Saturday, October 19, 2013

Google flies high -- but Motorola sinks further



The good news about Google in its third-quarter results aren't hard to find: The company beat analyst estimates for revenue and earnings per share. But there is bad news, and it hints at how the company's big mobile hardware investment may be a much longer-term proposition for a profit.


Nobody, save maybe for Google's competition, is complaining about the company's revenues: $14.89 billion total, $11.92 billion net, up 12 percent from Q3 2012. The projections were for $11.7 billion revenue, and a $10.36 EPS (for the latter, Google made $10.74). Small wonder Google's shares jumped some 5 percent in after-hours trading.


One sign of how Google's business could change up with the ongoing shift away from desktops and toward mobile devices, is the dropping cost-per-click, or CPC, rate. A metric that measures the average price for an ad, CPC fell 8 percent over last year, and 4 percent from Q2, even while paid clicks rose 26 percent year-over-year and went up 8 percent from Q2.


Carolina Milanesi, a research VP at Gartner, described these steady-rather-than-drastic changes as a consequence of the movement toward mobile ads, "where there is a reluctance to pay as much." On the other hand, "the main thing is that more users are clicking on the ads that Google is serving."


Some of that may be due to the recently launched Enhanced Campaigns ad system (courtesy of its acquisition of AdMob). But other hints of how that might be happening came during the quarterly analyst conference call, where Chief Business Officer Nikesh Arora talked about how localized product-listing ads (a major component of the mobile ad strategy) and the transition "from links to answers" has been playing out.


"We’re transitioning from links to answers," he said, referring to the way Google has been reworking its results via its Hummingbird tuneup, "and product-listing ads are part of that because they're a good experience for the user, especially on mobile devices." But he declined to comment "on how that will impact going forward."


If Google plans to continue making up in volume what it loses in individual sales, it may well be one of the few entities on the planet with the muscle and the means to do so.


But Motorola Mobility, the in-house hardware side of Google's mobile strategy, hasn't experienced a turnaround of its own. Instead, it's slid even further into the red, with a Q3 loss of $248 million. At least the dip wasn't as pronounced as in Q2, where Motorola lost $342 million. Total Q3 revenue: $1.18 billion, down from $1.78 billion last year.


The real question: Is anyone even surprised by such lackluster performance? Under Google's stewardship, Motorola hasn't differentiated itself except by being remarkably underwhelming in most every respect. The U.S.-made Moto X phones have stolen no thunder from the likes of Samsung's Galaxy S4, let alone the iPhone 5s, and its "Motomaker" customization system hasn't done much for sales either.


Milanesi's observation on this point was blunt: "It is hard to see what the advantage of having Moto is, considering the fact that they have lost close to $1 billion." But she also pointed out Google is "looking years ahead, not quarters ahead, a strategy that might make earnings analysis quite complex as we do not see the quick results on investments such as Moto."


On the analyst call, CFO Patrick Pichette reiterated a similar line: The company had a quality product in the Moto X, and it was still the early days for the new Motorola. How long those early days will go on is another story entirely -- especially with the mobile market fast becoming a settled field with Apple on top, Samsung under that, and everyone else far, far behind.


This article, "Google flies high -- but Motorola sinks further," was originally published at InfoWorld.com. Get the first word on what the important tech news really means with the InfoWorld Tech Watch blog. For the latest business technology news, follow InfoWorld.com on Twitter.


Source: http://akamai.infoworld.com/t/technology-business/google-flies-high-motorola-sinks-further-229051?source=rss_mobile_technology
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Teams Take A Step Closer To World Series


The Cardinals beat the Dodgers Friday night, and Detroit and Boston are back at Fenway on Saturday. Host Scott Simon talks with Howard Bryant of ESPN about the games and what's ahead for the World Series.



Copyright © 2013 NPR. For personal, noncommercial use only. See Terms of Use. For other uses, prior permission required.


SCOTT SIMON, HOST:


You know, this week there's been no shutdown of sports.


(SOUNDBITE OF MUSIC)


SIMON: The pennants are falling into place. The St. Louis Cardinals going back to the World Series after beating the Los Angeles Dodgers last night by a score of, I don't know, I had to go to sleep. It looked like about 50 to nothing. And tonight, in the American League, the Detroit Tigers roar back into Fenway Park. But would you bet against the Red Sox to win a game there? They lead the series three games to two. A bunch of reds could be in the World Series. For more we go to Howard Bryant of ESPN.com and ESPN The Magazine. He's at the studios of New England Public Radio. Howard, thanks for being with us.


HOWARD BRYANT: Good morning, Scott. It wasn't that bad. It wasn't 50 to nothing. It was 9 to nothing, but it felt like 50 to nothing.


SIMON: This is the fourth World Series the Cardinals will be going to in ten years. Now of course, as you realize, for a Cub fan, this is hard to say, b-b-b-b-b-but year in and year out the Cardinals are one of the great franchises, not only of all time, but of all now. How do they do it?


BRYANT: It's a fantastic thing. When you start looking at the Cardinals, I always refer to Major League Baseball as there are four legs to the table in terms of the four franchises that have been historically and successfully the most popular teams, is the Cardinals, the Red Sox, the Dodgers and the Yankees. And those teams stand above the rest every year for some reason, whether it's the Red Sox - even when the Red Sox underachieve, they were somehow the team that people wrote about and talked about and they were always, they had so much influence in Major League Baseball.


The Cardinals are the Midwest team. In a year where Stan Musial, the greatest Cardinal, passed away, they win the pennant. They've won 19 pennants, 22 pennants overall since 1883; they've won nine since 1996. And they do it the old-fashioned way, in a lot of different ways. They still go out and they get free agent players, but they have a lot of homegrown players.


They don't overspend, and gee, the kid, Michael Wacha - this kid has played - he's pitched nine starts in his career and he is the difference-maker right now. And how did they get Michael Wacha? By not giving Albert Pujols the $250 million and letting him go, and now this young homegrown talent pitched them into the World Series last night, giving up only two hits.


SIMON: Yeah. Let's go to the American League. As we mentioned, Boston is ahead three to two. So Detroit's not down by much, but did that second game put the series into a kind of groove?


