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Saturday, April 20, 2013
This Predator Helmet Can Make Even the Tiniest Vespa Badass
Thursday, April 18, 2013
Why I'll run the Boston Marathon again in 2014
Angry people set off the bombs at the Boston Marathon. We runners are angry, too, but we're going to use that as fuel to train harder and become better at the sport we love, so when we show up in 2014, we'll be ready to do our best in memory of those who fell on Monday.
Mike Merino (left) and oped contributor Ray Charbonneau rest after completing the Boston Marathon before the bombs went off April 15. Writes Mr. Charbonneau: 'Non-runners have asked me whether I'll be afraid to return to the marathon next year. They don't understand. If I were afraid, running is what I'd do to work through those feelings.'
Photo courtesy of the author
EnlargeFor my 22nd marathon, I volunteered to guide visually-impaired runner Mike Merino in the Boston Marathon. We were part of the Massachusetts Association for the Blind's "Team With A Vision." Mike and I tethered ourselves together at the start in Hopkinton and then wove our way through crowds of runners to the finish on Boylston Street.
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After I guided Mike across the line, we jammed ourselves in with hundreds of other tired, sweaty runners stumbling slowly forward to collect the medals commemorating our victory. We were a scrawny army wrapped in foil blankets ? survivors of a war we'd fought in flimsy uniforms and boots padded with lightweight foam, armed only with bodies loaded with pasta, oxygen from a beautiful spring day, and determination. The fight to finish in under four hours had taken all we had.
Then there was an explosion. While we were still trying to convince ourselves that the first blast was just an accident, maybe a short in a power transformer or a gas leak, another one went off. We knew then, though it wouldn't be confirmed until much later, that the real war had intruded, the one with bombs, flying shreds of metal and glass, three tragic deaths, and more than 150 people injured.?
My first response, and the first response of many of the people I know, wasn't fear. It was anger. We were mad, and are still mad, because running is our refuge, and it seems like someone is trying to take it away.
Running helps me process my thoughts. It distracts me just enough to let the back of my mind sort out whatever is bothering me. An hour's run is a straightforward task that gives me the comfort of knowing I've accomplished something that day. If I argue with my boss or get in a fight with my spouse, I can work through it by running a little faster. And a nice, long run is a few hours out of the day when I don't have to worry about yard work, bills, politics, crime, or terrorism.?
At least until Monday, when someone decided to make a point of some kind at the Boston Marathon.
Non-runners have asked me whether I'll be afraid to return to the marathon next year. They don't understand. If I were afraid, running is what I'd do to work through those feelings.
But running isn't just about escaping the stresses of daily life. We don't run just to get fit, for the competition, or to collect money for charities. Those are wonderful benefits, but they're not why we run. As Mike told me on Tuesday, "I run marathons because of something bigger than all that."
It starts with individual people, getting out on the road regularly, building fitness and training to run farther and faster. As they run, they find others who share their goals and start working together, having fun while encouraging each other to achieve even more. Some of those people organize events, and even more people, many of them non-runners, join in to help. Soon there are 27,000 people running together from Hopkinton to Boston with thousands more in volunteer jackets helping out, hundreds of thousands lining the roads to cheer and enjoy the spectacle, and millions donating to their friend's charity, watching on TV, and maybe even thinking, "Hey, I'll bet I can do that."
It's also about the next day, when the crowds are gone and you're out there by yourself, not for the glory, but because it's who you are, a runner. And it's about getting out there the next day and the next and the one after that.
Usually, distance runners toil on the side of the road, away from any spotlight other than the headlights from an oncoming car. Our sport only gets noticed in the US in passing, when the Summer Olympics are held in a convenient time zone or on the weekend of the Boston Marathon.
Now we're getting worldwide attention, but for all the wrong reasons. And it makes us mad.
Sure, lots of people were disappointed that they didn't get to finish their race, but that's not the real issue. Marathoners are used to the vagaries of the weather or a mid-race injury spoiling six months of training. It's frustrating, but there's always another race. The bombers appear to want to destroy that possibility of redemption.
Marathoners already know running Boston isn't a given. Most people have to qualify by running fast or collecting for a charity. If we aren't able to earn our way in, that's OK. But we are not willing to let someone else take our opportunity away.
Angry people set off the bombs in Boston on Monday. We runners are angry, too, but we're going to use that as fuel to train harder and become better at the sport we love, so when we show up in Hopkinton in 2014, we'll be ready to do our best in memory of those who fell on Monday.
Ray Charbonneau lives with his wife Ruth in Arlington, MA. He writes about qualifying for the 2014 Boston Marathon in his latest book, "Overthinking the Marathon." Find out more at Y42K.com.
