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Monday, April 30, 2012
Thursday, April 26, 2012
Everything You Need to Kill Time Until Your Team's Next NFL Draft Pick [Toolkit]
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Matchmaker, matchmaker: ?Big Nog?s? next bout, moving around title bouts, and Hector Lombard?s new home
Here's the latest in fights made and fighters signed by the UFC's yentes.
-- Somehow, not every heavyweight bout isn't on UFC 146. Antonio Rodrigo Nogueira will fight Cheick Kongo at UFC 149 in Calgary. This is Big Nog's first fight back since Frank Mir snapped his arm.
-- The moving around of title fights isn't over with Chael Sonnen's bout with Anderson Silva. Jose Aldo's title fight may move to UFC 147 in Brazil, which doesn't have a venue, and Dan Henderson may face Jon Jones for the UFC light heavyweight belt at UFC 149 in Calgary. With summer looming, few pay-per-view cards outside of UFC 148 in Las Vegas are set.
-- Though there isn't a fight yet scheduled for him, former Bellator champion Hector Lombard will make the move to the UFC. MMA Fighting found out from Bellator CEO Bjorn Rebney, and then Lombard confirmed the news on Twitter. His last loss was in 2006, and Rebney said he is confident Lombard will be the UFC middleweight champ.
-- Marcus LeVesseur will make his UFC debut against Cody McKenzie at UFC on Fuel 3 on May 15 in Virginia, taking the place of Aaron Riley. Wrestling fans will recognize LeVesseur as four-time D-III national champion. He's been fighting since 2003 and has a record of 21-5. TUF alum McKenzie is on a three-fight losing streak.
UPDATE: One more bout for your enjoyment. Mark Munoz will take on Chris Weidman at UFC on Fuel 4 on July 11. The just-announced event does not yet have a location, but is important in deciding who will fight for the middleweight belt next.
--
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Is Russia now the strongest backer of peace in Syria?
Russia has emerged as a strong backer of Kofi Annan's peace plan for Syria, and is now hammering Western nations for not doing enough to support it.
Russia today challenged Western countries to get behind United Nations envoy Kofi Annan's peace plan for Syria, or accept the blame for its failure.
Skip to next paragraphIt's a new role for Russia, which endured months of accusations that it was blocking a solution for strife-torn Syria after it vetoed two UN Security Council?resolutions in the past several months?calling for the removal of Syrian leader Bashar al-Assad.? ?
But last month, Moscow threw its weight behind Mr. Annan's plan to end the year-long uprising, which has killed more than 9,000 people by UN estimates. It called for a withdrawal of all government forces from Syrian towns and cities, followed by a shaky cease-fire that went into effect last Thursday and appears to be just barely holding despite multiple violations alleged on both sides.
Speaking in televised remarks today, Russian Foreign Minister Sergei Lavrov implied that the shoe is on the other foot now, with Moscow strongly backing the UN peace plan for Syria and willing to hold both Mr. Assad and his opponents to task but, he alleged, the effort is being undermined by unnamed Western and Arab countries.
"There are those who want Kofi Annan's plan to fail," Mr. Lavrov insisted. "Today, those who from the beginning foretold the failure of Annan's plan are doing a lot to see to it that this prophecy comes true? They are doing this by delivering arms to the Syrian opposition and stimulating the activity of rebels who continue to attack both government facilities and civilian facilities on a daily basis."
The cease-fire remains "quite fragile" because of the reluctance of those outside forces to fully back the Annan plan, Lavrov suggested, although he added that Assad bears a share of blame for the continuing uncertainty. "Of course, government forces are also taking measures to react to such provocations, and as a result it is not all going very smoothly yet," he said.
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Wednesday, April 25, 2012
Flexible Solar Panels Stack Cells on Sheets Printed Like OLEDs [Monster Machines]
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EyeRing finger-mounted connected cam captures signs and dollar bills, identifies them with OCR (hands-on)
Ready to swap that diamond for a finger-mounted camera with a built-in trigger and Bluetooth connectivity? If it could help identify otherwise indistinguishable objects, you might just consider it. The MIT Media Lab's EyeRing project was designed with an assistive focus in mind, helping visually disabled persons read signs or identify currency, for example, while also serving to assist children during the tedious process of learning to read. Instead of hunting for a grownup to translate text into speech, a young student could direct EyeRing at words on a page, hit the shutter release, and receive a verbal response from a Bluetooth-connected device, such as a smartphone or tablet. EyeRing could be useful for other individuals as well, serving as an ever-ready imaging device that enables you to capture pictures or documents with ease, transmitting them automatically to a smartphone, then on to a media sharing site or a server.