BRYANT: Second game changed everything. You've got back-to-back guys throwing no-hitters. You've got a 1-nothing lead on the road, you're up 5 to nothing, and then 5 to one with two outs in the eighth inning, so you're about to go home for three games, up two games to none, with your best pitcher on the mound.


David Ortiz hits a grand slam, you lose the game in the next inning. And all of a sudden everything turns around. Then they beat Verlander at home, you know, in Detroit, and so now instead of having a chance to go up three games to none, the Tigers are facing elimination. And the good news for the Tigers is that they've got their two best pitchers.


You've got Max Scherzer going tonight, who's probably going to win the Cy Young Award next month, and you've got Verlander if they win tonight, going to a game 7 and you don't want to face Verlander in a game 7. So on the one hand, the Red Sox are a game away from going to the World Series, but if you're the Tigers, you are the defending American League Champions. You went to the World Series last year, and you've got your two best pitchers going the next two games if it gets that far.


SIMON: Got to ask you quickly about Prince Fielder. I saw him slide into second base this week. It was like dredging the Panama Canal. He hasn't had a successful playoff series in a long time.


BRYANT: No, and it's tough. You look at all the stat guys and the Bill James people that I completely disagree with so many times when they talk about how there's no such thing as clutch hitting and there's a small sample size in the postseason. And I disagree with that. I think that what you do in the postseason, it's pressure. It's not comparing you to the regular season. It's what you do in this moment when everybody's watching.


If you look at Carlos Beltran last night...


SIMON: Oh, what a catch. Yeah.


BRYANT: What a catch. He got them going and he wins game 1 for them. He's an amazing, amazing offensive player and defensive player, and then you look at Prince Fielder who's had a terrible postseason. He needs to break out or people are going to wonder if he's a pressure player - at $214 million over nine years.


SIMON: Yeah. We actually have 20 seconds left. We're building into the clock. I got a tweet last night as you and I were watching the game I want to run by you. Thomas Alma writes: Sorry I don't share your love of the game. Professional sports are corrupt, child-like and pathetic. Howard, he's talking about us.


BRYANT: He really is. And he's not wrong, but we love them anyway.


SIMON: Thanks very much, Howard Bryant of ESPN.com and ESPN The Magazine. And you're listening to WEEKEND EDITION from NPR News.


Copyright © 2013 NPR. All rights reserved. No quotes from the materials contained herein may be used in any media without attribution to NPR. This transcript is provided for personal, noncommercial use only, pursuant to our Terms of Use. Any other use requires NPR's prior permission. Visit our permissions page for further information.


NPR transcripts are created on a rush deadline by a contractor for NPR, and accuracy and availability may vary. This text may not be in its final form and may be updated or revised in the future. Please be aware that the authoritative record of NPR's programming is the audio.


Source: http://www.npr.org/templates/story/story.php?storyId=237545159&ft=1&f=1055
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Study shows how Staph toxin disarms the immune system

Study shows how Staph toxin disarms the immune system


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Public release date: 16-Oct-2013
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Contact: Lisa Greiner
lisa.greiner@nyumc.org
646-592-3044
NYU Langone Medical Center / New York University School of Medicine



Findings point the way to new class of antibiotics



Researchers at NYU Langone Medical Center have discovered a new mechanism by which the deadly Staphylococcus aureus bacteria attack and kill off immune cells. Their findings, published today in the journal Cell Host & Microbe, explain a critical survival tactic of a pathogen that causes more skin and heart infections than any other microbe, and kills more than 100,000 Americans every year.


"What we've found is that Staph unleashes a multi-purpose toxin capable of killing different types of immune cells by selectively binding to surface receptors," says Victor J. Torres, PhD, assistant professor of microbiology, and senior author of the study. "Staph has evolved the clever ability to target the immune system at different stages."


Scientists have long known that Staph releases an arsenal of toxins to puncture immune cells and clear the way for infection. But only recently have they begun to understand exactly how these toxins work. Earlier this year, Dr. Torres and his team published a paper in Nature explaining how one of those toxins, a protein called LukED, fatally lyses T-cells, macrophages and dendritic cells, all types of white blood cells that help fight off infection. The LukED toxin, they showed, binds to a surface receptor called CCR5 (the same one exploited by HIV). "It attaches to the surface receptor and then triggers pore formation," says Dr. Torres. But their discovery failed to explain how the bacterial toxin kills other types of white blood cells, such as neutrophils, that lack the CCR5 receptor.


Their most recent work solves this puzzle, showing for the first time how receptors on neutrophils (a common type of white blood cell) also enable binding of the LukED toxin. The researchers found that LukED latches onto surface receptors called CXCR1 and CXCR2, creating the same deadly pores that it does when it latches onto CCR5 receptors. "The mechanism is the same," says Dr. Torres. "The strategy makes Staph deadlier in mice."


Neutrophils are the first responders. Upon infection, they race through the bloodstream to kill off the invading pathogen. "They're like the marines of the immune system," Dr. Torres says. T-cells, macrophages and dendritic cells rush in later, mounting a secondary attack to help the body clear the pathogen and remember it in the future. "Killing off the first responders completely disarms the immune system," Dr. Torres says.


LukED is just one piece of the puzzle, and more research is needed to understand other Staph toxins and how they work together to make the microbe deadlier. However, these recent insights hold promise for new medications that target LukED. Better treatments against Staph are desperately needed. In 2005, the Centers for Disease Control and Prevention estimated that more than half of the 478,000 people hospitalized for staph infections were resistant to methicillin, one of the most potent antibiotics available.


One therapeutic strategy is to block CCR5 receptors and spare the secondary immune response. "We know we can block CCR5 receptors without crippling the rest of the immune system. Some people lack CCR5 and they are perfectly healthy and immune to HIV as well," Dr. Torres says. "But just blocking CCR5 isn't enough." Drugs are available to block CXCR1 and CXCR2 receptors, but those will impair neutrophil recruitment and function. "The lesson is to target the toxin itself and prevent it from attaching to any receptors," Dr. Torres adds. "We have to think globally."