Source: http://rss.csmonitor.com/~r/feeds/csm/~3/EgVjyolm6_M/Why-I-ll-run-the-Boston-Marathon-again-in-2014
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Wednesday, April 17, 2013
Sources Say Amazon Acquired Siri-Like Evi App For $26M ? Is A Smartphone Coming?
When Siri arrived on the iPhone 4S it seemed like a magic piece of software. The future had arrived. But it wasn't alone. True Knowledge, a British startup with a natural language search engine developed in university labs had been working out what to do next. Siri was the 'boom' moment. They licensed Nuance?s voice recognition technology and created an app based on the True Knowledge engine, called Evi, which worked on any iPhone and Android. That clever move looks like it paid off. TechCrunch understands from sources that the company has been sold to Amazon for $26 million. However, calls to Amazon PR, backers Octopus Ventures and the founders of Evi have ben met with a stoney silence. A spokesperson for Octopus told us: "On this occasion Octopus will decline to comment on this specific portfolio company".Source: http://feedproxy.google.com/~r/Techcrunch/~3/1Kvbs9zeSYk/
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Saturday, April 13, 2013
NY jury awards $12 million to billionaire William Koch
By Bernard Vaughan
NEW YORK (Reuters) - A federal jury in New York on Friday awarded $12 million in punitive damages to U.S. billionaire William Koch in his dispute over the alleged misrepresentation of 24 bottles of wine he bought at auction.
Koch, 72, said he may use the proceeds to establish a fund to confront auction fraud and wine fraud.
The founder of Oxbow Group energy company, Koch had accused tech entrepreneur Eric Greenberg of knowingly selling him counterfeit bottles of wine at a 2005 Zachys auction.
"There's been a huge code of silence in this industry," Koch said after the jury decided on the damages in U.S. District Court in Manhattan. "My purpose is to shine a bright light on it."
Koch filed a federal lawsuit in 2007, accusing Greenberg, the San Francisco-based founder of several Internet companies, of fraud and misrepresentation and seeking $320,000, the amount he paid for the 24 bottles.
The jury on Thursday evening returned with a verdict that Koch should be compensated for the amount he spent on the wine, and on Friday the panel decided on the $12 million in punitive damages.
Koch shook hands with jurors and thanked them as they left the courtroom, saying he was "out of sight, over the moon" over the damages award.
Greenberg had denied the charges, saying any forgeries from his wine cellar got to the auction house by mistake. In closing arguments on Thursday, his attorney Arthur Shartsis said his client did not knowingly sell fakes.
"Clearly, the verdict is a disappointment because I believed all the consigned wine to be authentic," Greenberg said in a statement after the verdict.
He said he had offered Koch a full refund of his money when he learned that Koch "had issues with some of the wines he had purchased" and said he intended to appeal the verdict.
"We believe that we acted honorably and tried to do the right thing for all concerned," Greenberg said in the statement.
Experts for both sides agreed that the wine in one of the 24 bottles was fake. The authenticity of the other 23 bottles was unclear, although expert witnesses testified that some of the labels were copies of the originals.
None of the bottles had been opened nor had the wine been tasted.
In court, Greenberg's attorney argued that the New York-based Zachys auction house had sold the bottles "as is," meaning the buyer accepted the product in whatever condition it was at the time.
Koch's lawyer John Hueston said in court that Greenberg withheld information about the provenance and authenticity of his wine collection.
Koch, whose brother David Koch is a major supporter of conservative political causes, settled a separate lawsuit with the auction house in 2011, details of which were kept private.
(Additional reporting by Atossa Araxia Abrahamian; Editing by Ellen Wulfhorst and Phil Berlowitz)
Source: http://news.yahoo.com/ny-jury-awards-12-million-billionaire-william-koch-194113207.html
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Scientists find interferon, one of the body's own proteins, induces persistent viral infection
Apr. 9, 2013 ? Scientists at The Scripps Research Institute (TSRI) have made a counterintuitive finding that may lead to new ways to clear persistent infection that is the hallmark of such diseases as AIDS, hepatitis B and hepatitis C.
The study, reported in the April 12, 2013 issue of the journal Science, focused on the activity of the body's type 1 interferon (IFN-I) proteins. Since its discovery over 50 years ago, IFN-I has been believed to be an especially powerful antiviral agent that marshals the immune system's response against the body's foreign invaders. But in the new study, the TSRI scientists document in mice that IFN-I initiates persistent infection and limits the generation of an effective antiviral immune response.
