text:
JIM LEHRER: And to the analysis of Shields and Brooks, syndicated columnist Mark Shields, New York Times columnist David Brooks.
David, do you agree with Deborah Pryce that the — what she calls the thoughtful middle has been run out of Washington?
DAVID BROOKS, Columnist, New York Times: Yes, I do, and for a whole bunch of reasons. Redistricting is part of it. The team spirit is part of it.
Deborah Pryce is a fascinating example. I remember meeting with Deborah Pryce and a whole bunch of Republican moderates years ago. They knew their party was in trouble. They knew they needed to change course.
They couldn't get the resolve, the muster to actually change course. And now the Republican Party is in the state it's in.
Deborah Pryce is from the area around Columbus, Ohio. It's a swing district, very close. And as a result, she has run and had to face a series of tough competitions. She had to face a vicious campaign last time, where — vicious ads were run against her. She ran vicious ads against her opponent.
And at one point, Pryce told me, her mother called her up and said, "I'm ashamed of the ads you're running." It wasn't the opponent's ads that bothered her.
JIM LEHRER: Her own?
DAVID BROOKS: It was the ads she was running on her own behalf. And at a certain point, you come to a point where you say, "It's not worth it." And a lot of these folks are coming to that point.
GOP Retirements
JIM LEHRER: Mark, do you see Democrats having the same thoughtful middle deficit that Deborah Pryce is talking about?
MARK SHIELDS, Syndicated Columnist: I think it is. I think the redistricting really has a lot to do with it, Jim. In other words -- say, by redistricting, we organize the congressional districts so that you have a 70 percent, if you're a Democrat, a 70 percent Democratic seat, I have a 70 percent Republican seat, David has a 70 percent Republican seat, that means that the only worry we have is not an Election Day in general election, it's in a primary.
JIM LEHRER: It's a primary, yes.
MARK SHIELDS: And the only -- so it's on the left of the Democratic Party that you have to be nervous, so you're constantly looking at your left flank, whether it's MoveOn.org, on the right side, whether Club for Growth is going to come in and spend a couple hundred thousand dollars for you because you may have even suggested that, you know, a tax would be helpful, or necessary, or wise at a time of war.
DAVID BROOKS: If I could just add one thing...
JIM LEHRER: Yes, sure.
DAVID BROOKS: ... that's all true. Another part of it is the middle -- there are people who are centrist in Congress, but they're relatively quiet and they're relatively subdued.
When you go to a conservative dinner in Washington, there are academics, there are think-tankers, there are activists. When you go to a liberal dinner, there are academics, think-tankers, and activists. When you go to a middle dinner, a centrist dinner, there are a bunch of lobbyists.
They have not generated the ideas. They have not generated the institutions. The centrists in this world complain about it. They just haven't mobilized.
There's Heritage Foundation. There's Center for American Progress on these two ideological sides. There are very few institutions that give ideas to centrists.
MARK SHIELDS: Can I just say one thing about Ray LaHood?
JIM LEHRER: Sure...
MARK SHIELDS: Ray LaHood, in that piece...
JIM LEHRER: ... the Illinois Republican.
MARK SHIELDS: ... congressman, he's a man of the House. Washington will be a less civil and less humane place because Ray LaHood is leaving. This is somebody who never had an enemy's list. He refused to demonize people across the aisle.
I mean, Dick Durbin, the Senate Democratic whip, I mean, and a formidable partisan operative, told me that Ray LaHood was one of his three best friends in the entire Illinois delegation, which includes, I think, 14 Democrats.
JIM LEHRER: Dick Durbin is a liberal Democrat.
MARK SHIELDS: Yes...
JIM LEHRER: Leader of the...
MARK SHIELDS: And a dozen Democrats who don't make his list. My point is, he's somebody who's reached across the aisle. He's always accepted that the other person may have a point of view and there's goodwill. And I have to tell you, I mean, it's an enormous, enormous loss to have him go.
JIM LEHRER: David, unless I've missed something, I don't see a solution out there to this. Nobody's -- we're lamenting a problem, but it doesn't have a solution?
DAVID BROOKS: Well, leadership. You know, when I take members of Congress or they take me to lunch or dinner, I always leave that lunch or dinner with this phrase in my head: reasonable in private. In private...
JIM LEHRER: Reasonable in private?
DAVID BROOKS: They understand the flaws of their own arguments, the strengths of their own arguments. They hate the system they're trapped in. They feel conformed to meet the party line.
And it's only when they're retiring they can give interviews like we just saw, where they're a little more honest about Katrina and things like that.
But once they're there, they have to voice the team party line. And it will take a president, frankly, to get them out of those teams.
JIM LEHRER: Do you agree?
MARK SHIELDS: Well, I think we have the potential of both of these men, I mean, have demonstrated...
JIM LEHRER: Obama and McCain?
MARK SHIELDS: ... Obama and McCain, an inclination and an interest in working across the aisle. And I think that's -- I think that's encouraging in itself.
But I don't want to in any way underestimate, Jim, the importance of the redistricting. I mean, I think...
JIM LEHRER: But that's not going to get fixed? That's not...
MARK SHIELDS: Well, but it can be fixed. And it's fixed in Iowa. I mean, Iowa as a consequence has a delegation where the lines are drawn not on, you know, some political get-even or "gotcha" operation, but are drawn by an independent commission.
And, I mean, there have been attempts to do this. And I think the recognition -- for one thing, you can maximize the number of your own party if you say to people, "David, you can win with 55 percent." "No, no, I have to have 75 percent." It becomes a matter of ego and vanity to have these huge...
DAVID BROOKS: I agree with you totally, but the Senate is almost as polarized as the House, not quite, but almost as polarized. And there's obviously no redistricting in the Senate.
And there, I think, it's culture. It's loyalty to team replaces loyalty to the truth.
You go to these policy lunches on Tuesdays, if you're a senator. They give you the message of the week, especially on the Republican side, and you're supposed to hew to that message. And that's just a matter of culture. The redistricting hurts a lot, but I think there's also a culture here that has to be broken.
The Clintons at the convention
JIM LEHRER: The presidential campaign -- quickly here, Mark -- Hillary Clinton has now suggested that maybe there should be a vote on her during the Democratic convention. Obviously, she's going to lose it, but for symbolic reasons, et cetera, et cetera. What do you think of that idea?
