carbonnel; Editing by Janet Lawrence)
Bacterial genes tell the tale of an outbreak's evolutionPublic release date: 13-Nov-2011 [ | E-mail | Share ]
Contact: David Cameron david_cameron@hms.harvard.edu 617-432-0441 Harvard Medical School
Researchers at Harvard Medical School and Children's Hospital Boston have retraced the evolution of an unusual bacterial infection as it spread among cystic fibrosis patients by sequencing scores of samples collected during the outbreak, since contained. A significant achievement in genetic pathology, the work also suggests a new way to recognize adaptive mutationsto see evolution as it happensand sheds new light on how our bodies resist infection.
The results are to be published online November 13 in Nature Genetics.
Cystic fibrosis (CF) is a hereditary disease that renders the lungs susceptible to bacterial infection. Though there is no cure for CF, it is managed with antibiotics and therapies that remove mucous from the lungs. An infection that resists antibiotics can overwhelm the body's defenses and lead eventually to respiratory failure and death, but advances in care have increased the median life expectancy for Americans born with CF from six months in 1959 to nearly 40 years today.
Despite constant vigilance, outbreaks pose a particular risk at CF treatment centers, where otherwise rare strains of bacteria can spread between patients. In the 1990's, one such outbreak spread among CF patients followed at a single CF center in Boston. Thirty-nine people were infected with the strain, later identified as a new species of bacteria, Burkholderia dolosa.
The hospital implemented new infection control measures and has not seen a new case in more than six years. But the outbreak presented researchers with a rare opportunity: A new pathogen with a closed circle of infection and abundant samples collected over the span of a decade.
Roy Kishony was looking for just such a bug. The HMS professor of systems biology studies bacterial evolution, exploring such questions as how antibiotic resistance arises. Many of his experiments are conducted in the lab: Grow bacteria in a test tube, add just enough antibiotic to challenge it, and look for genetic changes over time. But people aren't test tubes, and Kishony wanted to investigate how a pathogen evolves in a natural context.
"Imagine if you could interrogate the bacteria," said Kishony, principal investigator on the study. "You would ask, 'what do you find most challenging in the human body?'"
In search of a good model system, Kishony and his graduate student Jean-Baptiste Michel consulted clinicians and found their way to Alex McAdam, an associate professor of pathology at Children's Hospital Boston who suggested B. dolosa. "I thought it would be interesting," McAdam said, "because we could also see how the organism changed during the course of an outbreak."
From that conversation grew a robust collaboration among a diverse team of scientists and clinicians, including Kishony's lab, McAdam and Greg Priebe, assistant professor of anesthesia at Children's and a microbiologist at the Channing Laboratory of Brigham and Women's Hospital, as well as collaborators in Michigan and Virginia. The team set out to sequence the genomes of 112 B. dolosa isolates taken from 14 of the infected patients, mapping genetic changes over time to reveal both the route of the infection's spread and which genes faced the greatest selective pressure in other words, how the bacteria evolved when challenged by human defenses and medical treatment.
Every time a cell divides, small copying errors can introduce slight changes in the new DNA. Some of those changes affect the cell's machinery, and some do not. To identify selective pressure on genes over generations, scientists compare the number of significant changes to the number of those that had no effecta measure called the dN/dS ratio.
"That's where we ran into a bit of a snag," said Michel, now a postdoctoral fellow at Harvard University and visiting faculty at Google, who analyzed the data with Tami Lieberman when both were graduate students in Systems Biology. When Michel and Lieberman, who share credit as first authors on the Nature Genetics paper, crunched the numbers on their B. dolosa samples, the dN/dS ratio was 1.0. Across the genomes of their entire sample set, the changes appeared perfectly random.
"It wasn't a small effect," Lieberman said. "It was no effect." But the finding defied previous observations and common sensebacteria face pressure from antibiotics, pressure from the immune system, pressure from one another. Even in test tubes, bacteria evolve.
Maybe, Lieberman suggested, they were asking the wrong question. What if the genome-wide dN/dS ratio was a red herring, when what they really wanted to know was what was happening to specific genes? "Tami had the key insight," said Kishony. If a mutation has any effect, it's typically harmful. Randomly tune your car, and you're apt to get a broken car. In a gene pool, purifying selection weeds out those harmful changes even as positive selection spreads helpful ones. Average those positive and negative effects, and both might disappear.
Sure enough, when Lieberman and Michel analyzed the same data another wayseparating genes that had mutated in multiple patients from those that had mutated just oncemost genes registered a dN/dS of slightly less than one, evidence of widespread purifying selection. Seventeen genes scored much higher, strong evidence of positive selection. Tellingly, bacteria from different patients showed pressure on the same genes, which evolved in similar ways.
"These data told us what the pathogen experiences as its main challenges," Kishony said. Some of those challenges were expected: Genes linked to antibiotic resistance, adhesion and immune response faced pressure to adapt.