"Our findings illuminate an unexpected role for IFN-I protein(s) in persistent infections, which has major implications for how we treat these infections," said Michael B. A. Oldstone, a professor in the Department of Immunology and Microbial Science at TSRI and senior investigator for the study.
Mystery of Immune Suppression
For decades, Oldstone and other virologists around the world have been trying to understand how some viruses manage to persist in their hosts.
One big clue, discovered only in recent years, is that some of these viruses are especially effective at getting into cells of the immune system known as dendritic cells. These cells serve as key detectors of infection and normally respond to viral infection by producing IFN-I proteins. They also produce both immune-enhancing proteins (cytokines/chemokines) to drive forward a vigorous immune response, as well as immune-suppressing proteins including interleukin-10 (IL-10) and PD-1, which act as a braking system that balances the immune response to keep within healthy (non-autoimmune) limits.
Persistent viruses can use this immune-suppressing effect for their own purposes. In several experimental models of persistent infections and in humans with persistent infections, a rise in IL-10 and PD-L1 is followed by declines in the function and numbers of antiviral T-cells. Many of the surviving T cells are rendered ineffectual -- a phenomenon called "T-cell exhaustion" or "hyporesponsiveness."
A Surprising Observation
To better understand how this immune-suppressing response develops, Oldstone and his team, including first authors John R. Teijaro and Cherie Ng, along with Brian Sullivan, looked in detail at the early events in a persistent viral infection. The team used a now-standard animal model that Oldstone developed almost 30 years ago: laboratory mice infected with lymphocytic choriomeningitis virus (LCMV) Clone (Cl) 13 strain.
One initial observation surprised them. "A day after infection, bloodstream levels of IFN-I were at least several times higher in the persistent infection, compared to a non-persistent LCMV infection," said Teijaro.
The persistent LCMV Cl 13 strain also turned out to be much better at infecting plasmacytoid dendritic cells -- which are considered the principal source of IFN-I proteins during viral infections. By contrast, the LCMV Armstrong (ARM) 53b strain, from which Cl 13 was derived, generated significantly less IFN-I and did not induce a persistent infection but rather generated antiviral effector CD8 T cells; this infection was terminated within 7 to 10 days. Cl 13 differs from ARM by only three amino acids (protein building blocks) of which just two are important; one in the glycoprotein for binding and entry into dendritic cells and the other in the viral polymerase that enhances viral replication.
Earlier Clearance and Fewer Malfunctions
The production of IFN-Is by plasmacytoid dendritic cells has been considered a normal and beneficial part of the immune reaction to a viral infection. "We usually think of IFN-I proteins as antiviral proteins, so that more IFN is better," said Ng. Indeed, when she and Teijaro used a monoclonal antibody to block IFN-I-alpha-beta (-a-b) receptor, activity just prior to or after infection with Cl 13, they observed a sharp drop in the production of IL-10 and PD-L1, loss of excessive cytokine/chemokine expression (cytokine storm) and maintenance of normal secondary lymphoid tissue architecture.
But the scientists found over the longer term a sharp drop in levels of immune-suppressing IL-10, as well as PD-L1, both inducers of T-cell exhaustion, was associated with restoration of antiviral immune response and virus clearance. And although blocking the IFN-I-a-b receptor led to higher bloodstream levels of virus in the first days after infection, it soon brought about a stronger, infection-clearing response.
"Even when we blocked IFN-I-a-b receptor after a persistent infection had been established and T-cell exhaustion had set in, we still saw a significantly earlier clearance of the virus," Ng said.
Blocking IFN-I-a-b receptor also prevented or reversed other immune malfunctions caused by the persistent LCMV strain, including a disruption of the structure of the spleen tissue and diminished T cell entry and maintenance within lymphoid structures in the spleen that contain dendritic cells. The interaction of dendritic cells with T cells is necessary to generate antiviral effector CD8 and CD4 T cells. "We saw a restoration of this lymphoid architecture, as well as an increase in a subset of antiviral T cells, natural killer cells and dendritic cells, and restoration of antiviral CD4 T cell function," said Teijaro.
Potentially Broad Applications
Oldstone and his team now plan to study IFN-I signaling pathways in further detail. In particular, they hope to determine whether the IFN-I-a-b receptor blocking strategy can work against chronic viral infections in humans. The scientists will also seek small pharmacologic molecules with the same function.
"Most of our findings in the LCMV model mirror what has been observed in human persistent infections, namely the upregulation of IL-10 and PD-L1, and the disruption of lymphoid architecture," said Oldstone.