###


Other NYU School of Medicine researchers contributing to the study are Tamara Reyes-Robles, Francis Alonzo III, PhD, Lina Kozhaya and Derya Unutmaz, MD.


The study was funded by grants from the National Institutes of Health, the NYU School of Medicine Development Funds, and an American Heart Association Scientist Development Grant.




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Study shows how Staph toxin disarms the immune system


[ Back to EurekAlert! ]
Public release date: 16-Oct-2013
[


| E-mail



| Share Share

]

Contact: Lisa Greiner
lisa.greiner@nyumc.org
646-592-3044
NYU Langone Medical Center / New York University School of Medicine



Findings point the way to new class of antibiotics



Researchers at NYU Langone Medical Center have discovered a new mechanism by which the deadly Staphylococcus aureus bacteria attack and kill off immune cells. Their findings, published today in the journal Cell Host & Microbe, explain a critical survival tactic of a pathogen that causes more skin and heart infections than any other microbe, and kills more than 100,000 Americans every year.


"What we've found is that Staph unleashes a multi-purpose toxin capable of killing different types of immune cells by selectively binding to surface receptors," says Victor J. Torres, PhD, assistant professor of microbiology, and senior author of the study. "Staph has evolved the clever ability to target the immune system at different stages."


Scientists have long known that Staph releases an arsenal of toxins to puncture immune cells and clear the way for infection. But only recently have they begun to understand exactly how these toxins work. Earlier this year, Dr. Torres and his team published a paper in Nature explaining how one of those toxins, a protein called LukED, fatally lyses T-cells, macrophages and dendritic cells, all types of white blood cells that help fight off infection. The LukED toxin, they showed, binds to a surface receptor called CCR5 (the same one exploited by HIV). "It attaches to the surface receptor and then triggers pore formation," says Dr. Torres. But their discovery failed to explain how the bacterial toxin kills other types of white blood cells, such as neutrophils, that lack the CCR5 receptor.


Their most recent work solves this puzzle, showing for the first time how receptors on neutrophils (a common type of white blood cell) also enable binding of the LukED toxin. The researchers found that LukED latches onto surface receptors called CXCR1 and CXCR2, creating the same deadly pores that it does when it latches onto CCR5 receptors. "The mechanism is the same," says Dr. Torres. "The strategy makes Staph deadlier in mice."


Neutrophils are the first responders. Upon infection, they race through the bloodstream to kill off the invading pathogen. "They're like the marines of the immune system," Dr. Torres says. T-cells, macrophages and dendritic cells rush in later, mounting a secondary attack to help the body clear the pathogen and remember it in the future. "Killing off the first responders completely disarms the immune system," Dr. Torres says.


LukED is just one piece of the puzzle, and more research is needed to understand other Staph toxins and how they work together to make the microbe deadlier. However, these recent insights hold promise for new medications that target LukED. Better treatments against Staph are desperately needed. In 2005, the Centers for Disease Control and Prevention estimated that more than half of the 478,000 people hospitalized for staph infections were resistant to methicillin, one of the most potent antibiotics available.


One therapeutic strategy is to block CCR5 receptors and spare the secondary immune response. "We know we can block CCR5 receptors without crippling the rest of the immune system. Some people lack CCR5 and they are perfectly healthy and immune to HIV as well," Dr. Torres says. "But just blocking CCR5 isn't enough." Drugs are available to block CXCR1 and CXCR2 receptors, but those will impair neutrophil recruitment and function. "The lesson is to target the toxin itself and prevent it from attaching to any receptors," Dr. Torres adds. "We have to think globally."


###


Other NYU School of Medicine researchers contributing to the study are Tamara Reyes-Robles, Francis Alonzo III, PhD, Lina Kozhaya and Derya Unutmaz, MD.


The study was funded by grants from the National Institutes of Health, the NYU School of Medicine Development Funds, and an American Heart Association Scientist Development Grant.




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| Share 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.




Source: http://www.eurekalert.org/pub_releases/2013-10/nlmc-ssh101113.php
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Titanic violin sells more nearly $1.45M at auction


LONDON (AP) — A violin believed to have played on the Titanic before the doomed vessel sank beneath the waves has sold for 900,000 pounds (some $1.45 million) at auction.

An unidentified bidder on Saturday won the violin, whose metal fixtures appear corroded by seawater and is no longer playable. It is thought to have belonged to bandmaster Wallace Hartley, who was among the disaster's more than 1,500 victims.

Auctioneer Henry Aldridge and Son says the violin has been subject to numerous tests to check its authenticity since it was discovered in 2006. It said earlier this year that the violin was Hartley's "beyond reasonable doubt."

The German-made violin was a gift from Hartley's fiancee Maria Robinson, and was engraved with the words "For Wallace on the occasion of our engagement from Maria."

Source: http://news.yahoo.com/titanic-violin-sells-more-nearly-1-45m-auction-154058842.html
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Bethenny Frankel Says Jason Hoppy Is Living in Her House!



By Victoria Moorhouse

A lover of Mad Men, #ManicureMondays, statement shoes, and anything Boy Meets World.




When Ellen noted she hasn’t been invited over pal Bethenny Frankel‘s humble abode, Bethenny gave her a reason why—and revealed a fact you might not believe! Apparently it’s because her ex-husband—Jason Hoppy—still lives there!


OK! News: Bethenny Frankel Gets New Ink 


That’s what she said! Ellen DeGeneres appears on Bethenny’s talk show today as the first guest, clearing up rumors that the two aren’t exactly close friends. Those fictional myths were quickly put to rest as Ellen and Bethenny mutually reveal their admiration and love for each other. Seriously, these two have a friendship that seems like it’s built on solid ground.



But an interview with Ellen wouldn’t be the same without a little wit, and that’s when the secret came out. After Bethenny tells her audience that she’s hung out with Ellen and Portia at their house, Ellen says, “You have not invited me to your house, but I’ve invited you to mine, so that has happened.” Bethenny’s response? “My ex-husband lives in my house, Ellen.”


Yep, she said it! Do you think that means Bethenny still lives there, too? Did she move into a different apartment? Thoughts?