MARK SHIELDS: The only thing worse than a vote on the floor for Hillary Clinton, her being nominated, is perhaps not having a vote on the floor. I mean, in other words, if the protests are going to be part of the story...
JIM LEHRER: So that would take the edge off...
MARK SHIELDS: It might take the edge off. I would say this. You know, we're seeing this week why Sen. Clinton was not on the long list or the short list for vice president. I mean, we're seeing abundant evidence of it. I mean, from Bill Clinton's frosty non-endorsement of -- and sort of petulant non-endorsement of Sen. Obama.
JIM LEHRER: Just a couple of weeks ago?
MARK SHIELDS: Yes...
JIM LEHRER: ... on interviews.
MARK SHIELDS: ... ABC. And then Sen. Obama scurrying, saying, no, no, he thought he was set up for that question. He told the New York Post yesterday that they were trying to push President Clinton.
I just -- I think, Jim, what we have here is -- it's interesting. Hillary Clinton has gone from an interesting, independent, formidable political figure in her own right, which she became during the primaries, especially that string of victories, and it was an impressive performance.
Now we're back to thinking of them as the Clintons, which is a soap opera and it's a psychodrama. And this is not helpful going in.
The comparable experiences, 1976, with Reagan and Ford, where that party was never put back together after Kansas City, 1980, where Jimmy Carter probably couldn't have won against Ronald Reagan under any circumstance, but with Ted Kennedy, that was divided, and '68 with the Democrats.
JIM LEHRER: How do you see it?
DAVID BROOKS: But those were at least ideological fights. This is a fight about nothing.
MARK SHIELDS: That's right.
DAVID BROOKS: Except personal power.
JIM LEHRER: Is it really a fight about nothing?
DAVID BROOKS: Well, it's a fight about naked politics. I mean, it's existing on two levels.
On the public level, it's sort of a new age therapy group, where they say, "We need to have catharsis. We need to have closure. We need to heal the chi and the feng shui," or whatever that stuff is. "We need peace."
But that's not what it's really about. Those are just the talking points. There is some negotiations going beneath the level over I don't know what, speeches at the convention, who gets what job in an administration. At some level, it's got politics, and this is just being used as leverage. I can't -- personally don't think they'll have the vote.
MARK SHIELDS: I can't either, David.
JIM LEHRER: You don't think they will?
MARK SHIELDS: I can't either. But, I mean, you know, why do they have them on two separate nights? I mean, there's only four nights of the convention. So that means half the nights...
JIM LEHRER: They're going to have Hillary Clinton on Tuesday night and have Bill Clinton on Wednesday night.
MARK SHIELDS: And Bill Clinton on Wednesday night. I mean, at least the Republicans are quarantining Bush and Cheney to Monday night, on Labor Day, you know, so that they're in and out, out of the Twin Cities.
JIM LEHRER: Some people are suggesting, David, that maybe the Clintons don't want Barack Obama to win after all.
DAVID BROOKS: Yes, I...
JIM LEHRER: You don't go with that?
DAVID BROOKS: ... I remain innocent about this. I could be naive, but I just believe people generally want their party to win, even if it's not -- but there is...
JIM LEHRER: So you think they'll suck it up by the time of...
DAVID BROOKS: Oh, I think so, but there's an ethos that, "We're going to be hard. We're going to be tough. You want to admire that. We're going to be ruthless. Ruthless is good." And you see that in the Clintons.
And, frankly, you see it in the McCain and Obama in the way they flip-flop on all these various issues. There's an ethos now that the more ruthless you are, the more macho you are, that proves you're a tough customer and you're the best thing. No holds barred, we're going after this thing.
Strategies of McCain, Obama
JIM LEHRER: Meanwhile, Mark, both Obama and McCain have been talking a lot about energy, energy, energy, energy. Are they saying anything important this week?
MARK SHIELDS: Well, I mean, for McCain, it's been a godsend, because McCain is trying to make energy a proxy for the economy. He's in terrible shape on the economy, whether it's, you know, being branded too close to Bush, carrying the Republican brand on unemployment, inflation, economic growth, and sort of a pessimism.
But if he can make energy sort of the proxy for the economy, it kind of works for him, I think in the sense of off-shore drilling. You've seen -- I don't know what will be the consequence, Jim, of Obama, you know, moving to a compromise on...
JIM LEHRER: On drilling and...
MARK SHIELDS: ... off-shore drilling, but I do think that McCain feels that this is the one advantage he's been given. And he's just trying to grab it, because he's obviously lost his advantage -- because of the president and his own initiatives to save his legacy, I think, on Iran and on Iraq, he's been deprived of some of his talking points and his positions.
JIM LEHRER: But a lot has been made about the fact that McCain had a couple of commercials this week that seemed to be pulling away from Bush as best he can. What do you think?
DAVID BROOKS: Well, you'd better. You know, 80 percent of the country thinks the country is going in the wrong direction. You'd better. You'd better move away.
And I think it's obviously the smart thing to do. The thing he's got to do -- and I'm told the thing he's going to do in the convention -- is give a narrative of where the Republican Party went wrong. Those Republican moderates who are leaving the House...
JIM LEHRER: We'll be hearing some of that, you think?
DAVID BROOKS: We will be hearing some of that.
JIM LEHRER: From John McCain, we'd be -- we would be...
DAVID BROOKS: In his speech, he'll distance himself. He's got to distance himself not only from the Bush, but the recent history of the party.
And he's got to hit Obama. I agree with Mark. The energy thing has been the best issue McCain has. On the stupid political sense, he's talking about off-shore drilling, not that it will help, but he's forced Obama into a series of policy shifts which detract from his era of new politics, the windfall profits tax, totally stupid tax, the petroleum reserve, and sort of agreeing to off-shore drilling.
He's dented Obama and put him really on the defensive. On substance, of course, none of these things will make any difference. But on politics, it's working for McCain.
MARK SHIELDS: It's fascinating, Jim, I mean, that John McCain preempted the Ronald Reagan phrase, "We're worse off than we were four years ago." I mean, that shows to me a sensitivity of the charge that he's running for George Bush's third term. He's trying somehow to immunize himself against that charge by his being more critical of the last four years and what's gone on than even is Obama.