One of the most striking findings among such genes was a stop codon, seen in about 70 percent of the strains, in a previously unstudied enzyme linked to genes involved in the synthesis of lipopolysaccharide (LPS), also known as endotoxin. The Priebe lab and collaborators had previously observed an unusual degree of LPS variation among B. dolosa strains and now had a genetic mechanism to explain it. "That finding was a real 'aha' moment for me," said Priebe, who suggested that the enzyme could be disappearing as the bacteria adapted to evade the immune system, adhere to its host or improve a function still undiscovered.
But other challenges were a surprise, for example propelling furious changes in genes linked to growth under low-oxygen conditions typical of the lung of a CF patient. "This method suggests therapeutic directions we didn't know were important," Michel said, "and drug targets we didn't know existed."
The team's findings could help researchers better understand a pathogen's strengths and weaknesses, the mechanisms by which it adapts to our defenses, and potential targets for new therapies. The researchers next hope to study the diversity generated by a pathogen's evolution within a single patient, to learn more about the different challenges posed throughout the human body.
The questions are still evolving.
###
This research was funded by the National Institutes of Health, the New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases, and the Harvard Catalyst.
Citation:
Nature Genetics, online publication, Nov 13, 2011
"Parallel bacterial evolution within multiple patients identifies candidate pathogenicity genes," by Lieberman et al
Harvard Medical School http://hms.harvard.edu> has more than 7,500 full-time faculty working in 11 academic departments located at the School's Boston campus or in one of 47 hospital-based clinical departments at 17 Harvard-affiliated teaching hospitals and research institutes. Those affiliates include Beth Israel Deaconess Medical Center, Brigham and Womens Hospital, Cambridge Health Alliance, Childrens Hospital Boston, Dana-Farber Cancer Institute, Forsyth Institute, Harvard Pilgrim Health Care, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Childrens Center, Massachusetts Eye and Ear Infirmary, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Schepens Eye Research Institute, Spaulding Rehabilitation Hospital, and VA Boston Healthcare System.
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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.
Bacterial genes tell the tale of an outbreak's evolutionPublic release date: 13-Nov-2011 [ | E-mail | Share ]
Contact: David Cameron david_cameron@hms.harvard.edu 617-432-0441 Harvard Medical School
Researchers at Harvard Medical School and Children's Hospital Boston have retraced the evolution of an unusual bacterial infection as it spread among cystic fibrosis patients by sequencing scores of samples collected during the outbreak, since contained. A significant achievement in genetic pathology, the work also suggests a new way to recognize adaptive mutationsto see evolution as it happensand sheds new light on how our bodies resist infection.
The results are to be published online November 13 in Nature Genetics.
Cystic fibrosis (CF) is a hereditary disease that renders the lungs susceptible to bacterial infection. Though there is no cure for CF, it is managed with antibiotics and therapies that remove mucous from the lungs. An infection that resists antibiotics can overwhelm the body's defenses and lead eventually to respiratory failure and death, but advances in care have increased the median life expectancy for Americans born with CF from six months in 1959 to nearly 40 years today.
Despite constant vigilance, outbreaks pose a particular risk at CF treatment centers, where otherwise rare strains of bacteria can spread between patients. In the 1990's, one such outbreak spread among CF patients followed at a single CF center in Boston. Thirty-nine people were infected with the strain, later identified as a new species of bacteria, Burkholderia dolosa.
The hospital implemented new infection control measures and has not seen a new case in more than six years. But the outbreak presented researchers with a rare opportunity: A new pathogen with a closed circle of infection and abundant samples collected over the span of a decade.
Roy Kishony was looking for just such a bug. The HMS professor of systems biology studies bacterial evolution, exploring such questions as how antibiotic resistance arises. Many of his experiments are conducted in the lab: Grow bacteria in a test tube, add just enough antibiotic to challenge it, and look for genetic changes over time. But people aren't test tubes, and Kishony wanted to investigate how a pathogen evolves in a natural context.
"Imagine if you could interrogate the bacteria," said Kishony, principal investigator on the study. "You would ask, 'what do you find most challenging in the human body?'"
In search of a good model system, Kishony and his graduate student Jean-Baptiste Michel consulted clinicians and found their way to Alex McAdam, an associate professor of pathology at Children's Hospital Boston who suggested B. dolosa. "I thought it would be interesting," McAdam said, "because we could also see how the organism changed during the course of an outbreak."
From that conversation grew a robust collaboration among a diverse team of scientists and clinicians, including Kishony's lab, McAdam and Greg Priebe, assistant professor of anesthesia at Children's and a microbiologist at the Channing Laboratory of Brigham and Women's Hospital, as well as collaborators in Michigan and Virginia. The team set out to sequence the genomes of 112 B. dolosa isolates taken from 14 of the infected patients, mapping genetic changes over time to reveal both the route of the infection's spread and which genes faced the greatest selective pressure in other words, how the bacteria evolved when challenged by human defenses and medical treatment.