Photos: #TransformationTuesday: The Real Housewives 


Watch: Evelyn Lozada Talks Beauty Secrets 


What do you think about what Bethenny revealed? Tweet @OKMagazine and leave a comment below.



Source: http://okmagazine.com/get-scoop/bethenny-frankel-says-jason-hoppy-is-living-in-her-house/
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'Pulp Fiction' Castmembers Reunite for Quentin Tarantino's Prix Lumiere Award


LYON, France – Quentin Tarantino brought out the big guns – including Harvey Weinstein, Uma Thurman and Harvey Keitel – when he received the Prix Lumiere at the film festival here Friday night.



The Prix Lumiere, which has been awarded to Clint Eastwood, Milos Forman, Gerard Depardieu, and Ken Loach in the five years since its inception, was envisioned by Cannes and Lumiere film festivals head Thierry Fremaux to become the Nobel prize of filmmakers to honor their bodies of work.


At an exceptionally emotional tribute and award ceremony, which preceded a brief backstage government ceremony in which he was awarded the Commander of Arts and Letters by French culture minister Aurelie Filippetti, the director was honored by his longtime friends and creative collaborators.


PHOTOS: Quentin Tarantino's 'Django Unchained' NYC Premiere


Tim Roth got the evening off to a bawdy start with a few well-placed swears, but the mood soon turned more sweet and serious as producers Lawrence Bender and Weinstein took the stage. The famously demanding Weinstein credited Tarantino for both of his businesses success.


"My first company, Miramax, was the house that Quentin built, and my second company, The Weinstein Company, is the house that Quentin saved," he said, showing an uncharacteristic soft spot when adding that Tarantino is "tough minded and tough, but really one of the most compassionate human beings I know."


Keitel, who took the stage next, was moved by Weinstein's words and grew teary as he began to talk about the director. "Damn, I'm not going to make it through this," he said when composing himself, before comparing his relationship with Tarantino to a great romance. "I always felt we were meant for each other and nothing could keep us apart. Maybe if he had been a woman we could have gotten married, had kids," he joked. "Working with Quentin is like reading a great novel or hearing a great symphony or piece of music -- it changes you. You don't know how, but it has."


With a barrage of superlatives that required Fremaux to translate from her "terribly" hand-written speech on the back of the day's program, Thurman declared: "For all your wildness, your work always has aspirations for justice, freedom from oppression, courage, and most of all love and passion."


PHOTOS: 25 of Fall's Most Anticipated Movies


"You have been an explosion of dynamite in the art of cinema itself," she said, comparing him to Alfred Nobel, the inventor of dynamite and the namesake of the Nobel Prize. "You invented your own dynamite, your 'cinemite.' May your legacy be your fearlessness and the flicker of light projected through the darkness of a movie house forever be your fuse."


"I don't have words for how I feel -- probably one of the first times that has happened to me," said Tarantino. He credited the actors onstage for bringing his characters to life, and Bender and Weinstein for backing him and his dreams throughout his career.


"I have always thought of myself as a lone wolf, but always because I never really had a family, but these people are my family. Their affection and respect is all I ever want," he said, just before Thurman presented him with the award.


He thanked the roaring crowd, the city of Lyon - where film was invented by the Lumiere brothers in 1895 - and France as well. "Cinema is my religion and France is my Vatican," he said, causing much confusion in the crowd. "I probably just insulted you a little bit with that but it was the best example I could come up with."


"I don't know where I would be if the Lumiere brothers' mother and father had never met," he said. "Probably somewhere selling 'Royale with Cheese.' "


Source: http://feedproxy.google.com/~r/thr/international/~3/v5FdrLm_bfI/story01.htm
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Let's Talk About Whatever You Want Right Now

Let's Talk About Whatever You Want Right Now

Hello there, happy Friday! We have a government again! (Sort of.) You know you don't want to work anymore, and neither do we. Let's do nothing together. And by nothing, I mean let's discuss topics of your choice in the Kinja™ below.

Read more...


    






Source: http://feeds.gawker.com/~r/gizmodo/full/~3/Qmflwaz0X2A/@marioaguilar
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Friday, October 18, 2013

A Fight Over Vineyards Pits Redwoods Against Red Wine





Environmental groups are fighting to stop the leveling of 154 acres of coastal redwoods and Douglas firs to make way for grapevines.



Courtesy Friends of the Gualala River


Environmental groups are fighting to stop the leveling of 154 acres of coastal redwoods and Douglas firs to make way for grapevines.


Courtesy Friends of the Gualala River


In the California wine mecca of Sonoma County, climate change is pitting redwood lovers against red wine lovers.


This Friday morning, a coalition of environmental groups are in a Santa Rosa, Calif., courtroom fighting to stop a Spanish-owned winery from leveling 154 acres of coast redwoods and Douglas firs to make way for grapevines.


Redwoods only grow in the relatively cool coastal region of Northern California and southern Oregon. Parts of this range, such as northwestern Sonoma County, have become increasingly coveted by winemakers.


Chris Poehlmann, president of a small organization called Friends of the Gualala River, says the wine industry is creeping toward the coast as California's interior valleys heat up and consumers show preferences for cooler-weather grapes like pinot noir.


"Inexorably, the wine industry is looking for new places to plant vineyards," says Poehlmann, whose group is among the plaintiffs.


California's Department of Forestry and Fire Protection, or CalFire, approved the redwood-clearing project in May 2012.


"So we sued them," says Dave Jordan, the legal liaison for the Sierra Club's Redwood Chapter, another of the plaintiffs. The Center for Biological Diversity is the third plaintiff.


The groups filed suit in June 2012 on the grounds that state officials violated California's environmental protection laws by approving the plan.


Redwoods are considered among the most spectacular of all trees. The biggest trees on Earth by height, redwoods can stand more than 350 feet tall. Some are more than 2,000 years old.


However, the redwoods at the center of this conflict are not old-growth trees. The area was clear-cut more than 50 years ago, and most of the redwoods on the site are less than 100 feet tall. Which is why Sam Singer argues: "There are no forests [on this site]."


