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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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Monday, April 1, 2013
6000 died in Syria in March, deadliest month yet
BEIRUT (AP) ? More than 6,000 people were killed in the Syrian civil war in March alone, according to a leading activist group that reported it was the deadliest month yet in the 2-year-old conflict.
The head of the Syrian Observatory for Human Rights said an increase in shelling and clashes around the country led to the high toll, which is incomplete because fighters on both sides tend to underreport their dead.
"Both sides are hiding information," Rami Abdul-Rahman said by phone from Britain, where he is based. "It is very difficult to get correct info on the fighters because they don't want the information to hurt morale."
The increase also likely represents the further spread of the civil war throughout the country.
Clashes continue to rage in the northern city of Aleppo and around the capital Damascus as well as in the central city of Homs.
And in recent weeks, rebels in the southern province of Daraa along the Jordanian border have seized towns and military bases from the government with the help of an increased influx of foreign-funded weapons.
The Observatory, which opposed President Bashar Assad's regime, said the March dead included 298 children, 291 women, 1,486 rebel fighters and army defectors and 1,464 government soldiers. The rest were unidentified civilians and fighters.
The government does not provide death tolls for the civil war.
That toll solidly beat the second most deadly month, when airstrikes, clashes and shelling killed more than 5,400 people in August 2012, Abdul-Rahman said.
He said his total death toll for the conflict through the end of March is 62,554, a number he said he guessed only reflected about half of the actual dead.
He said many deaths go unreported by the government or rebel fighters and that there are tens of thousands detained in regime and rebel prisons whose fates are not known.
The United Nations said in February that 70,000 people had been killed since the start of the conflict. It has not updated its number since.
Source: http://news.yahoo.com/6000-died-syria-march-deadliest-month-yet-163824539.html
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Jewish Business Ethics: Proper Marketing and Selling | Jewish Journal
March 31, 2013 | 5:30 am
Posted by?Rabbi Dr. Shmuly Yanklowitz
There is a famous business concept called caveat emptor (buyer beware). In secular society, as long as a seller does not blatantly lie or actively conceal a defect, it is the full responsibility of the buyer to exercise due diligence and to inspect what is being purchased. Jewish law takes a totally different approach: It is presumed that no defects or problems exist in a product or property if they are not disclosed explicitly by the seller.
We are well aware of fictional examples in literature and old movies of the quack doctor who promises miracle cures. This goes further back than you might think, and was prevalent in the entire Western world. One of the more famous comic Italian operas is Gaetano Donizetti?s L?Elisir d?Amore (?The Elixir of Love?), in which quack Dr. Dulcamara (?Bittersweet?) touts an elixir that cures everything from apoplexy to diabetes, though it is actually just repackaged Bordeaux wine. In this country, the creation of the Food and Drug Administration (FDA) in 1906 regulated the drug industry in a helpful way, so that drugs no longer contained dangerous substances like cocaine, heroin, and opium. However, new marketing schemes have continued to emerge and flourish as long as people were unaware of the deception. In the 1920s, for example, numerous ?miracle? cures based on radium were sold to the general public in everything from water to bread to suppositories. Today, of course, companies sell radon detectors so homeowners can tell if there is radon gas (and thus a risk for lung cancer) in their basements.
In looking back to these bygone eras, we should not feel smug about how sophisticated we are today, for we still are fooled by deceptive marketing practices. You may think that that bottled water has to come from a pristine spring in the wilderness, that ?natural? is just as good as ?organic,? or that the FDA has accurately defined and regulated all these terms. If so, you are in error.
For example, many people drink bottled water, unaware that the source of that water is ordinary tap water.? Nestl?? Waters? 5-gallon bottles of water come from the municipal tap water of Woodridge, Illinois, while Aquafina (owned by PepsiCo) also bottles its water from municipal tap water. Even worse, a Coca-Cola subsidiary makes ?Vitaminwater,? which sounds like healthful, vitamin-fortified water, but at 130 calories and 33 grams of sugar it is quite the opposite. To make matters worse, several government- and privately-sponsored studies have concluded that tap water is more closely regulated than the bottled water industry. (Additional benefits of drinking tap water instead of bottled water include less waste disposal and lower spending.) In our search for healthy food products, we see labels such as ?natural? as well as ?organic.? The U. S. Department of Agriculture regulates and certifies the production of organic food, and excludes many harmful substances: ?Synthetic fertilizers, sewage sludge, irradiation, and genetic engineering may not be used.? For multi-ingredient food items, a label of ?organic? means that at least 95 percent or more of the content must be organic.