We peeked at EyeRing during our visit to the MIT Media Lab this week, and while the device is buggy at best in its current state, we can definitely see how it could fit into the lives of people unable to read posted signs, text on a page or the monetary value of a currency note. We had an opportunity to see several iterations of the device, which has come quite a long way in recent months, as you'll notice in the gallery below. The demo, which like many at the Lab includes a Samsung Epic 4G, transmits images from the ring to the smartphone, where text is highlighted and read aloud using a custom app. Snapping the text "ring," it took a dozen or so attempts before the rig correctly read the word aloud, but considering that we've seen much more accurate OCR implementations, it's reasonable to expect a more advanced version of the software to make its way out once the hardware is a bit more polished -- at this stage, EyeRing is more about the device itself, which had some issues of its own maintaining a link to the phone. You can get a feel for how the whole package works in the video after the break, which required quite a few takes before we were able to capture an accurate reading.
EyeRing finger-mounted connected cam captures signs and dollar bills, identifies them with OCR (hands-on) originally appeared on Engadget on Wed, 25 Apr 2012 13:53:00 EDT. Please see our terms for use of feeds.
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Steam for Linux is coming, and after waiting epochs what's a few more months?
It's been a long-running saga as to when Linux users will finally see some native gaming action on Steam, but according to Phoronix that happy day will likely arrive within "months." Valve has been busily hiring Linux OpenGL boffins, including people recommended by Phoronix's founder, Michael Larabel, who certainly seems to be on the inside track. His photo above offers some proof of progress: it shows Left 4 Dead 2 running natively on Ubuntu 11.10 with AMD Catalysts drivers. Why has it taken so long since news of a Linux client was first floated (and officially denied) back in 2010? Larabel attributes it to Valve's "flat management structure" that allows its developers to work on what they want. (And you still question the importance of hierarchy?)
Steam for Linux is coming, and after waiting epochs what's a few more months? originally appeared on Engadget on Wed, 25 Apr 2012 06:19:00 EDT. Please see our terms for use of feeds.
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Ex-PM cleared of major charges in Iceland crisis trial
REYKJAVIK (Reuters) - Iceland's former prime minister was found innocent on Monday of three major charges of negligence related to the country's 2008 economic collapse, and guilty of a smaller count that carried no prison sentence.
The verdict by a special court was seen by many as little more than a slap on the wrist for Geir Haarde, the only leader in the world to face prosecution over the global crisis. He had faced up to two years in prison if found guilty of the more serious charges, including neglecting to deal with an overblown banking sector.
Haarde looked on and showed no visible emotion as the 15-judge court issued its verdict, convicting him of failing to hold dedicated cabinet meetings ahead of the crisis. About 70 people, including his family and political supporters, attended the session.
Moments later, he told reporters that the judges had tried to appease a public opinion angry at a political elite perceived as fostering an unsustainable banking system that grew to 10 times Iceland's GDP just before the meltdown.
"It is absurd," a furious-looking, red-faced Haarde said.
"It is obvious that the majority of the judges have found themselves pressed to come up with a guilty verdict on one point, however minor, to save the neck of the parliamentarians who instigated this," he added.
Outside the court, a protester banged on a pot, in a repeat of the gesture that Icelanders carried out at the height of the crisis in the streets outside parliament. The protests were the biggest ever seen in Iceland, occasionally turning violent in a nation renowned for its peaceful nature.
All of Iceland's top banks went under in 2008 just days after the collapse of Lehman Brothers, which led to a freeze on global interbank lending. The country's crown currency nosedived and many Icelanders who had taken out foreign currency loans found themselves saddled with even bigger piles of debt.
Despite the anger, many Icelanders say the 61-year-old Haarde, generally seen as a decent person who was too soft in his role as prime minister, should not have been the only politician put on the stand.
"He was the captain on the bridge, but there were more ministers," said Arni Einarsson, a pensioner. "The politicians thought that Iceland was like the Titanic - unsinkable."
"NOT UNIQUE"
Prime Minister Johanna Sigurdardottir, who served in Haarde's cabinet during the boom years that preceded the crisis, said the verdict had taken her by surprise.
"I never thought the charges were sufficient to warrant the indictment and subsequent trial," she told state television.
Haarde said that while his government could have done something different in the run up to the island's worst-ever crisis, he doubted he could have stopped it.