JIM LEHRER: But Obama, that is his major theme, is it not? You want another Bush term, vote for McCain.
DAVID BROOKS: Right, and it's the smart thing. It's sticking in the polls. The only thing I would say, in times of change, there are occasions when the conservative candidate wins because people want change, but not that much change. And there's an opening there for McCain, if he can articulate a sort of reform that's not radical change. He hasn't done that yet.
MARK SHIELDS: The argument that Obama is confronting is this. Independents and Democrats have doubts about Obama. They're not sure who he is. They don't have doubts about George W. Bush. They know where they stand on him. And so, if he can tie McCain to him, that works than trying to simply fill in his own biography.
JIM LEHRER: And I thought this worked really well tonight. Thank you both very much.


text:
The Netherlands had over 2,500 EVSE (charging stations) installed by the end of 2011. Amsterdam has the highest density of EVSE in the world, with more than 600 stations installed per 780,000 inhabitants.
IA-HEV Task 18 has held workshops on creating EV cities of the future in Newcastle, London, Istanbul, Barcelona, and Los Angeles. Will your city be next?
The Task focus is on the life cycle assessment (LCA) of electric vehicles (EVs). The objective is to learn how electric drivetrain vehicles should be designed for optimal recyclability, minimal resource consumption, and proper recycling or disposal.
IA-HEV Task 20, Quick Charging Technology, brings experts to discuss business cases, communication, batteries, and interoperability. Join in the dialogue about making EVs work for both drivers and industry.
IA-HEV Task 21 addresses lithium-ion batteries performance over time. Accelerated ageing testing seeks to simulate the process of driving an EV within a much shorter time to understand its impact upon the battery.
IA-HEV Annual Report over 2015 now ready for download, Hybrid and Electric Vehicles: The Electric Drive Commutes.
Just published: M. Nikowitz (Ed.), Advanced Hybrid and Electric Vehicles, Springer 2016. Published as part of "Lecture Notes in Mobility", this contributed volume presents the results of Task 17 "System Integration" of the HEV TCP.
Final report on IEA HEV TCP Task 24 work on the Economic Impact of E-mobility is ready. Individual country reports of the Task participants Austria, Belgium, Denmark, France, Germany, the Netherlands, Switzerland and USA are also available.
Learn how to become involved...
IA-HEV welcomes countries and organizations that will both benefit from and contribute to the sharing of information and resources on hybrid and electric vehicles.
As more models of plug-in electric vehicles reach the commercial marketplace, the role of the private sector within IA-HEV is growing. Several Tasks (projects on special topics) include industry experts along with IA-HEV's traditional participation from governmental and research organizations.
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subset: commoncrawl


text:
Bubs 50th brings the house down
June 11, 2013
More than 200 Tufts Beelzebubs alumni or "Bub alums" came back to the Hill over Memorial Day Weekend, bringing with them countless family and friends to celebrate the group's 50th anniversary.
The weekend kicked off on Friday, May 23, with a dinner at Michael Horwitz's home in Chestnut Hill. Says Horwitz, A81, FG82, A16P, of welcoming so many old friends for reunion, "The opportunity to spend four days and nights with 200-plus Bub alums spanning five decades, along with their spouses, partners, and families was like nothing I've ever experienced. Drawing Bubs from around the world, the multi-generational experience solidified the strong relationship we have with the university."
On Friday, Bubs met up to rehearse for the concerts to come over the next couple of days, attended a workshop entitled "Bubs on Screen: An Inside Look at The Sing-Off, Glee, and Pitch Perfect," and toured the "50 Years of Fun Through Song" Bubs history exhibition at the Aidekman Art Gallery. Dinner at Dewick capped off the first of many exciting days.
Saturday included more rehearsals, as well as a family cookout and games, pizza dinner, and the much-anticipated Traditions Concert at the Chevalier Theater in Medford. Hundreds of Bubalums and their loved ones, as well as more than 230 Tufts and local community members, attended the free event to hear old favorites sung in groups divided by decade. Says Horowitz, "'Nothing Compares', solo by Greg Binstock, A03, brought the house down for sure."
Read the full concert recap from 88.9 WERS.
On Sunday, the campus was quiet and cold with blustery winds and the threat of rain—but the sung on, convening on the library roof for a history parade of the Hill. Little Jumbos marched with kazoos and flags touting the 50th anniversary logo, as the founders of the group took alumni around to Bub hot spots like West Hall, where the name Beelzebubs was first picked in 1963, and the anniversary plaque on the President's Lawn that literally shows how the Bubs have made their mark on the Tufts community.
Watch the Bubs sing to commemorate the plaque.
Of alumni visiting the marker, Horowitz says, "Hopefully you'll recall a Bub or two who brightened your day during your time at Tufts."
Bubalums also met earlier in the day at Goddard Chapel for a Remembrance Service, honoring fellow Bubs who have passed away. More workshops offered ample opportunity to share stories, ideas, and advice. The sessions included topics on life post-Bubs, the group's evolution in music and performance, as well as looking towards the next generations.
The weekend wouldn't have been complete without another concert, this time in Cohen, where the decade groupings were tossed aside so Bubs old and new could sing together in whichever styles they chose. Alumni closed out the reunion with a gala at the Marriott in Kendall Square.
"The Bubs would not be who they are without Tufts, and Tufts would not be Tufts without the Bubs," says Horowitz. "The Office of Alumni Relations was incredibly supportive of our efforts to provide a first class reunion experience for our constituents, and all came away with even stronger connections to each other and to Tufts."
Photos courtesy of Joseph Savitch.


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Items for It's Your Business can be submitted online at http://cjonline.com/business, by email to firstname.lastname@example.com or by mail to The Topeka Capital-Journal, 616 S.E. Jefferson, Topeka, 66607. Items and photographs will run in print as space permits.
Bob Washatka, of Topeka, has joined the The Great Game of Business team as a business coach, helping to implement the open-book management practices outlined in the book "The Great Game of Business." Washatka has more than 30 years of experience in sales, marketing and business ownership. He can be reached at (785) 256-0195 or www.greatgame.com.