Every time a cell divides, small copying errors can introduce slight changes in the new DNA. Some of those changes affect the cell's machinery, and some do not. To identify selective pressure on genes over generations, scientists compare the number of significant changes to the number of those that had no effecta measure called the dN/dS ratio.
"That's where we ran into a bit of a snag," said Michel, now a postdoctoral fellow at Harvard University and visiting faculty at Google, who analyzed the data with Tami Lieberman when both were graduate students in Systems Biology. When Michel and Lieberman, who share credit as first authors on the Nature Genetics paper, crunched the numbers on their B. dolosa samples, the dN/dS ratio was 1.0. Across the genomes of their entire sample set, the changes appeared perfectly random.
"It wasn't a small effect," Lieberman said. "It was no effect." But the finding defied previous observations and common sensebacteria face pressure from antibiotics, pressure from the immune system, pressure from one another. Even in test tubes, bacteria evolve.
Maybe, Lieberman suggested, they were asking the wrong question. What if the genome-wide dN/dS ratio was a red herring, when what they really wanted to know was what was happening to specific genes? "Tami had the key insight," said Kishony. If a mutation has any effect, it's typically harmful. Randomly tune your car, and you're apt to get a broken car. In a gene pool, purifying selection weeds out those harmful changes even as positive selection spreads helpful ones. Average those positive and negative effects, and both might disappear.
Sure enough, when Lieberman and Michel analyzed the same data another wayseparating genes that had mutated in multiple patients from those that had mutated just oncemost genes registered a dN/dS of slightly less than one, evidence of widespread purifying selection. Seventeen genes scored much higher, strong evidence of positive selection. Tellingly, bacteria from different patients showed pressure on the same genes, which evolved in similar ways.
"These data told us what the pathogen experiences as its main challenges," Kishony said. Some of those challenges were expected: Genes linked to antibiotic resistance, adhesion and immune response faced pressure to adapt.
One of the most striking findings among such genes was a stop codon, seen in about 70 percent of the strains, in a previously unstudied enzyme linked to genes involved in the synthesis of lipopolysaccharide (LPS), also known as endotoxin. The Priebe lab and collaborators had previously observed an unusual degree of LPS variation among B. dolosa strains and now had a genetic mechanism to explain it. "That finding was a real 'aha' moment for me," said Priebe, who suggested that the enzyme could be disappearing as the bacteria adapted to evade the immune system, adhere to its host or improve a function still undiscovered.
But other challenges were a surprise, for example propelling furious changes in genes linked to growth under low-oxygen conditions typical of the lung of a CF patient. "This method suggests therapeutic directions we didn't know were important," Michel said, "and drug targets we didn't know existed."
The team's findings could help researchers better understand a pathogen's strengths and weaknesses, the mechanisms by which it adapts to our defenses, and potential targets for new therapies. The researchers next hope to study the diversity generated by a pathogen's evolution within a single patient, to learn more about the different challenges posed throughout the human body.
The questions are still evolving.
###
This research was funded by the National Institutes of Health, the New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases, and the Harvard Catalyst.
Citation:
Nature Genetics, online publication, Nov 13, 2011
"Parallel bacterial evolution within multiple patients identifies candidate pathogenicity genes," by Lieberman et al
Harvard Medical School http://hms.harvard.edu> has more than 7,500 full-time faculty working in 11 academic departments located at the School's Boston campus or in one of 47 hospital-based clinical departments at 17 Harvard-affiliated teaching hospitals and research institutes. Those affiliates include Beth Israel Deaconess Medical Center, Brigham and Womens Hospital, Cambridge Health Alliance, Childrens Hospital Boston, Dana-Farber Cancer Institute, Forsyth Institute, Harvard Pilgrim Health Care, Hebrew SeniorLife, Joslin Diabetes Center, Judge Baker Childrens Center, Massachusetts Eye and Ear Infirmary, Massachusetts General Hospital, McLean Hospital, Mount Auburn Hospital, Schepens Eye Research Institute, Spaulding Rehabilitation Hospital, and VA Boston Healthcare System.
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
We've mentioned using bread tags as quick cord labels before, but if you don't have 10 loaves of bread lying around, you can easily make your own using just a hole punch and a milk jug. ![[ Back to EurekAlert! ]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_sMjHTZQLn5tyKFaqrooIkKqZAlUHWY2WGzG3QNgvaXCgnx7BmKFJ0wczzMdVuDOkdq2mTm_gQUF-JMuB7y1zR6B7MjMjoifshsesqRk_Q=s0-d){kind=small}
Public release date: 13-Nov-2011
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