Singer is a spokesman for Artesa Vineyards and Winery, which is owned by the Spanish Codorniu Group and which first proposed the development project in 2001. Singer says that the two old-growth redwood trees on the property will be spared.


But the thousands of trees slated for removal are between 50 and 80 feet tall, according to Poehlmann. He says the trees provide wildlife habitat and stabilize the soil against erosion, which has been a major problem for streams in the area that once harbored runs of salmon and steelhead trout.





Coast redwood trees stand at Muir Woods National Monument in Mill Valley, Calif. Redwoods are the biggest trees on Earth by height — they can grow more than 350 feet tall. But their range is quite limited: They only grow along the coast of Northern California and southern Oregon.



Justin Sullivan/Getty Images


Coast redwood trees stand at Muir Woods National Monument in Mill Valley, Calif. Redwoods are the biggest trees on Earth by height — they can grow more than 350 feet tall. But their range is quite limited: They only grow along the coast of Northern California and southern Oregon.


Justin Sullivan/Getty Images


The project planners have even estimated this timber to represent 1.25 million board feet of "merchantable" lumber.


Dennis Hall, a higher official with CalFire, says his department's approval of Artesa's project in 2012 came only after a lengthy review process found that it would not significantly damage the environment.


"We did an [environmental impact report] for the project," Hall says. "It was an extreme and exhaustive analysis of potential impacts to the environment." The report deemed most of these potential impacts to be "less-than-significant."


Still, Poehlmann feels CalFire has been too lenient on proposals by developers to level trees. "They are acting as if they are actually the 'department of deforestation,' " he says.


The tensions go beyond this case: Friends of the Gualala River and the Sierra Club's Redwood Chapter have gone to court several times in the past decade to successfully stop timberland conversion projects proposed by winery groups and which had been approved by the state. Among these fights was the battle to save the so-called Preservation Ranch, a 19,000-acre parcel that developers planned to partially deforest and replant with vines. Earlier this year, the developer sold the property to The Conservation Fund.


But from 1979 to 2006, 25 conversions of forest to agriculture occurred in Sonoma County at an average rate of 21 acres per year, according to county officials.


At least a few tree-clearing projects have occurred without permission. High-profile winemaker Paul Hobbs didn't bother getting a permit before he leveled 8 acres of redwoods in 2011 with plans to plant wine grapes. He remains a superstar winemaker and was tagged earlier this year by Forbes as "The Steve Jobs of Wine."


And it's not just redwoods that are at stake as vineyards expand their terrain. California's oaks aren't subject to the same environmental protections as more commercially valuable species like redwoods and Douglas fir, according to CalFire's Hall. And Northern California's oak forest, near the coast as well as inland, is being lost at fast rates to vineyard expansions, says Adina Merenlender, an environmental biologist with the University of California, Berkeley.


Merenlender says oak trees tend to be overlooked by the general public, which is more easily impressed by redwoods. Yet oak forests, she says, provide habitat for vastly more species than do redwood forests.


Sara Cummings with the Sonoma Vintners, a wine industry trade group, says new vineyards are usually planted within what she calls the region's "agricultural footprint" — land that is already designated by county planners as "agricultural." Moreover, she says, more than half the county's wine growers are members of the California Sustainable Winegrowing Program.


But Merenlender is concerned about future expansion into land not previously farmed.


"We're already seeing a lot of acquisition of coastal lands," she says. "Investments are moving north and west, toward the coast."


The issue, it seems, is a global one. A 2013 study predicted that global warming will cause a dramatic shift in the world's wine regions. The report warns that wilderness areas in British Columbia and remote regions of China — one of the world's fastest-growing winemaking regions — may become increasingly coveted by the industry.


"But at least we'll have plenty of wine to drink, "Poehlmann quips, "while we bemoan the fact that our forests are all used up."


Source: http://www.npr.org/blogs/thesalt/2013/10/18/237136077/a-fight-over-vineyards-pits-redwoods-against-red-wine?ft=1&f=1053
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Reid Says Cruz Wants to Run for President (Taegan Goddard's Political Wire)

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Tanning gene linked to increased risk of testicular cancer, according to NIH scientists

Tanning gene linked to increased risk of testicular cancer, according to NIH scientists


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PUBLIC RELEASE DATE:

18-Oct-2013



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Contact: Robin Mackar
rmackar@niehs.nih.gov
919-541-0073
NIH/National Institute of Environmental Health Sciences





A gene important in skin tanning has been linked to higher risk for testicular cancer in white men, according to a study led by scientists from the U.S. National Institutes of Health and the University of Oxford in England. Nearly 80 percent of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.


The research appeared online October 10, 2013 in the journal Cell, and is the result of an integrated analysis of big data supported by laboratory research. The team suspected that variations in a gene pathway controlled by the tumor suppressor gene p53 could have both positive and negative effects on human health.


"Gene variations occur naturally, and may become common in a population if they convey a health benefit," said Douglas Bell, Ph.D., author on the paper and researcher at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. "It appears that this particular variant could help protect light-skinned individuals from UV skin damage, like burning or cancer, by promoting the tanning process, but it permits testicular stem cells to grow in the presence of DNA damage, when they are supposed to stop growing."


Bell explained that p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.


To conduct the analysis, Xuting Wang, Ph.D., of NIEHS, co-author and lead bioinformatics scientist on the paper, led a data mining expedition to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.


"In the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved," Wang noted.


The group at the Ludwig Institute for Cancer Research at the University of Oxford, led by Gareth Bond, Ph.D., performed complex experiments to confirm the molecular mechanism that linked the variant with cancer and tanning.


"White males with a single nucleotide variation in KITLG, called the G allele, have the highest odds of having testicular cancer. In fact, the twofold to threefold increased risk is one of the highest and most significant among all cancer GWAS conducted within the past few years," said Bond. "The high frequency of this allele in light skin individuals may explain why testicular cancer is so much more frequent in people of European descent than those of African descent."


Bond said although the G allele increases testicular cancer risk, it may explain why testicular tumors are often easily cured with chemotherapy. "Most other tumors have a mutant p53, but in these testicular cell tumors, the p53 is functioning properly, and the drugs used for testicular cancer appear to work in concert with p53's tumor suppression function to kill the cancer cells."


