Arizona sends Harvard home with a thump, 74-51

SALT LAKE CITY (AP) ? Sometimes, it's rough being the smartest guy in the room.

Harvard freshman point guard Siyani Chambers knows.

He'll be heading back to Harvard missing part of his front tooth ? all part of a wicked basketball lesson provided by Arizona in a 74-51 crushing of the Crimson on Saturday in the NCAA tournament.

Mark Lyons matched a career high with 27 points to lead the sixth-seeded Wildcats (27-7), who showed how a real basketball school does it when March rolls around.

"The history of Arizona speaks for itself," coach Sean Miller said. "This time of year, we not only represent ourselves, but all the great players and teams of the past."

This will be Arizona's 15th appearance in the Sweet 16. The Wildcats are heading to Los Angeles for a West Regional matchup against Sunday's winner between Ohio State and Iowa State.

And Harvard ? well, it's back to class, though Chambers may want to stop by the dentist's office first.

"We got the rebound, we were on a fast break, I went in the air, came down, and before I knew it, my tooth was out," he said, in describing the inadvertent elbow he took early in the second half from Arizona guard Kevin Parrom.

Luckily, teammate Christian Webster was on the ball. He walked over to retrieve the tooth fragment and hand it back to its owner.

But there wasn't much to salvage by that point.

Harvard (20-10) missed its first 13 shots and 20 of its first 22 while falling behind 30-9. The Ivy League champs, who shot 52 percent in their upset win over New Mexico on Thursday, made only 27 percent in this one.

"We had some open opportunities early, and once we missed some, we kind of got our heads down and they took advantage of it," coach Tommy Amaker said.

Laurent Rivard, the Canadian guard who made five 3-pointers in the upset Thursday, shot 1-for-6 this time. He missed two early, then shot two airballs in the second half and finished with three points.

"They played me different than New Mexico did," Rivard said. "Stayed on me, forced us to finish inside. That changed the game."

Indeed, this was nothing like Thursday, when the upset over a physically imposing New Mexico team riled up the Harvard twitterrati and sparked dreams of nets somehow being cut down with a slide rule.

Yes, Amaker's program could be redefining what's possible in the Ivy League.

But Arizona, a team that hasn't lost to an opponent outside of the Pac-12 this season, had too much height, too much speed, too much talent to be slowed by this Harvard team.

"They pounced on us from the beginning," Webster said. "I think it took us by surprise how hard they played, how physical they were, their length and size and speed. From there, it was just an uphill battle."

Indeed, it was over early and a couple vignettes told the story.

Forward Solomon Hill (13 points, 10 rebounds) spotted up for a 3-pointer, drained it, then looped his fingers over his eyes ? the 3-point goggles ? right by the Harvard bench, in Amaker's face. On Harvard's next possession, Hill rebounded a missed shot, took the ball coast to coast and jammed with both hands, then bumped chests violently with Parrom.

Moments later, Lyons made a backdoor cut and took an alley-oop pass from Jordin Mayes for an easy layup.

Bad enough that happens to a defense once in a game. But on the next possession, Lyons and Mayes combined for an absolute carbon-copy of the same play.

"My teammates got me the ball in the right position and I was able to make shots today," said Lyons, a senior who came to Arizona from Xavier along with his coach.

Impressive as the back-to-back oops were, Chambers will remember another play better.

He was trying to make a jump pass, when Parrom left his feet, as well, to block it. His elbow bashed Chambers' lip and he grimaced in pain. Helped off the floor with the tooth in hand, he was wincing on the bench, where TV cameras caught a clear shot of his newly jagged right incisor.

"That showed how physical the game was," Rivard said. "It wasn't even close to the rim. Guys were scratching and clawing. But it was an accident."

Chambers came back shortly after and made a 3. He finished with six points.

Kenyatta Smith, Harvard's tallest player at 6-foot-8, led the Crimson with 10 points. Also shut down was Wesley Saunders. Saunders led Harvard with 18 points against New Mexico, but went 1-for-11 for eight points against Arizona.

"They're 7-feet, 6-9, 6-8," Amaker said. "They're in front of the rim, around the rim. They make it very difficult to finish."

Arizona, meanwhile, was every bit as good on offense as it was on defense. The Wildcats made 55 percent of their shots, led by Lyons' 12-for-17 night.

Source: http://news.yahoo.com/arizona-sends-harvard-home-thump-74-51-003031097--spt.html

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Source: http://www.empowernetwork.com/evinanderson/blog/how-to-launch-a-product-and-make-profits-with-network-marketing/

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Bloomberg, mayor group tout big gun control push (The Arizona Republic)

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New US-EU talks threatened by agriculture spats

WASHINGTON (AP) ? President Barack Obama used Washington's grandest stage ? the State of the Union speech ? to announce negotiations with Europe aimed at creating the world's largest free trade agreement. Just weeks later, there are signs that old agriculture disputes could be deal-killers.