Hollyn Smith has been hired by The Columbian Theatre Foundation as gift shop coordinator for the OZ Museum in Wamego. The Kansas State University graduate has taught classes at Catt's Dance Studio in Wamego and coached the Wamego High School Dazzlers. The OZ Museum recently updated its website at www.ozmuseum.com. Smith can be reached at (785) 458-8686 or email@example.com.
Mayor Larry Wolgast has announced the following appointments to two community boards in Topeka:
■ Alisa Snavely, to the Topeka Housing Authority, filling an unexpired term ending Dec. 31, 2016. Snavely is the tax director for Berberich, Trahan & Co.
■ Amy Cohen, to the Topeka Human Relations Commission, filling an unexpired term ending Dec. 31, 2015. Cohen is employed by the Disability Rights Center of Kansas and the YWCA Family Peace Initiative.
David J. Rebein, of Dodge City, has been selected to serve as 2014-15 treasurer and Eagles Chair for the Kansas Association for Justice. Rebein, a graduate of Washburn University and The University of Kansas School of Law, is a partner in the Rebein Bangerter Rebein law firm, which has offices in Dodge City and Tampa, Fla.
The Kansas Adjutant General's Department recognized the following employees for their years of service at the state July 16 at Nickell Armory in Topeka:
■ 30 years — Kerwin Nichols, Yolanda Rightmeier, Be Van Truong and Jane Welch.
■ 25 years — Janice Harper.
■ 20 years — Jean Copeland, Terri Ploger-McCool, Paul Rader, Dave Rapson, Bret Rowe and Danita Simnitt.
■ 15 years — Randy Bradford, Jason Bryant, John Burris, Thomas DeWitt, Scott Higgins, Stephen Larson and Emily Marsh.
■ 10 years — Roland Anderson, Stanton Beckett, Robert Bryant, Stephanie Burdett, Stephen Claspill, Dennis Colsden, Martin Currier, Cheri Froetschner, Henry Garcia, Rhonda Gotschall, Darrin Griffin, Ricky Hall, Scott Heston, Randy Knight, James Leftwich, George Matthias Jr., Darby Prine, William Rector, Karen Thompson, Steven West, Steven Will, Rodney Williams, Ivan Woltje, Joseph Wright, Keith Yoder and Michael Yoho.
■ 5 years — Valerie Arkell, Lyle Babcock Sr., Jeffrey Brummett, Julie Carey, Richard Dechant Jr., Charles Eichem, Scott Ekberg, Harry Heintzelmann, Jesse Hodgson, Scott Humphrey, John Hurst, John Lyons, Colin Mulloy, Sandra Norman, Daniel Scott, Jesse Smith, Jeffrey Terrell, Jonathan York and David Young.
Brig. Gen. Robert E. Windham Jr. assumed command of the Kansas Army National Guard during a ceremony July 12 at the Museum of the Kansas National Guard in Topeka. Windham, who serves as director of the Army Network Enterprise Center at Fort Riley, was promoted from colonel to brigadier general before the command change. He succeeds Brig. Gen. Eric Peck, who retired as assistant adjutant general and commander of the KNG.
Melissa Still, of Topeka, was one of 10 Kansas State University master's graduates in interior architecture and product design selected to compete at the International Woodworking Fair's annual Design Emphasis Student Furniture Design Competition next month in Atlanta. Still's project is a retro slipper chair.
The Jerry Brosius Team helped Prudential First, Realtors in Topeka earn two regional quarterly awards from Prudential Real Estate Network & Relocation Services by claiming first place for residential units for the first quarter in Kansas. Prudential First was awarded first place for residential units and second place for gross commission income for the first quarter in the Midwest region.
The Kansas Housing Resources Corp. is accepting applications for the Moderate Income Housing Program through noon Sept. 5. Awards will be
announced in October.
For more information, contact Fred Bentley at firstname.lastname@example.com or James R. Behan at jrbehan@kshousing


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Help us salute our soldiers
What defines a true hero?
According to Webster, a hero is simply defined as: one that shows great courage.
Well, the Jennings Daily News is honored to report that we come across our fair share of heroes each year when we compile material for our annual "Salute to Soldiers" section.
So many local men and women have remarkable stories of courage and commitment to share, and once again this year, we are asking people to share them with our readers.
Considering Jennings has always been a military town without a base, and Jeff Davis Parish is no stranger to service men and women, we know there are plenty of untold stories out there.
But by sharing these stories, many who read them gain a better understanding and appreciation of, not just war, but also the brave soldiers who serve and continue to serve their country.
The Jennings Daily News is currently searching for our heroes in hiding.
If you have a story to tell – or know of someone who's story needs to be told – contact us at 824-3011. It doesn't matter if they served in the Pacific, in Europe or in Africa – or if they are serving today – heroes are made the minute that oath is taken to serve and protect.
Area residents are also encouraged to send in photos of their loved ones who have served, plan to serve or are still serving in the United States military.
In addition to photos, family members and friends can also send "letters of thanks" to be printed in the upcoming special section.
Jeff Davis Parish residents, let our soldiers know how much we appreciate them by sharing your thoughts with us.
Pictures, brief bios, letters and/or cards of thanks can be mailed to the Jennings Daily News at 238 North Market Street or can be emailed to firstname.lastname@example.com.
Meanwhile, the Jennings Daily News would also like to use this section to honor our veterans of past wars. In Jeff Davis Parish, we are in no short supply of heroes, especially with the Southwest Louisiana War Veterans Home located just around the corner.
Families of veterans are also encouraged to take part in this tribute by sending in pictures and info about their loved ones, as well.
Again, residents are encouraged to either mail or email their info as soon as possible.
In closing, the Jennings Daily News salutes the men and women who fight to ensure our freedom – yesterday, today and tomorrow.
In all honesty, none of us can thank them enough.
Short URL: https://www.jenningsdailynews.net/?p=25753


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I am here officially raising Avatar to up to 1/4th (25%) your point value.
Additionally, I am going to allow Allies (but not Ally Groups) worth up to 25% of your point value.
This contradicts the PDF, which I'll get to updating as soon as I figure out how...
Also, the SM range limit applies to Allies as well, but it is being increased to -4 to +4.