###


NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit http://www.niehs.nih.gov. Subscribe to one or more of the NIEHS news lists to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications.


About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
NIH...Turning Discovery Into Health


Reference: Zeron-Medina J, Wang X, Repapi E, Campbell MR, Su D, Castro-Giner F, Davies B, Peterse EFP, Sacilotto N, Walker GJ, Terzian T, Tomlinson IP, Box NF, Meinshausen N, De Val S, Bell DA, Bond GL. 2013. A polymorphic p53 response element in the KIT ligand gene influences cancer risk and has undergone natural selection. Cell; http://dx.doi.org/10.1016/j.cell.2013.09.017 [Online 10 October 2013].


Grant numbers: 01ES100475, Z01ES046008




Contact:


Robin Mackar, NIEHS

(919) 541-0073


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Tanning gene linked to increased risk of testicular cancer, according to NIH scientists


[ Back to EurekAlert! ]

PUBLIC RELEASE DATE:

18-Oct-2013



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Contact: Robin Mackar
rmackar@niehs.nih.gov
919-541-0073
NIH/National Institute of Environmental Health Sciences





A gene important in skin tanning has been linked to higher risk for testicular cancer in white men, according to a study led by scientists from the U.S. National Institutes of Health and the University of Oxford in England. Nearly 80 percent of white men carry a variant form of this gene, which increased risk of testicular cancer up to threefold in the study.


The research appeared online October 10, 2013 in the journal Cell, and is the result of an integrated analysis of big data supported by laboratory research. The team suspected that variations in a gene pathway controlled by the tumor suppressor gene p53 could have both positive and negative effects on human health.


"Gene variations occur naturally, and may become common in a population if they convey a health benefit," said Douglas Bell, Ph.D., author on the paper and researcher at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. "It appears that this particular variant could help protect light-skinned individuals from UV skin damage, like burning or cancer, by promoting the tanning process, but it permits testicular stem cells to grow in the presence of DNA damage, when they are supposed to stop growing."


Bell explained that p53 stimulates skin tanning when ultraviolet light activates it in the skin. It then must bind a specific sequence of DNA located in a gene called the KIT ligand oncogene (KITLG), which stimulates melanocyte production, causing the skin to tan.


To conduct the analysis, Xuting Wang, Ph.D., of NIEHS, co-author and lead bioinformatics scientist on the paper, led a data mining expedition to sieve through many different data sets. The team selected possible leads from the intersection of more than 20,000 p53 binding sites in the human genome, 10 million inherited genetic variations genotyped in the 1000 Genomes Project, and 62,000 genetic variations associated with human cancers identified in genome-wide association studies (GWAS). These data sets were gathered through joint efforts of thousands of researchers from around the world.


"In the end, one variant in the p53 pathway was strongly associated with testicular cancer, but also, surprisingly, displayed a positive benefit that is probably related to tanning that has occurred as humans evolved," Wang noted.


The group at the Ludwig Institute for Cancer Research at the University of Oxford, led by Gareth Bond, Ph.D., performed complex experiments to confirm the molecular mechanism that linked the variant with cancer and tanning.


"White males with a single nucleotide variation in KITLG, called the G allele, have the highest odds of having testicular cancer. In fact, the twofold to threefold increased risk is one of the highest and most significant among all cancer GWAS conducted within the past few years," said Bond. "The high frequency of this allele in light skin individuals may explain why testicular cancer is so much more frequent in people of European descent than those of African descent."


Bond said although the G allele increases testicular cancer risk, it may explain why testicular tumors are often easily cured with chemotherapy. "Most other tumors have a mutant p53, but in these testicular cell tumors, the p53 is functioning properly, and the drugs used for testicular cancer appear to work in concert with p53's tumor suppression function to kill the cancer cells."


###


NIEHS supports research to understand the effects of the environment on human health and is part of NIH. For more information on environmental health topics, visit http://www.niehs.nih.gov. Subscribe to one or more of the NIEHS news lists to stay current on NIEHS news, press releases, grant opportunities, training, events, and publications.


About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.
NIH...Turning Discovery Into Health


Reference: Zeron-Medina J, Wang X, Repapi E, Campbell MR, Su D, Castro-Giner F, Davies B, Peterse EFP, Sacilotto N, Walker GJ, Terzian T, Tomlinson IP, Box NF, Meinshausen N, De Val S, Bell DA, Bond GL. 2013. A polymorphic p53 response element in the KIT ligand gene influences cancer risk and has undergone natural selection. Cell; http://dx.doi.org/10.1016/j.cell.2013.09.017 [Online 10 October 2013].


Grant numbers: 01ES100475, Z01ES046008




Contact:


Robin Mackar, NIEHS

(919) 541-0073


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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.




Source: http://www.eurekalert.org/pub_releases/2013-10/nioe-tgl101813.php
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iPhone aces JD Power satisfaction survey

iPhone aces JD Power satisfaction survey

Once again, the iPhone has come out on top in J.D. Power's U.S. Wireless Smartphone Satisfaction Study. Verizon and AT&T customers favor the iPhone the most, with Samsung favored by T-Mobile and Sprint users.

T-Mobile just began selling the iPhone 5 in April of this year; JD Power's poll took place from February to August, so it's probable that their lack of love for the iPhone is based on relative unfamiliarity. It'll be interesting to see how these figure compare in a year, now that the iPhone is squarely part of T-Mobile's product offerings.

Some bright news for beleaguered BlackBerry - the Z10 faired well in the poll. Nokia's Lumia 920 and Samsung's Galaxy Note II were also strong performers. JD Power's poll shows that Sprint users are more likely to factor features into their smartphone buying decisions, while T-Mobile customers are more price-driven.

What's your experience? Are you happy with the performance of your iPhone? Who's your carrier? Sound off in the comments!


    






Source: http://feedproxy.google.com/~r/TheIphoneBlog/~3/HF9U4DrSZW8/story01.htm
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'This is time for a reconciliation'

WASHINGTON (AP) — Senate leaders announced last-minute agreement Wednesday to avert a threatened Treasury default and reopen the government after a partial, 16-day shutdown. Congress raced to pass the measure by day's end.