"Look at what the leaders of the central banks of the U.S., the UK have said repeatedly - they didn't see this crisis coming. The IMF didn't see this crisis coming," he told Reuters after the verdict, which was broadcast live on TV.
"Look at what is happening in Greece, Spain, Portugal, Ireland, Italy. Our situation is not unique."
Haarde, who had pleaded innocent to all charges, said he is considering taking his case to the European Court of Human Rights.
Eirikur Bergmann, political science professor at the Bifrost University north of the capital, called the ruling "a slap on the wrist".
"He's not convicted on any of the charges leading up to the crisis - sponsoring the system that proved unsustainable," said Bergmann. "It is an in-between ruling to calm both sides of society."
Though the economy is recovering from the crisis and Iceland successfully completed a bailout program led by the International Monetary Fund, people remain distrustful of state institutions. Polls show that parliament has the support of only 10 percent of the public.
Capital controls remain in place, damaging the economic recovery.
(Writing by Alistair Scrutton, additional reporting by Omar Valdimarsson in Reykjavik and Anna Ringstrom and Niklas Pollard in Stockholm; Editing by Alessandra Rizzo)
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Tuesday, April 24, 2012
Johns Hopkins researchers uncover genes at fault for cystic fibrosis-related intestinal obstruction
![[ Back to EurekAlert! ]](http://www.eurekalert.org/images/back2e.gif){kind=small}
Public release date: 23-Apr-2012[ | E-mail |
Share ] Contact: Audrey Huang
audrey@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
Researchers at Johns Hopkins have identified a gene that modifies the risk of newborns with cystic fibrosis (CF) developing neonatal intestinal obstruction, a potentially lethal complication of CF. Their findings, which appeared online March 15 in PLoS Genetics, along with the findings of their Toronto-based colleagues, published April 1 in Nature Genetics, may lead to a better understanding of how the intestines work and pave the way for identifying genes involved in secondary complications of other disorders.
Soon after birth, most babies excrete their first stool, a tar-like substance called meconium. But not babies with neonatal intestinal obstruction, or meconium ileus (MI), which affects 15 percent of newborns with CF and, rarely, newborns without CF. Their stool is different.
"It is abnormally viscous due to high protein content and low levels of hydration, and the child can't move it through the intestine," says Garry Cutting, M.D., professor of pediatrics at the Johns Hopkins McKusick-Nathans Institute of Genetic Medicine.
The condition results in death if not treated by surgery or enema. But why some newborns with CF get it and others don't is not well understood. To better understand why this is so and to develop models for finding so-called modifier genesgenes that modify the effects of other genesCutting and his colleagues aimed to figure out which modifier genes contribute to the development of MI. (From their previous work, they already knew that modifier genes contribute to its development.)
Working with Toronto-based collaborators, members of Cutting's team looked for gene variants that occur in CF patients with MI. They knew that CF is caused by disruption of the CFTR gene, which encodes for a cell membrane protein, so they thought that maybe the genes that alter CFTR's activity and cause MI might also encode for cell membrane proteins; after all, a cell membrane protein is more likely to interact with a nearby cell membrane protein than with a protein that's deep inside the cell. They tested DNA samples from 3,763 CF patients611 who had had MI and 3152 who hadn'tto compare genes that encode for cell membrane proteins to those that encode for unrelated proteins. Three of the 155 genes tested that encode for cell membrane proteins correlated with risk for MI, compared with none of the 231 genes tested that encode for unrelated proteins.
"These genes have common variants that all of us happen to be carrying around," says Cutting, "and just by chance, if you have a child with CF, these common variants play a role in modifying risk for meconium ileus." The researchers wanted to look for additional gene variants associated with an increased risk for MI, using a different approach.
In an earlier study, Cutting's team had found a region of human chromosome 8 to be linked to MI. To pinpoint which gene within that region leads to the condition, the researchers analyzed the DNA of 133 families with at least two CF children, at least one of whom previously had MI. The DNA was tested to determine which parts of chromosome 8 parents had passed down to their children who had MI.
Using this approach, the researchers found variants of the methionine sulfoxide reductase (MSRA) genein this case, a particular combination of DNA alterations close to and within the genethat appeared significantly more often in children who had MI. In an unrelated CF patient population from Canada, they found evidence of the same link between MSRA and MI, which helped confirm their results.
While the researchers now knew that CF patients with a certain MSRA gene variant tended to have had MI as newborns, they didn't yet know whether MSRA actually plays a role in MI and hence whether it is truly a modifier gene. To address this question, they turned to mice engineered to have CF that tend to die from intestinal obstruction and developed three genetically modified versions of these mice: one with both MSRA genes intact, one with only one intact, and one with none intact. The fewer the copies of intact MSRA genes, the more likely the mice were to survive. In other words, the loss of MSRA protected the mice from fatal intestinal obstruction.