European Union leaders don't want the negotiations to include discussions on their restrictions on genetically modified crops and other regulations that keep U.S. farm products out of Europe. But Obama says it's hard to imagine an agreement that doesn't address those issues. Powerful U.S. agricultural lobbies will do their best to make sure Congress rejects any pact that fails to address the restrictions.

"Any free trade agreement that doesn't cover agriculture is in trouble," said Cathleen Enright, executive vice president at the Biotechnology Industry Organization, which promotes biotechnology, including genetically modified products.

That would threaten the dream of a behemoth free trade deal between the world's two largest trading partners that together account for more than half of the world economy. It would lower tariffs and remove other trade barriers for most industries. Some analysts say the deal could boost each economy by more than a half-percentage point annually and significantly lower the cost of goods and services for consumers.

Agricultural issues have long bedeviled attempts to expand free trade across the Atlantic and have led each side to file complaints against the other before the World Trade Organization, an arbitrator in trade disputes. While the U.S. protests EU restrictions, Europeans want the U.S. to reduce agricultural subsidies.

Genetically modified organisms, or GMOs, have been a core part of the dispute. Agricultural scientists change the genetic makeup of agricultural products to improve their quality and boost production. In Europe, there is widespread public opposition to GMOs. The EU argues that the risks of altering the genetic pool are unknown. It has strict rules and imposes a heavy burden of proof before such crops can be grown or imported in the EU.

U.S. companies say that genetically modified products have been proved safe by scientific studies and are being excluded based on irrational fears. They accuse Europe of trying to help their own farmers by keeping out American products.

While they have little expectation that the EU would end the restrictions, they say it would be a victory if it clarified what it describes as opaque rules and also set timelines for considering products. Regulators now take what they call a precautionary approach, declining approval of products until they can be more certain of their safety.

But any move to water down the regulations could provoke a backlash in Europe.

"My reading of the mood in Europe around genetically modified crops is that it's extremely negative," said Paul DeGrauwe, a professor of economics at the London School of Economics. "It's going to be very difficult."

Indeed, the top EU trade negotiator, Commissioner Karel De Gucht, seemed to rule out a compromise in remarks this month: "A future deal will not change the existing legislation. Let me repeat: no change."

The U.S. and the EU have similarly intractable disagreements on what the two sides call sanitary issues in meats. U.S. poultry products are restricted in the EU because U.S. companies use chlorine to sanitize the meat. Pork is also restricted because U.S. farmers use a feed additive that makes pigs leaner. The two sides partially resolved disputes over U.S. beef after an agreement that U.S. farmers would restrict hormones in cows intended for the European market.

Some European officials say the agricultural differences should be discussed after a major trade deal is completed. This month, French President Francois Hollande called for excluding sensitive issues, including the sanitary standards, from the talks. In the past, France has been among the most adamant of the European countries about protecting agricultural interests.

Obama, in a talk with his export council this month, suggested this could be a deal-breaker.

"There are certain countries whose agricultural sector is very strong, who tended to block at critical junctures the kinds of broad-based trade agreements that would make it a good deal for us," he said. "If one of the areas where we've got the greatest comparative advantage is cordoned off from an overall trade deal, it's very hard to get something going."

Powerful U.S. agricultural groups could probably block a trade deal from winning approval in Congress. In interviews, representatives of many of these groups said they would oppose a deal that didn't address the regulatory differences.

Robert Thompson, an academic at Johns Hopkins University and a former economist for the Agriculture Department, said that the agricultural issues could easily upend the talks.

"I'm not expecting an agreement to emerge any time soon," he said. "I'm thinking years."

Of course, the rhetoric at the beginning of talks might not preclude compromise in the end. In his talk with the export council, Obama expressed optimism. He noted that austerity measures in response to the debt crisis in the EU have caused European countries to look to a free trade deal as a rare opportunity to boost the economy and improve competitiveness.

"I think they are hungrier for a deal than they have been in the past," he said.

___

Melvin reported from Brussels.

___

Follow Desmond Butler on Twitter at http://twitter.com/desmondbutler

Follow Don Melvin on Twitter at http://twitter.com/Don_Melvin

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/89ae8247abe8493fae24405546e9a1aa/Article_2013-03-23-US-EU-Trade/id-6f0309c29ae04a56a2f9f0c2d7def4ee

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Quirky Lyme disease bacteria: Unlike most organisms, they don't need iron, but crave manganese

Mar. 21, 2013 ? Scientists have confirmed that the pathogen that causes Lyme Disease -- unlike any other known organism -- can exist without iron, a metal that all other life needs to make proteins and enzymes. Instead of iron, the bacteria substitute manganese to make an essential enzyme, thus eluding immune system defenses that protect the body by starving pathogens of iron.