Conceivably, the IFN-I-a-b receptor-blocking strategy could have broad clinical applications. In terms of viruses alone, chronic HIV, hepatitis B and hepatitis C infections collectively are found in hundreds of millions of people worldwide. Other common persistent viruses include Epstein-Barr virus, cytomegalovirus and cancer-causing human papilloma virus. Researchers have estimated that the average person at any one time carries at least several persistent, often silent viral infections.
Other contributors to the study, "Persistent LCMV infection is controlled by blockade of type 1 interferon signaling," were Kathleen C. F. Sheehan and Robert D. Schreiber of Washington School of Medicine at St. Louis; and Megan J. Welch, Andrew M. Lee, and Juan Carlos de la Torre of TSRI.
The study was supported by the National Institutes of Health grants AI009484, AI057160 and AI077719, as well as an American Heart Association Fellowship (11POST7430106).
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The above story is reprinted from materials provided by The Scripps Research Institute.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- J. R. Teijaro, C. Ng, A. M. Lee, B. M. Sullivan, K. C. F. Sheehan, M. Welch, R. D. Schreiber, J. Carlos de la Torre, M. B. A. Oldstone. Persistent LCMV Infection Is Controlled by Blockade of Type I Interferon Signaling. Science, 2013; 340 (6129): 207 DOI: 10.1126/science.1235214
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Source: http://feeds.sciencedaily.com/~r/sciencedaily/most_popular/~3/jq2JIzicfHA/130411142815.htm
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Tuesday, April 2, 2013
Singapore prime minister visits White House
WASHINGTON (AP) ? President Barack Obama says he appreciates an outstanding partnership between the United States and Singapore on military, economic and other matters in Asia.
Obama ignored questions from reporters about an alarming development in the Pacific region with North Korea announcing plans to restart its nuclear facilities. Neither Obama nor Prime Minister Lee Hsien Loong (lee haz-ee-en lahng) mentioned it in their brief remarks.
Instead, they focused on touting their bilateral cooperation. Lee says Singapore is looking forward to hosting Navy warships as the U.S. shifts its military presence to the Asia-Pacific.
THIS IS A BREAKING NEWS UPDATE. Check back soon for further information. AP's earlier story is below.
Singapore's prime minister on Tuesday becomes the third Asian leader to visit the White House this year, as President Barack Obama pursues closer ties with countries in the region in his second term.
It's Lee Hsien Loong's first Oval Office meeting in six years and comes as the U.S. pushes for completion by fall of a trans-Pacific free trade pact. Singapore, a close ally, is one of 11 countries taking part in the negotiations.
The U.S. and Singapore also have strong defense ties. Next week, the U.S. will begin rotational deployments of Navy vessels in Singapore, part of its efforts to shift American military presence toward the Asia-Pacific as the U.S. disentangles itself from a decade of conflict in Iraq and Afghanistan.
Defense cuts at home and turmoil in the Middle East have raised doubts in Asia about the U.S. ability to sustain its "pivot" to the region. But Obama made his diplomatic priorities clear by traveling to Myanmar, Cambodia and Thailand soon after his November re-election, and then by hosting the leaders of Japan and Brunei. South Korea's new president will visit in May.
"The prime minister's visit underscores the strategic importance the president places on Asia and the value we place on our relationship with Singapore as a key partner," a White House statement announcing Lee's trip said.
Lee is the eldest son of Singapore's founding prime minister, Lee Kuan Yew. He last visited the U.S. for a nuclear security summit in 2010. He'll address the U.S. Chamber of Commerce after his White House meeting.
While much attention is currently on Northeast Asia, and North Korea's threats to attack the U.S. and South Korea, Lee's four-day visit also takes place against the backdrop of tensions in the South China Sea, where assertive Chinese actions near disputed islands have unnerved other claimants in Southeast Asia.
Singapore itself is not a claimant, but its prosperity depends on commerce through those busy waters. It is a strong supporter of the U.S. security presence in the region, although it retains cordial ties with China.
Underscoring the administration's efforts to sustain its Asian diplomacy, the foreign ministers of two U.S. treaty allies in the region, the Philippines and South Korea, were also in Washington Tuesday for meetings with Secretary of State John Kerry, who travels to Northeast Asia next week.
Before meeting with Philippine Foreign Secretary Albert del Rosario, Kerry expressed deep concern about tensions in the South China Sea and called for the territorial disputes there worked out through arbitration.
During his visit, Singapore's Lee is also meeting with Defense Secretary Chuck Hagel, Treasury Secretary Jacob Lew and Kerry. He'll also travel to New York City and meet with Mayor Michael Bloomberg.
Source: http://news.yahoo.com/singapore-prime-minister-visits-white-house-070811591--politics.html
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