You were once a small spark of consciousness, a spirit, if you will, perhaps tied to a place, or a tree, or even a rock. Or perhaps you roamed free. Whatever the case, your memory of this time is hazy. You weren't quite intelligent yet, not back then. You desired little, but one driving desire you had was hard for your simple psyche to express yet all the same, you desired worship.
Sometime, you gained self-awareness. This occurred when someone started believing in you. Your mind went through an instant evolution, and you suddenly realized that you wanted worship. Using your new abilities granted through being believed in, you used your still limited power to reinforce this belief. Largely, people start believing in spirits through times of great and desperate need, so perhaps you satisfied this need. Or perhaps someone was thanking the spirit of a place for a fortunate occurrence, so you gave them a sign that you were there and acknowledged their thanks. At this point, you became a god.
What you do after this, is up to you. No matter what the decision is, though, know this the moment you became a god, you began craving worship. You thrive on it the more worship you have, the more powerful you become. Prayer replenishes your divine energies, and belief in you lets you grow more powerful. How you gain this worship is where you may differ from other gods. Do you help your followers by spreading a message of peace, or are you a ruthless tyrant, ruling through fear?
The world is split into two major continents, Terra Antiquus and Terra Novus. Terra Novus is a wild place, untamed with people who may or may not be civilized. Terra Antiquus has many powerful kingdoms. In order of military power:
The kingdom of Stay The Heck Out, ruled by xenophobic dwarves and mad-scientist gnomes.
The republic of Midplains, consisting of brave men, mercantile dwarves and creative elves.
The kingdom of Sylva, the forest nation of the elitist elves.
The principality of Gruggmire, a loose coalition of ogre and orc tribes.
The kingdom of Grenold, filled with happy halflings.
They have their own gods, though Midplains and Grenold are at least somewhat open to new religions. There are also many smaller kingdoms filled with a mixture of peoples and smaller, pagan gods.
The most popular god is Iosephus, the great god of good. He is worshiped throughout the Midplains, Sylva and Grenold, with minor cults in the other major kingdoms and minor kingdoms.
Another popular god is Meh, the god of apathy and neutrality. He tries not to get involved much, though, and doesn't mind if his followers pay tribute to other gods, as well.
Another somewhat popular god is Stynn, a god who refused to put any vowels in his name. He is, while not exactly evil, not very nice, either. He is worshipped in Gruggmire, with minor cults in the other kingdoms.
Geographically speaking, there is a large woodland to the west on the continent of Terra Antiquus, with large grasslands in the middle. South of the grasslands there is a rocky and sandy desert region. South of that are large mountains. In the very north there are also mountains. The kingdom Stay the Heck Out spans over the northern mountains and encroaches a bit into the woodlands and the plains. Midplains takes up most of the plains, except for a small bit to the east where Grenold lies. Sylva consists of all the woodlands that aren't in Stay the Heck out. Gruggmire's region is that of swamps in the south of the grasslands, and the desert to the south of that.


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|2 reviews in total
When a series of auto mishaps cause several traffic jams, John Beck must
save the day or run the risk of his wife, Shelly Fabares, and the kids
running off on vacation without him.
The accidents alone were amusing. Abe Vigoda as a crash helmet-wearing driver instructor to student Nedra Volz ("There's a hole. Should I go in there?"); Wink Martindale as a frustrated golfer who takes his revenge out on the interstate when two truckers drive by and ruin his game (Martindale's calm demeanor as he sends those golf balls out into the traffic was hilarious.) and finally the truckers themselves wreck, one carrying vodka and the other oranges. Guess what they ended up doing?
The stories involve Desi Arnaz trying to get to his pregnant wife (Christopher Norris) who is being driven to the hospital by a cab driver named Snake (Vic Tayback); Ed MacMahon and Rue McLanahan as a wealthy, unhappy couple (odd casting, but they all but stole the show); the unhappy band with LIsa Hartman as a lead singer and ubiquitous acting staple Larry Hankin as the guitarist, and Fabares and Beck's unhappy marriage.
All end up stuck in the traffic mishaps, with Beck trying to find Fabares with the kids in the camper, Arnaz borrowing the band's car phone to call the cab company to find Norris, and McLanahan trading her fur for a better spot in line to use the port-a-potty. Hands down, the McLanahan-McMahon resolution, while nice and neat, is terribly cute, especially with ol' Ed on that motorbike at the end.
With guest appearances galore, from Lyle Waggoner as the incompetent traffic controller to Marcia Wallace all but reprising her 'Bob Newhart' role as the traffic division secretary, this movie watches like a less cliched episode of Love Boat without the problem-solving crew, except for Beck, that is.
And yes, the band performance at the end was the perfect conclusion to this light-hearted bit of fun.
This is definitely a guilty-pleasure movie. Such a stellar cast! I mean, Ed McMahon!! The rock band that gets stuck in the traffic jam and ends up playing to the crowd out of the back of their truck--IT'S CLASSIC!
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Just read on several sites how the latest model for Verison will Dual boot into Windows 8.1 and Android.
Is there a way to add this to the existing / original Android M8
Where did you read that?
Theres no way they would release a verison with 2 operating systems especially when android has been widly available for the device. Theres currently no version of a bootloader that has the right environment for windows adding an android boot to there bootloader "to try and even get back to android" Unfortunetly android is open sourse and windows is not, they would have to release there sourcecode to the developing world if they wanted to dual boot with android and they wont. so its up to us to exctract it on our end to make android 's boot loader able to dual boot into windows and hopefully find a way to get back.
For some users the most exciting prospect of the HTC One (M8) for Windows may come from the fact that it shares the same hardware as the One (M8). It's possible that the developer community will be able to load the firmware from the HTC One (M8) onto the device in a dual boot configuration with Windows Phone 8 so users can switch between the operating systems as they please.
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no subjectDate: 2012-04-19 04:14 pm (UTC)
From: kenn_el
You're probably totally correct! I was still wary of anything in the mini back when Levitz was being cute about the whole Earth 1/Earth 2 question, though, and the contents of the crates could have been going to Metropolis, and it wouldn't have meant that Helena operated in Metropolis. The 'Batman' comment just makes no sense coming from Batman's daughter, and seemed to indicate at the time that the character was pre-Flashpoint Helena. If anyone knows how Batman does it, it's his daughter/partner, and I can't imagine that the Earth 1 Bats is THAT much more impressive than his Earth 2 counterpart.
no subjectDate: 2012-04-19 04:55 pm (UTC)
From: kenn_el
Just considering the fact that Earth 2 Bruce is both Helena's father AND Batman to her Robin, it's highly unlikely that she'd be that impressed with Earth 1 Bruce, as she seems to be in the example you cited. That's more the pre-Flashpoint Helena's style.