Cutting and his colleagues don't know how exactly the loss of MSRA reduces risk for fatal intestinal obstruction, but they suspect that MSRA's ability to alter the activity of specific intestinal enzymes may be the key. They suspect that with reduced levels of MSRA, the enzymes are free to do their job breaking down proteins that make up meconium so that meconium can pass through the intestines and be evacuated normally at birth.
The researchers' work on MSRA could shed light on how meconium normally gets broken down in the intestines. Moreover, use of the techniques pioneered by Cutting and his colleagues may lead to identification of modifier genes that play roles in other complications of CF, like lung function, and in other diseases caused by a single gene, like Huntington's disease.
###
The studies were funded by the National Institutes of Health (NHLBI and NIDDK) and the Cystic Fibrosis Foundation.
Authors on the PLoS Genetics paper are: Lindsay B. Henderson, Vishal K. Doshi, Scott M. Blackman, Kathleen M. Naughton, and Garry R. Cutting of Johns Hopkins; Rhonda G. Pace and Michael R. Knowles of University of North Carolina at Chapel Hill; Jackob Moskovitz of University of Kansas, Lawrence; Peter R. Durie of Hospital for Sick Children, Toronto, Ontario, Canada; and Mitchell L. Drumm of Case Western Reserve University.
Authors on the Nature Genetics paper are: Lei Sun, Johanna Rommens, Weili Li, Peter R Durie, Lisa Strug of University of Toronto, Toronto, Ontario, Canada; Harriet Corvol, Annick Clement and Pierre-Yves Bolle of Pierre et Marie Curie University, Paris, France ; Xin Li, Theodore Chiang, Fan Lin, Ruslan Dorfman, Rashmi V Parekh, Mary Corey, Julian Zielenski of the Hospital for Sick Children, Toronto, Ontario, Canada; Pierre-Franois Busson of St Antoine Hospital, Paris, France; Diana Zelenika of Centre National de Gnotypage, Evry, France ; Scott Blackman, Vishal Doshi, Lindsay Henderson, Kathleen Naughton and Garry R Cutting of Johns Hopkins; Wanda K O'Neal, Rhonda G Pace, Jaclyn R Stonebraker, Sally D Wood and Fred A Wright, and Michael R. Knowles of University of North Carolina at Chapel Hill; and Mitchell L. Drumm of Case Western Reserve University.
On the Web:
http://www.hopkinsmedicine.org/geneticmedicine/
http://www.hopkinsmedicine.org/geneticmedicine/People/Faculty/cutting.html
http://www.plosgenetics.org/home.action
http://www.nature.com/ng/index.html
[ | 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.
Public release date: 23-Apr-2012[ | E-mail |
Share ] Contact: Audrey Huang
audrey@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
Researchers at Johns Hopkins have identified a gene that modifies the risk of newborns with cystic fibrosis (CF) developing neonatal intestinal obstruction, a potentially lethal complication of CF. Their findings, which appeared online March 15 in PLoS Genetics, along with the findings of their Toronto-based colleagues, published April 1 in Nature Genetics, may lead to a better understanding of how the intestines work and pave the way for identifying genes involved in secondary complications of other disorders.
Soon after birth, most babies excrete their first stool, a tar-like substance called meconium. But not babies with neonatal intestinal obstruction, or meconium ileus (MI), which affects 15 percent of newborns with CF and, rarely, newborns without CF. Their stool is different.
"It is abnormally viscous due to high protein content and low levels of hydration, and the child can't move it through the intestine," says Garry Cutting, M.D., professor of pediatrics at the Johns Hopkins McKusick-Nathans Institute of Genetic Medicine.
The condition results in death if not treated by surgery or enema. But why some newborns with CF get it and others don't is not well understood. To better understand why this is so and to develop models for finding so-called modifier genesgenes that modify the effects of other genesCutting and his colleagues aimed to figure out which modifier genes contribute to the development of MI. (From their previous work, they already knew that modifier genes contribute to its development.)