What about ?natural? food? The FDA has this to say about ?natural?: ?[The] FDA has not developed a definition for use of the term natural or its derivatives.? Thus, all those pesticides, genetically modified food, and ?sewage sludge? that are excluded from organic food may well be in ?natural? food, and these are not required to be listed on the nutrition label. Unfortunately, many large agribusinesses have subsidiary companies that sound small and organic, but which use food that have pesticides and other harmful substances.
Finally, many people are concerned about consuming too much sodium, but will ?reduced? or ?low? sodium products be a better option? Fortunately, there are definitions here, but you may still take in far too much sodium. Of the two, ?low sodium? is often the best option, as it means 140 mg of sodium or less per serving (don?t forget to check the serving size as well). ?Reduced sodium? means at least 25 percent less than the regular product. Thus, if a ?normal? soup contains a staggering 900 mg of sodium per cup, the reduced sodium version can have 675 mg per cup, which in a 2.5-serving can would still give you nearly 1,700 mg of sodium, already more than the daily suggested serving for children, older adults, and people with diabetes or advanced kidney disease.
In consumer cases, the Federal Trade Commission sometimes catches the more outrageous marketing schemes. In 2012, for example, they successfully ordered Oreck to stop claiming that their vacuum cleaners could reduce the risk of flu, asthma, and other airborne illnesses, and forced Nivea to stop claiming that its skin cream could make people lose weight. However, the FTC also acted against a more insidious trend to mask commercials as news stories.? The FTC forced the cessation of fake news sites such as ?News 6 News Alerts? and ?Health News Health Alerts? by six companies selling acai berry weight-loss programs. These companies used fake news sites to pretend that major media organizations had aired stories confirming the false claims of weight loss.??
The American concept of caveat emptor is unjust, as it presumes that the consumer has as much power and ability to find good information as huge corporations do to spread the bad kind. We should be smarter consumers but the onus ultimately should be, as in Jewish law, almost completely on the seller to actively reveal any problems. If the owner does not disclose problems or defects, they have violated the prohibition of geneivat da?at, deception (Choshen Mishpat 228:6). If a product has a defect that is not actively disclosed then the buyer has the right to return the item for a full refund (Choshen Mishpat 232:3), since the transaction was a mekach ta?ut, false sale. This disclosure may not be broad but must be very specific to the problem (Choshen Mishpat? 232:7). To determine whether or not a certain type of defect needs to be disclosed, we employ minhag hamakom, the customs and norms of the land/region (Choshen Mishpat 232:6). With the marketplace as complex and convoluted as it is, it is only just to shift responsibility for improper marketing to the seller.
?
Rabbi Shmuly Yanklowitz is the Founder and President of Uri L'Tzedek, the Senior Rabbi at Kehilath Israel, the Founder and C.E.O. of The Shamayim V?Aretz Institute and is the author of "Jewish Ethics & Social Justice: A Guide for the 21st Century.? In 2012 and 2013, Newsweek named Rav Shmuly one of the top 50 rabbis in America."
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Newly approved blood thinner may increase susceptibility to some viral infections
Apr. 1, 2013 ? A study led by researchers at the University of North Carolina indicates that a newly approved blood thinner that blocks a key component of the human blood clotting system may increase the risk and severity of certain viral infections, including flu and myocarditis, a viral infection of the heart and a significant cause of sudden death in children and young adults.
For the past 50 years, people with the heartbeat irregularity, atrial fibrillation, and others at increased risk for forming potentially life-threatening blood clots have been given the anticoagulant drug warfarin. Recently, the U.S. Food and Drug Administration approved the use of the blood-thinner Dabigatran etexilate (called Pradaxa?) for atrial fibrillation patients. The drug inhibits thrombin, the body's central coagulation activator of the blood clotting system.