The Dow Jones industrial average soared on the news that the threat of default was fading, flirting with a 200-point gain in morning trading.


"This is a time for reconciliation," said Senate Majority Leader Harry Reid of the agreement he had forged with the GOP leader, Sen. Mitch McConnell of Kentucky.


McConnell said that with the accord, Republicans had sealed a deal to have spending in one area of the budget decline for two years in a row, adding, "we're not going back."


One prominent tea party lawmaker, Sen. Ted Cruz of Texas, said he would oppose the plan, but not seek to delay its passage.


That was a key concession that signaled a strong possibility that both houses could act by day's end. That, in turn, would allow President Barack Obama to sign the bill into law ahead of the Thursday deadline that Treasury Secretary Jacob Lew had set for action to raise the $16.7 trillion debt limit.


Officials said the proposal called for the Treasury to have authority to continue borrowing through Feb. 7, and the government would reopen through Jan. 15.


There was no official comment from the White House, although congressional officials said administration aides had been kept fully informed of the negotiations.


In political terms, the final agreement was almost entirely along lines Obama had set when the impasse began last month. Tea party conservatives had initially demanded the defunding of the health care law as the price for providing essential federal funding.


Under a strategy set by Obama and Reid, Democrats said they would not negotiate with Republicans in exchange for performing what the White House called basic functions of keeping the government in operation and preventing Treasury from defaulting on its obligations.


A long line of polls charted a steep decline in public approval for Republicans in the course of what Sen. John McCain, R-Ariz., pronounced a "shameful episode" in the nation's history.


While the emerging deal could well meet resistance from conservatives in the Republican-controlled House, the Democratic Leader, Rep. Nancy Pelosi of California, has signaled she will support the plan and her rank and file is expected to vote for it in overwhelming numbers.


That raised the possibility that more Democrats than Republicans would back it, potentially causing additional problems for House Speaker John Boehner as he struggles to manage his tea party-heavy majority.


Boehner and the House Republican leadership met in a different part of the Capitol to plan their next move. A spokesman, Michael Steel, said afterward that no decision had been made "about how or when a potential Senate agreement could be voted on in the House."


The developments came one day before the deadline Lew had set for Congress to raise the current $16.7 trillion debt limit. Without action by lawmakers, he said, Treasury could not be certain it had the ability to pay bills as they come due.


In addition to raising the debt limit, the proposal would give lawmakers a vote to disapprove the increase. Obama would have the right to veto their opposition, ensuring he would prevail.


House and Senate negotiators would be appointed to seek a deficit-reduction deal. At the last minute, Reid and McConnell jettisoned a plan to give federal agencies increased flexibility in coping with the effects of across-the-board cuts. Officials said that would be a topic for the negotiations expected to begin shortly.


Despite initial Republican demands for the defunding of the health care law often derided as "Obamacare," the pending agreement makes only one modest change in the program. It requires individuals and families seeking subsidies to purchase coverage to verify their incomes before qualifying.


There were some dire warnings from the financial world a day after the Fitch credit rating agency said Tuesday it was reviewing its AAA rating on U.S. government debt for possible downgrade.


John Chambers, chairman of Standard & Poor's Sovereign Debt Committee, told "CBS This Morning" on Wednesday that a U.S. government default on its debts would be "much worse than Lehman Brothers," the investment firm whose 2008 collapse led to the global financial crisis.


Aides to Reid and McConnell said the two men had resumed talks, including a Tuesday night conversation, and were hopeful about striking an agreement that could pass both houses.


It was expected to mirror a deal the leaders had neared Monday. That agreement was described as extending the debt limit through Feb. 7, immediately reopening the government fully and keeping agencies running until Jan. 15 — leaving lawmakers clashing over the same disputes in the near future.


It also set a mid-December deadline for bipartisan budget negotiators to report on efforts to reach compromise on longer-term issues like spending cuts. And it likely would require the Obama administration to certify that it can verify the income of people who qualify for federal subsidies for medical insurance under the 2010 health care law.


But that emerging Senate pact was put on hold Tuesday, an extraordinary day that highlighted how unruly rank-and-file House Republicans can be, even when the stakes are high. Facing solid Democratic opposition, Boehner tried in vain to write legislation that would satisfy GOP lawmakers, especially conservatives.


Boehner crafted two versions of the bill, but neither made it to a House vote because both faced certain defeat. Working against him was word during the day from the influential group Heritage Action for America that his legislation was not conservative enough — a worrisome threat for many GOP lawmakers whose biggest electoral fears are of primary challenges from the right.


The last of Boehner's two bills had the same dates as the emerging Senate plan on the debt limit and shutdown.


But it also blocked federal payments for the president, members of Congress and other officials to help pay for their health care coverage. And it prevented the Obama administration from shifting funds among different accounts — as past Treasury secretaries have done — to let the government keep paying bills briefly after the federal debt limit is reached.


Boehner's inability to produce a bill that could pass his own chamber likely means he will have to let the House vote on a Senate compromise, even if that means it would pass with strong Democratic and weak GOP support. House Republican leaders have tried to avoid that scenario for fear that it would threaten their leadership, and some Republicans worried openly about that.


___


Associated Press writers David Espo, Andrew Taylor, Charles Babington, Stephen Ohlemacher, Henry C. Jackson and Donna Cassata contributed to this report.


Source: http://news.yahoo.com/deal-reached-avoid-default-open-government-165353575--finance.html
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Next-generation gene sequencing can identify invasive carp species in Chicago area waterways

Next-generation gene sequencing can identify invasive carp species in Chicago area waterways


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Public release date: 17-Oct-2013
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Contact: Wen-Tso Liu
wtliu@illinois.edu
217-333-8442
University of Illinois College of Engineering






A project to map the microbes present in the digestive systems of fish species holds promise for monitoring the presence of Asian carp in Chicago area waterways and ultimately preventing their spread, according to a study published in Nature's ISME Journal. The work, funded through the U.S. Environmental Protection Agency Great Lakes Restoration Initiative, is being conducted by researchers from the University of Illinois at Urbana-Champaign and the U.S. Geological Survey (USGS).