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Discussion in 'Android Devices' started by rab393, Aug 14, 2013.
My phone is in safe mode and have re-booted with up volume button but still in safe mode. Help
U tried a battery pull then boot?
Moved to the GS3 Forum
Dunno if this is still applicable, but way back when, devices would boot-up in safe mode accidentally due to stuck keys/buttons (i.e., dirt / dust getting between the key/buttons and the edge of the case, etc.).
Hope that might help!
Yeah. On the s3 though, you get into safe mode by tapping repeatedly the menu capacitive button while it boots so i doubt it would apply this time mate
Thanks everyone. Bought my S3 at Costco. Finally took it back there. They took out battery and sim card, rebooted and it came up.


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Gut bacteria trigger colitis in animal models and are suspected to aggravate inflammatory bowel diseases. We have recently reported that Escherichia coli accumulates in murine ileitis and exacerbates small intestinal inflammation via Toll-like receptor (TLR) signaling.
Methodology and Principal Findings
Because knowledge on shifts in the intestinal microflora during colitis is limited, we performed a global survey of the colon flora of C57BL/10 wild-type (wt), TLR2-/-, TLR4-/-, and TLR2/4-/- mice treated for seven days with 3.5% dextrane-sulfate-sodium (DSS). As compared to wt animals, TLR2-/-, TLR4-/-, and TLR2/4-/- mice displayed reduced macroscopic signs of acute colitis and the amelioration of inflammation was associated with reduced IFN-gamma levels in mesenteric lymph nodes, lower amounts of neutrophils, and less FOXP3-positive T-cells in the colon in situ. During acute colitis E. coli increased in wt and TLR-deficient mice (P<0.05), but the final numbers reached were significantly lower in TLR2-/-, TLR4-/- and TLR2/4-/- animals, as compared to wt controls (P<0.01). Concentrations of Bacteroides/ Prevotella spp., and enterococci did not increase during colitis, but their numbers were significantly reduced in the colon of DSS-treated TLR2/4-/- animals (P<0.01). Numbers of lactobacilli and clostridia remained unaffected by colitis, irrespective of the TLR-genotype of mice. Culture-independent molecular analyses confirmed the microflora shifts towards enterobacteria during colitis and showed that the gut flora composition was similar in both, healthy wt and TLR-deficient animals.
Conclusions and Significance
DSS-induced colitis is characterized by a shift in the intestinal microflora towards pro-inflammatory Gram-negative bacteria. Bacterial products exacerbate acute inflammation via TLR2- and TLR4-signaling and direct the recruitment of neutrophils and regulatory T-cells to intestinal sites. E. coli may serve as a biomarker for colitis severity and DSS-induced barrier damage seems to be a valuable model to further identify bacterial factors involved in maintaining intestinal homeostasis and to test therapeutic interventions based upon anti-TLR strategies.
Citation: Heimesaat MM, Fischer A, Siegmund B, Kupz A, Niebergall J, Fuchs D, et al. (2007) Shift Towards Pro-inflammatory Intestinal Bacteria Aggravates Acute Murine Colitis via Toll-like Receptors 2 and 4. PLoS ONE 2(7): e662. https://doi.org/10.1371/journal.pone.0000662
Academic Editor: Alejandro Aballay, Duke University Medical Center, United States of America
Received: May 20, 2007; Accepted: June 22, 2007; Published: July 25, 2007
Copyright: © 2007 Heimesaat et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by grants from the Deutsche Forschungsgemeinschaft to U.B.G., O.L., R.R.S., C.L. (KFO104/ project 6; SFB633/ projects A7, B6, Z1), to B.S. (Emmy-Noether-Programm of the DFG, 749/3-4, 749/5-1) and to M.F. (DFG-SPP1110/ project Fr448/4-3). A.F. is supported by a grant from the Sonnenfeld Foundation Berlin, Germany.
Competing interests: The authors have declared that no competing interests exist.
In inflammatory bowel diseases (IBD) the disturbance of intestinal barrier functions results in increased immunoreactivity against bacterial antigens [1]–[3]. Patients with active intestinal inflammation display accumulation of commensal Escherichia coli or Bacteroides spp. at inflamed tissue sites [4]–[6]. These bacterial groups, also suspected to trigger intestinal inflammation in acute graft-versus-host-disease after bone marrow transplantation [7], can further potentiate immunopathology by translocation via microlesions and ulcerations [5], [8]. The role of the commensal intestinal microflora in colitis has been studied in a number of experimental models [9], [10], but detailed knowledge on the gut microbiota composition in acute intestinal inflammation is still limited. Recently, we have demonstrated that acute murine ileitis is accompanied by a rigorous E. coli overgrowth in the terminal ileum. During acute inflammation, E. coli numbers increased by up to nine orders of magnitude and their presence was found to be essential for the induction and progression of ileal immunopathology [8]. High numbers of E. coli in the inflamed ileum point towards an important role of bacterial lipopolysaccharide (LPS) in the exacerbation of acute intestinal inflammation. LPS and products from Gram-positive bacteria are recognized by toll-like-receptors (TLRs) 4 and 2, respectively, both of which are expressed in the murine intestinal mucosa [11]. Similar observations have been made in human IBD where TLRs are upregulated at inflamed tissue sites [12], [13]. In line with this, we found that LPS-mediated TLR4 signaling is responsible for a major part of the immunostimulatory potential of E. coli in acute ileitis, whereas TLR2, the main receptor for Gram-positive bacteria, was not involved [14].