To cause disease, Borrelia burgdorferi requires unusually high levels of manganese, scientists at Johns Hopkins University (JHU), Woods Hole Oceanographic Institution (WHOI), and the University of Texas reported. Their study, published March 22, 2013, in The Journal of Biological Chemistry, may explain some mysteries about why Lyme Disease is slow-growing and hard to detect and treat. The findings also open the door to search for new therapies to thwart the bacterium by targeting manganese.

"When we become infected with pathogens, from tuberculosis to yeast infections, the body has natural immunological responses," said Valeria Culotta, a molecular biologist at the JHU Bloomberg School of Public Health. The liver produces hepcidin, a hormone that inhibits iron from being absorbed in the gut and also prevents it from getting into the bloodstream. "We become anemic, which is one reason we feel terrible, but it effectively starves pathogens of iron they need to grow and survive," she said.

Borrelia, with no need for iron,has evolved to evade that defense mechanism. In 2000, groundbreaking research on Borrelia's genome by James Posey and Frank Gherardini at the University of Georgia showed that the bacterium has no genes that code to make iron-containing proteins and typically do not accumulate any detectable iron.

Culotta's lab at JHU investigates what she called "metal-trafficking" in organisms? -- the biochemical mechanisms that cells and pathogens such as Borrelia use to acquire and manipulate metal ions for their biological purposes.

"If Borrelia doesn't use iron, what does it use?" Culotta asked.

To find out, Culotta's lab joined forces with Mak Saito, a marine chemist at WHOI, who had developed techniques to explore how marine life uses metals. Saito was particularly intrigued because of the high incidence of Lyme Disease on Cape Cod, where WHOI is located, and because he specializes in metalloproteins, which contain iron, zinc, cobalt, and other elements often seen in vitamin supplements. The metals serve as linchpins, binding to enzymes. They help determine the enzymes' distinctive three-dimensional shapes and the specific chemical reactions they catalyze.

It's difficult to identify what metals are within proteins because typical analyses break apart proteins, often separating metal from protein. Saito used a liquid chromatography mass spectrometer to distinguish and measure separate individual Borrelia proteins according to their chemical properties and infinitesimal differences in their masses. Then he used an inductively coupled plasma mass spectrometer to detect and measure metals down to parts per trillion. Together, the combined analyses not only measured the amounts of metals and proteins, they showed that the metals are components of the proteins.

"The tools he has are fantastic," Culotta said. "Not too many people have this set of tools to detect metalloproteins."

The experiments revealed that instead of iron, Borrelia uses that element's next-door neighbor on the periodic chart, manganese, in certain Borrelia enzymes. These include an amino peptidase and an important antioxidant enzyme called superoxide dismutase.

Superoxide dismutase protects the pathogens against a second defense mechanism that the body throws against them. The body bombards pathogens with superoxide radicals, highly reactive molecules that cause damage within the pathogens. Superoxide dismutase is like an antioxidant that neutralizes the superoxides so that the pathogens can continue to grow.

The discoveries open new possibilities for therapies, Culotta said. "The only therapy for Lyme Disease right now are antibiotics like penicillin, which are effective if the disease is detected early enough. It works by attacking the bacteria's cell walls. But certain forms of Borrelia, such as the L-form, can be resistant because they are deficient in cell walls."

"So we'd like to find targets inside pathogenic cell that could thwart their growth," she continued. "The best targets are enzymes that the pathogens have, but people do not, so they would kill the pathogens but not harm people." Borrelia's distinctive manganese-containing enzymes such as superoxide dismutase may have such attributes.

In search of new avenues of attack, the groups are planning to expand their collaborative efforts by mapping out all the metal-binding proteins that Borellia uses and investigating biochemical mechanisms that the bacteria use to acquire manganese and directs it into essential enzymes. Knowing details of how that happens offers ways to disrupt the process and deter Lyme Disease.

The authors of the new study are J. Daphne Aguirre, Hillary Clark, Christine Vazquez, Shaina Palmere, and Culotta (JHU Bloomberg School of Public Health); Saito and Matthew McIlvin (WHOI); Denise Grab (JHS School of Medicine); Janakiram Seshu (University of Texas); and P. John Hart (University of Texas Health Science Center).