Working with Toronto-based collaborators, members of Cutting's team looked for gene variants that occur in CF patients with MI. They knew that CF is caused by disruption of the CFTR gene, which encodes for a cell membrane protein, so they thought that maybe the genes that alter CFTR's activity and cause MI might also encode for cell membrane proteins; after all, a cell membrane protein is more likely to interact with a nearby cell membrane protein than with a protein that's deep inside the cell. They tested DNA samples from 3,763 CF patients611 who had had MI and 3152 who hadn'tto compare genes that encode for cell membrane proteins to those that encode for unrelated proteins. Three of the 155 genes tested that encode for cell membrane proteins correlated with risk for MI, compared with none of the 231 genes tested that encode for unrelated proteins.
"These genes have common variants that all of us happen to be carrying around," says Cutting, "and just by chance, if you have a child with CF, these common variants play a role in modifying risk for meconium ileus." The researchers wanted to look for additional gene variants associated with an increased risk for MI, using a different approach.
In an earlier study, Cutting's team had found a region of human chromosome 8 to be linked to MI. To pinpoint which gene within that region leads to the condition, the researchers analyzed the DNA of 133 families with at least two CF children, at least one of whom previously had MI. The DNA was tested to determine which parts of chromosome 8 parents had passed down to their children who had MI.
Using this approach, the researchers found variants of the methionine sulfoxide reductase (MSRA) genein this case, a particular combination of DNA alterations close to and within the genethat appeared significantly more often in children who had MI. In an unrelated CF patient population from Canada, they found evidence of the same link between MSRA and MI, which helped confirm their results.
While the researchers now knew that CF patients with a certain MSRA gene variant tended to have had MI as newborns, they didn't yet know whether MSRA actually plays a role in MI and hence whether it is truly a modifier gene. To address this question, they turned to mice engineered to have CF that tend to die from intestinal obstruction and developed three genetically modified versions of these mice: one with both MSRA genes intact, one with only one intact, and one with none intact. The fewer the copies of intact MSRA genes, the more likely the mice were to survive. In other words, the loss of MSRA protected the mice from fatal intestinal obstruction.
Cutting and his colleagues don't know how exactly the loss of MSRA reduces risk for fatal intestinal obstruction, but they suspect that MSRA's ability to alter the activity of specific intestinal enzymes may be the key. They suspect that with reduced levels of MSRA, the enzymes are free to do their job breaking down proteins that make up meconium so that meconium can pass through the intestines and be evacuated normally at birth.
The researchers' work on MSRA could shed light on how meconium normally gets broken down in the intestines. Moreover, use of the techniques pioneered by Cutting and his colleagues may lead to identification of modifier genes that play roles in other complications of CF, like lung function, and in other diseases caused by a single gene, like Huntington's disease.
###
The studies were funded by the National Institutes of Health (NHLBI and NIDDK) and the Cystic Fibrosis Foundation.
Authors on the PLoS Genetics paper are: Lindsay B. Henderson, Vishal K. Doshi, Scott M. Blackman, Kathleen M. Naughton, and Garry R. Cutting of Johns Hopkins; Rhonda G. Pace and Michael R. Knowles of University of North Carolina at Chapel Hill; Jackob Moskovitz of University of Kansas, Lawrence; Peter R. Durie of Hospital for Sick Children, Toronto, Ontario, Canada; and Mitchell L. Drumm of Case Western Reserve University.
Authors on the Nature Genetics paper are: Lei Sun, Johanna Rommens, Weili Li, Peter R Durie, Lisa Strug of University of Toronto, Toronto, Ontario, Canada; Harriet Corvol, Annick Clement and Pierre-Yves Bolle of Pierre et Marie Curie University, Paris, France ; Xin Li, Theodore Chiang, Fan Lin, Ruslan Dorfman, Rashmi V Parekh, Mary Corey, Julian Zielenski of the Hospital for Sick Children, Toronto, Ontario, Canada; Pierre-Franois Busson of St Antoine Hospital, Paris, France; Diana Zelenika of Centre National de Gnotypage, Evry, France ; Scott Blackman, Vishal Doshi, Lindsay Henderson, Kathleen Naughton and Garry R Cutting of Johns Hopkins; Wanda K O'Neal, Rhonda G Pace, Jaclyn R Stonebraker, Sally D Wood and Fred A Wright, and Michael R. Knowles of University of North Carolina at Chapel Hill; and Mitchell L. Drumm of Case Western Reserve University.
On the Web:
http://www.hopkinsmedicine.org/geneticmedicine/
http://www.hopkinsmedicine.org/geneticmedicine/People/Faculty/cutting.html
http://www.plosgenetics.org/home.action
http://www.nature.com/ng/index.html
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
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Why Exercise Warm-Ups Might Be Even More Important Than You Thought [Sports]
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