In blocking thrombin activity, the drug disturbs the protease cascade of molecular events that normally occurs in coagulation. While clot formation is reduced, the new study shows it may also cause an unintended consequence. "Our findings show that blocking thrombin reduces the innate immune response to viral infection," says study senior author Nigel Mackman, PhD, the John C. Parker Distinguished Professor of Medicine in the division of hematology and director of the UNC McAllister Heart Institute. "The use of the new generation of blood thinners might increase the risk and severity of flu and myocarditis."
A report of the research appears in the March 2013 issue of The Journal of Clinical Investigation.
Mackman points out that viral infections such as dengue fever trigger activation of the coagulation system but it was considered a bad thing. He says studies on bacterial infections have found that the last product of the "clotting cascade" (the process that occurs in blood clot formation) -- fibrin -- helps activate immune cell macrophages that boosts the immune system.
"But it seems that the antiviral mechanism of the clotting system is not via fibrin but rather via thrombin; namely, its activation of protease activated receptor proteins such as PAR-1," says Mackman. "The new study was aimed at finding out if PAR-1 plays any role in virus infections, a question of importance to the use of Pradaxa? and the development of antithrombotic drugs that target PAR-1 on platelets."
To find the answer, Mackman and colleagues used mice in which the PAR-1 gene is deleted and subjected then to infection with a virus that causes myocarditis. They found that loss of PAR-1 mediated signaling after infection with the cardiotrophic virus resulted in increased viral buildup in the heart, cardiac injury and, later, increased impairment of heart function.
Moreover, the absence of PAR-1 signaling was associated with a slower response to the virus of the innate immune soon after viral infection. The innate immune system provides early defense against disease causing organisms. The defense is almost immediate.
The researchers treated normal mice with Pradaxa?. They showed that thrombin inhibition increased cardiac virus load and cardiac injury after viral infection in a similar manner to a deficiency of PAR-1. In addition, they infected the PAR-1 deficient mice with influenza A and found that PAR-1 signaling was important in controlling the virus load in the lung in the early phase after infection. These results suggest that thrombin and PAR-1 mediate important early antiviral signals after infection.
"Pradaxa? inhibits clot formation by reducing fibrin deposition and platelet aggregation." said Mackman. "Importantly, Pradaxa? might not only facilitate significant lifesaving effects in reducing cardiac death but may also interfere with other processes in the body.
"The results we generated were completely unexpected and in fact our hypothesis was that PAR-1 deficient mice would be protected from viral myocarditis because they would have reduced inflammation," Mackman added. "We are now determining if the traditional long term anticoagulant warfarin has the same effect on viral infection or is this specific to the new blood thinner."
The majority of the study was a collaboration between the Mackman group at UNC and the Charit? -- Universit?tsmedizin in Berlin, Germany, and other groups at UNC, including at the Gillings School of Global Public Health, and across the USA.
The first-author is Silvio Antoniak, PhD, a postdoctoral researcher in Mackman's lab. Other co-authors from Mackman's lab were A. Phillip Owens III, PhD; Martin Baumnacke, MD; and Julie C. Williams, PhD.
The study was supported by the Myocarditis Foundation through a research grant to Silvio Antoniak. Additional funds were provided by the National Heart, Lung and Blood Institute (NHLBI), a component of the National Institutes of Health.
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The above story is reprinted from materials provided by University of North Carolina Health Care.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- Silvio Antoniak, A. Phillip Owens, Martin Baunacke, Julie C. Williams, Rebecca D. Lee, Alice Weith?user, Patricia A. Sheridan, Ronny Malz, James P. Luyendyk, Denise A. Esserman, JoAnn Trejo, Daniel Kirchhofer, Burns C. Blaxall, Rafal Pawlinski, Melinda A. Beck, Ursula Rauch, Nigel Mackman. PAR-1 contributes to the innate immune response during viral infection. Journal of Clinical Investigation, 2013; 123 (3): 1310 DOI: 10.1172/JCI66125
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Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/ANitGbFwha4/130401132058.htm
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