Asian carp is a term used to refer to several invasive fish species including silver, bighead and black carp. Bighead carp and silver carp have already invaded much of the Mississippi River basin, where they compete for food with native species and dominate aquatic communities. Bighead carp and silver carp are considered one of the most severe aquatic invasive species threats facing the Great Lakes today, according to the Asian Carp Regional Coordinating Committee (ACRCC). The ACRCC is coordinating the efforts of federal, state, local and private resource management agencies to develop an Asian carp control program. Efforts to control the fish include research to understand their physiology and behavior and how they differ from that of native species, with an eye toward developing effective monitoring and management systems.



Gut microbiotathe microbial communities present in the digestive tracts of living thingsare unique, according to Wen-Tso Liu, co-author of the study and a professor of civil and environmental engineering at the University of Illinois. For that reason, careful analysis of fish gut microbiota can reveal host-specific biomarkers shed in fish feces that indicate the presence of a specific species, promising the development of precise monitoring systems. Since fish feces are plentiful in waterways, monitoring could be easier than with techniques that have focused on detecting the DNA of the targeted species in sloughed-off skin tissue, Liu says.


The researchers used a next-generation gene sequencing technology called 16S pyrosequencing, which focuses on the 16S rRNA gene sequences, to analyze the gut microbiota of the invasive silver carp and the native gizzard shad. They successfully discovered potential biomarkers for silver carp and are working to refine them, Liu says.


In addition, the research illuminated some important similarities and differences in the species. For example, he says, gizzard shad harbor microbial communities that are 10 times more diverse than that of silver carp, showing that their digestive processes are significantly more complicated. The researchers also discovered a common food-source microbe, which proves that the fish compete for the same food.


"This is why invasive species can be dangerous," he says. "They can eat the same food, and if the invasive species consumes more food, then the native species can be out-competed and their population will start to decline, leading to ecological disaster."


On the strength of these findings, the researchers are beginning an extensive project to confirm their findings in the fish species in the Chicago Riverapproximately 50 different onesin order to map their gut microbiota and develop biomarkers for each species. The results will lead to a precise monitoring methodology, but the benefits will likely extend further, Liu says.


"There is a lot more beyond just monitoring," Liu says. "We will also learn more about the diversity of fish, their diets, how their diets are related to their gut microbiota and how they metabolize inside the gut."


###


The scientific article, "Fish gut microbiota analysis differentiates physiology and behavior of invasive Asian carp and indigenous American fish," by Lin Ye, Jon Amberg, Duane Chapman, Mark Gaikowski, and Wen-Tso Liu, is available on the ISME Journal website.




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Next-generation gene sequencing can identify invasive carp species in Chicago area waterways


[ Back to EurekAlert! ]
Public release date: 17-Oct-2013
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Contact: Wen-Tso Liu
wtliu@illinois.edu
217-333-8442
University of Illinois College of Engineering






A project to map the microbes present in the digestive systems of fish species holds promise for monitoring the presence of Asian carp in Chicago area waterways and ultimately preventing their spread, according to a study published in Nature's ISME Journal. The work, funded through the U.S. Environmental Protection Agency Great Lakes Restoration Initiative, is being conducted by researchers from the University of Illinois at Urbana-Champaign and the U.S. Geological Survey (USGS).


Asian carp is a term used to refer to several invasive fish species including silver, bighead and black carp. Bighead carp and silver carp have already invaded much of the Mississippi River basin, where they compete for food with native species and dominate aquatic communities. Bighead carp and silver carp are considered one of the most severe aquatic invasive species threats facing the Great Lakes today, according to the Asian Carp Regional Coordinating Committee (ACRCC). The ACRCC is coordinating the efforts of federal, state, local and private resource management agencies to develop an Asian carp control program. Efforts to control the fish include research to understand their physiology and behavior and how they differ from that of native species, with an eye toward developing effective monitoring and management systems.



Gut microbiotathe microbial communities present in the digestive tracts of living thingsare unique, according to Wen-Tso Liu, co-author of the study and a professor of civil and environmental engineering at the University of Illinois. For that reason, careful analysis of fish gut microbiota can reveal host-specific biomarkers shed in fish feces that indicate the presence of a specific species, promising the development of precise monitoring systems. Since fish feces are plentiful in waterways, monitoring could be easier than with techniques that have focused on detecting the DNA of the targeted species in sloughed-off skin tissue, Liu says.


The researchers used a next-generation gene sequencing technology called 16S pyrosequencing, which focuses on the 16S rRNA gene sequences, to analyze the gut microbiota of the invasive silver carp and the native gizzard shad. They successfully discovered potential biomarkers for silver carp and are working to refine them, Liu says.


In addition, the research illuminated some important similarities and differences in the species. For example, he says, gizzard shad harbor microbial communities that are 10 times more diverse than that of silver carp, showing that their digestive processes are significantly more complicated. The researchers also discovered a common food-source microbe, which proves that the fish compete for the same food.


"This is why invasive species can be dangerous," he says. "They can eat the same food, and if the invasive species consumes more food, then the native species can be out-competed and their population will start to decline, leading to ecological disaster."


On the strength of these findings, the researchers are beginning an extensive project to confirm their findings in the fish species in the Chicago Riverapproximately 50 different onesin order to map their gut microbiota and develop biomarkers for each species. The results will lead to a precise monitoring methodology, but the benefits will likely extend further, Liu says.


"There is a lot more beyond just monitoring," Liu says. "We will also learn more about the diversity of fish, their diets, how their diets are related to their gut microbiota and how they metabolize inside the gut."


###


The scientific article, "Fish gut microbiota analysis differentiates physiology and behavior of invasive Asian carp and indigenous American fish," by Lin Ye, Jon Amberg, Duane Chapman, Mark Gaikowski, and Wen-Tso Liu, is available on the ISME Journal website.




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Source: http://www.eurekalert.org/pub_releases/2013-10/uoic-ngs101713.php
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