Acute colitis induced by the barrier-damaging agent dextran-sulfate-sodium (DSS) is exacerbated by gut bacteria, as evidenced by the amelioration of inflammation in germ-free animals and in mice treated with antibiotics [15]. Early studies on roles of bacterial LPS in triggering acute intestinal inflammation revealed that LPS-hyporesponsive C57BL and C3H mice displayed reduced macroscopic signs of colitis as compared to controls and were protected from inflammatory responses initiated by elevated serum LPS levels during inflammation [16]. Another study reported that DSS-induced colitis activity varies with the mouse strain used, but claims that the severity of colitis does not differ in LPS-unresponsive as compared to control mice, irrespective of their genetic background [17]. Furthermore, TLR-mediated sensing of gut bacteria has been suggested to play a role in intestinal homeostasis and TLR4 was shown to limit bacterial translocation during colitis [18]–[21]. In contrast, recent findings demonstrated that TLR-signaling via the adapter protein MyD88 is essential for spontaneous development of colitis in IL10-deficient mice [22]. However, global gut flora analysis in DSS-induced barrier-damage, which could account for some of the contradictory results mentioned above, has not been performed and bacterial species most abundant in acute colitis have not been investigated so far. To further extend our knowledge on potential roles of a bacterial interplay with innate immunity in acute colitis, we performed a global survey of the intestinal microflora and determined numbers of inflammatory cells in DSS-treated C57BL/10 mice lacking TLRs 2 and/or 4. Because major groups of gut bacteria cannot be cultivated, we complemented classical microbiological analyses with culture-independent molecular approaches such as denaturing-gradient-gel-electrophoresis (DGGE) based on separation of PCR-amplified bacterial 16S rRNA gene fragments [8], [14]. Besides identification of gut residents specifically associated with the severity of DSS-induced colitis, we also studied the impact of TLRs 2 and 4 on i) macroscopic signs of acute colitis, ii) changes in relevant immune cell populations in the inflamed colon, and iii) the composition and dynamics of the intestinal microflora in healthy and diseased TLR-deficient animals.
Severity of acute intestinal inflammation depends on TLR2- and TLR4-signaling
We have recently demonstrated that commensal E. coli increase and exacerbate small intestinal inflammation in C57BL/10 mice via LPS-mediated TLR4-signaling [8], [14]. To determine whether TLR2 or TLR4 may be involved in the aggravation of acute colitis, we compared macroscopic signs of disease in C57BL/10 wild-type (wt) mice and animals lacking TLR2, TLR4, or both (Figure 1). After seven days of DSS-treatment, wt mice developed severe signs of colitis as indicated by a total clinical score of 11.3±1 (Figure 1A). In contrast, TLR2-/-, TLR4-/-, and TLR2/4-/- animals displayed significantly (P<0.001) lower clinical scores of 7.1±1.6, 7.0±3, and 4.2±2.3, respectively, as compared to wt animals, thus indicating that colitis is exacerbated via TLR2- and TLR4-signaling (Figure 1A). Furthermore, reduced macroscopic signs of colitis in TLR2-/-, TLR4-/-, and TLR2/4-/- were associated with diminished inflammatory activity as demonstrated by lower IFN-gamma concentrations (Figure 1B) in colonic mesenteric lymph nodes.
(A) Severity of colitis in DSS-treated animals. Clinical outcome of colitis was recorded in wt mice (WT, n = 10) and in mice lacking TLR2 (TLR2-/-, n = 10), TLR4 (TLR4-/-, n = 12), or both (TLR2/4-/-, n = 11). Clinical parameters of colitis were monitored daily (see methods). The data sets from two independent experiments were pooled. Total colitis scores were analyzed at day eight after DSS-treatment for seven days.
(B) IFN-gamma concentrations in supernatants of colonic MLN cultures from wt and TLR-deficient animals. Supernatants from MLN cultures of wt mice (WT, black bars, n = 3), and animals lacking TLR2 (TLR2-/-, n = 4), TLR4 (TLR4-/-, n = 5), or both (TLR2/4-/-, n = 4) with colitis were analyzed at day eight after DSS-treatment for seven days.
(A/B) Mean values, standard deviations and significance levels (as compared to the wt animals) determined by Student's t-test are indicated (***, P<0.001).
TLR2- and TLR4-dependent accumulation of effector immune cells in the inflamed colon
The acute stage of DSS-colitis is characterized by recruitment of neutrophils and T-cells to damaged tissue areas [23]. In addition, there is strong evidence that regulatory T-cells accumulate at inflamed tissue sites in DSS-treated mice and in IBD patients [23], [24]. However, their numbers in diseased animals have not been investigated so far. Therefore, we quantified CD3+ total T-cells, FOXP3+ regulatory T-cells, and myeloperoxidase+ neutrophils by immunohistochemistry of colon sections in situ. The results demonstrated that numbers of CD3+ T-cells were slightly increased in the colons of DSS-treated wt and TLR2-deficient, but not TLR4- and TLR2/4-deficient mice, as compared to the respective naive animals (Figure 2). Most strikingly, the numbers of neutrophils and FOXP3+ regulatory T-cells in the inflamed colon were significantly lower in the colons of TLR2-/-, TLR4-/-, and TLR2/4-/- mice as compared to DSS-treated wt animals (Figure 2). Independent histochemical analyses of HE-stained tissue sections and histological scoring by two pathologists (C.L. and H.A.L.) showed that DSS-induced tissue damage and histopathological changes in the colon were similar in wt, TLR2-/-, and TLR4-/- mice, but significantly reduced in TLR2/4-/- mice, as compared to the wt animals (not shown).
Numbers of T-cells, regulatory T-cells, and neutrophils in the colon of DSS-treated wt mice and mice lacking TLR2 and/ or TLR4. The average number of cells positive for CD3, FOXP3, or myeloperoxidase from at least five high power fields (HPF, 400×magnification) per animal were determined microscopically in immunostained colon sections of wt mice (WT), and animals lacking TLR2 (TLR2-/-), TLR4-/- (TLR4-/-), or both (TLR2/4-/-) at day eight after DSS-treatment for seven days (C, grey circles). Healthy animals served as controls (H, white circles). The numbers of analyzed animals are given in parenthesis. Mean values (black bars), and significance levels (as compared to wt animals with colitis) determined by Student's t-test are indicated (*, P<0.05; **, P<0.01; ***, P<0.001).