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Story Source:

The above story is reprinted from materials provided by Woods Hole Oceanographic Institution.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Journal Reference:

1. J. D. Aguirre, H. M. Clark, M. McIlvin, C. Vazquez, S. L. Palmere, D. Grab, J. Seshu, P. J. Hart, M. Saito, V. C. Culotta. A Manganese-Rich Environment Supports Superoxide Dismutase Activity in a Lyme Disease Pathogen, Borrelia burgdorferi. Journal of Biological Chemistry, 2013; DOI: 10.1074/jbc.M112.433540

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/strange_science/~3/IcB1FSF_Mvk/130321205712.htm

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Babbel acquires PlaySay in bid to bolster US language learning presence

Babbel's been doing a solid job of picking up users as it attempts to help people around the world learn new tongues over their lunch breaks, but evidently, it's not picking up steam in the US as well as it would like. The remedy? Buy the market share one so desires. Today, the company has announced the acquisition of San Francisco's own PlaySay -- a language learning company that has been tearing up every app store it approaches since launching at TechCrunch Disrupt in September of 2011. With that, however, comes some pretty unfortunate news for users. PlaySay apps are going to be yanked 45 days from now, with website visitors funneled over to Babbel's site. Moreover, we've confirmed that none of PlaySay's technologies will be integrated into Babbel's programs, and that only PlaySay's founder (Ryan Meinzer) will remain on staff as an "adviser."

We've got nothing but love for Babbel's software, but what this means for consumers is simple: one less player in the space, and a dead-end for the technology that was developed in order to launch PlaySay. Of course, we aren't going to pretend that this type of thing doesn't happen all of the time, but alas....

Filed under: Software

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Source: Babbel

Source: http://www.engadget.com/2013/03/21/babbel-acquires-playsay-language-learning-deal/

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Insights into the immune system, from the fates of individual T cells

Thursday, March 21, 2013

By charting the differing fates of individual T cells, researchers have shown that previously unpredictable aspects of the adaptive immune response can be effectively modeled. The crucial question: What determines which of the immune system's millions of cells will mobilize to fight an acute infection and which will be held back to survive long-term, forming the basis of the immunological memory? The scientists' findings, published in the journal Science, could have implications for improved immunotherapy and vaccination strategies.

The scientists found that the immediate immune response to an infection or tumor is mounted by a relatively tiny fraction of the so-called CD8+ T cells that are capable of recognizing the associated antigen. These few rapidly expand into giant populations of short-lived T cells targeted at killing infected cells or cancer cells. Meanwhile the vast majority remain in smaller populations geared toward longevity, to help ensure that the immune system will remember the antigen when it appears again in the future.

"Up to now, it was only possible to observe groups of immune cells during the response to an infection," says Prof. Dirk Busch of the Technische Universitaet Muenchen (TUM). "We have developed technology that enables us to observe individual T cells." Together with innovative cell processing technology, the researchers brought theoretical systems biology and clinical expertise to bear on this investigation, a collaboration of TUM, the University of Heidelberg, the Helmholtz Center Munich, the German Cancer Research Center (DKFZ), and the National Center for Infection Research (DZIF).

Marking the threshold of predictability

A single T cell is theoretically capable of generating an adaptive immune response by developing into diverse and expanding populations, fighting the acute infection as well as providing lasting memory for the future. But a fundamental question ? whether an effective response is predetermined on the level of an individual T cell or emerges from the commingled fates of multiple cells ? had never been put to the test. Another unresolved question concerned the order in which populations of short-lived killer cells and long-lived memory cells develop.

To address these questions, researchers at TUM began by introducing specially marked T cells into mice and then triggering a specific immune reaction. Around seven days later, they were able to determine how many descendant cells, and what kinds, had been generated by individual T cells. Biomathematical modeling, using an approach co-developed with the group of Prof. Thomas Hoefer at Heidelberg, helped to explain what the data showed. "One can't predict which 'career paths' the descendants of an individual killer T cell will take, " says first author Veit Buchholz, a medical resident at TUM. "This is a matter of chance, like a single roll of the dice. To generate a predictable immune response, we have found that a sample of at least 50 individual cells is needed."

From analysis of many of the huge populations of short-lived killer cells and the relatively tiny populations of long-lived memory cells, the researchers were able to reconstruct the T cells' development program and predict their behavior: All of the cells proceed along the same path of development, but they don't go the same distance. That is, the few cells that generate giant populations of short-lived infection fighters have gone through the same stage as those fated to produce memory cells ? but they have left that stage behind to provide immediate protection.

Beyond the results themselves, another important outcome of this study is increased confidence in the combined power of the in vivo and in silico approaches. "The fact that the experimental results confirmed our predictions in detail has strongly supported our theory," says Prof. Hoefer, leader of the Heidelberg group.

There are several ways these findings could become important in the setting of human health, the researchers explain ? in improving the effectiveness of immunotherapy against cancer, for example, or in optimizing treatment for older people, who tend to have significantly fewer copies of a given type of immune cell. "The future memory cell stands at the beginning of an expansion process with two extreme forms of differentiation," Buchholz says, "and ideally there should be a balance, so that the memory pool is not depleted. So we can think about how to tweak vaccination schemes to first allow expansion and not let differentiation kick in too early."

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Technische Universitaet Muenchen: http://www.tum.de

Thanks to Technische Universitaet Muenchen for this article.

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