Development of a complex gut flora in TLR2-/- and TLR4-/- mice
To determine whether sensing of gut bacteria via TLR4 or TLR2 has a general impact on the composition of the intestinal microflora (which could influence the outcome of colitis), we performed a global molecular survey of the colon microbiota in healthy C57BL/10 mice lacking TLR2, TLR4, or both receptors (Figure 3). Therefore, offspring mice were sacrificed, and the bacterial communities within the colon characterized by analysis of cloned bacterial 16S rRNA genes in DNA libraries (Figure 3A), as well as by high-resolution DGGE (Figure 3B). Comparative analysis of 16S rRNA gene libraries revealed that the overall diversity and composition of the gut microflora did not differ significantly among healthy TLR2-/-, TLR4-/-, and TLR2/4-/- mice, as compared to wt animals (Figure 3A). The number and position of bands in DGGE profiles showed that the molecular pattern of the colon flora of TLR2-/-, TLR4-/-, and TLR2/4-/- mice were similar to the reference pattern of wt animals, showing 100%, 92%, and 92% concordance, respectively. Two DGGE bands that were less intense in mice lacking TLR4 (Figure 3B, grey arrows) when compared to wt or TLR2-/- animals contained DNA from so far uncultured bacteria of the Bacteroidales group (Figure 3B). The fact that i) bacteria represented by the upper band completely absent in TLR4-/- mice were present in the luminal colon contents from TLR4-/- animals that grew up in another facility (Figure 3B, black arrow), and ii) that the lower band was detected in one of the TLR4-/- animals (Figure 3B) provided strong evidence that these differences are most likely caused by interindividual variability.
Detailed molecular investigations of the colon microbiota in three months old C57BL/10 mice lacking TLR2, TLR4, or both were performed by analysis of 16S rRNA gene libraries (A) or high-resolution DGGE (B) with primers HDA-1-GC and HDA-2 (see methods).
(A) Results from gene library analysis. Complete 16S rRNA genes were amplified from total luminal colon content DNA isolated from wt mice (WT, n = 3), and from mice (n = 3 each group) lacking TLR2 (TLR2-/-), TLR4 (TLR4-/-), or both (TLR2/4-/-). The amplicons were cloned and sequenced as described in the Methods section. Bars represent percentage amounts of gut bacterial groups indicated on the Y-axis.
(B) Results from DGGE analysis of PCR-amplified total bacterial 16S rRNA gene fragments. Each lane shows DGGE profiles of the bacterial flora from the colon of healthy wt mice, and animals lacking TLR2 (TLR2-/-), TLR4 (TLR4-/-), or both (TLR2/4-/-). Mice of identical age (three months) originated from two different animal facilities (as indicated above the lanes). DNA bands, which were absent or weak in DGGE profiles from TLR4-/- and TLR2/4-/- animals are marked by grey arrows. Bacterial species identified by sequence analysis of 16S rRNA gene fragments in the corresponding bands are indicated on the left. Total numbers of DGGE bands in the profile from wt animals were counted and set to 100% in the reference pattern (RP). Presence and absence of bands in profiles from the respective TLR-deficient animals was recorded and similarity values were calculated and expressed as % similarity to the wt RP. The DGGE profiles are representative for at least three mice per group and experiment. Results were reproduced in two independent experiments.
Characterization of gut flora changes in acute colitis
In order to characterize potential gut flora shifts during DSS-induced barrier damage and to identify gut residents abundant in colitis, we performed a global survey of the gut flora in C57BL/10 mice with or without colitis (Figures 4A and 5). Molecular monitoring of the intestinal bacterial communities by DGGE (Figure 4A) demonstrated that the acute stage of colitis was characterized by a shift towards members of the Enterobacteriaceae (Figure 4A). In addition, bacterial communities in the colon from diseased mice were less complex, indicating a loss in bacterial diversity during acute inflammation (Figure 4A). Sequence analysis of bacterial 16S rRNA gene fragments from individual DGGE bands revealed that previously undescribed members of the Bacteroidales group, Bryantella spp., Tannerella spp., clostridia, and lactobacilli disappeared and were not detected in the inflamed colon (Figure 4A). In contrast, a DGGE band containing 16S rRNA genes from bacteria of the Clostridiales group was more prominent in samples from the inflamed colon, providing evidence that these bacteria might accumulate during colitis.
(A) DGGE profiles of the colon flora in healthy and diseased wt mice. Results are shown for C57BL/10 wt mice without DSS-treatment or at day eight after DSS-treatment for seven days (as indicated above the lanes). Bacterial species were identified by comparative sequence analyses of 16S rRNA gene fragments amplified from DNA eluted from respective DNA bands. The DGGE profiles are representative for at least three mice per group and experiment.
(B) DGGE profiles of the colon flora in healthy and diseased TLR2/4-/- mice. DGGE profiles of luminal intestinal bacteria from wt and TLR2/4-/- mice were generated by PCR-based analysis of total DNA from colon contents of mice with or without colitis at day eight after DSS-treatment for seven days (as indicated). Bacterial species were identified by comparative sequence analysis of 16S rRNA gene fragments amplified from DNA eluted from respective DNA bands. The DGGE profiles are representative for at least three mice per group and experiment.
(A/B) Primers GC968F and R1378 (Heimesaat et al., 2006) were used for amplification. Results were reproduced in at least two independent experiments.
Bacterial counts of (A) Gram-negative (E. coli, Bacteroides/ Prevotella spp.) and (B) Gram-positive bacteria (Enterococcus spp., clostridia and lactobacilli) in luminal colon contents from healthy animals (H) and from mice with colitis at day eight after DSS-treatment for seven days (C) as determined by culture. Bacterial species were identified by biochemical analysis and reconfirmed by comparative sequence analyses of 16S rRNA genes. Results are shown for wt mice (WT, above) and for mice lacking TLR2 (TLR2-/-), TLR4 (TLR4-/-), or both (TLR2/4-/-) as indicated on the x-axis. Animal numbers analyzed are given in parentheses. The data sets were pooled from two independent experiments. The boxes represent 75th % and 25th % percentiles of medians (indicated by black bars within the boxes. Maximum and minimum values are indicated by lines above and below boxes, respectively. Significance levels were determined by Mann-Whitney-U-Test. Underlined P values shown in black were calculated from comparisons of healthy versus diseased animals. P values shown in grey were calculated from the bacterial number in diseased animals (all versus WT).
A global culture analysis of the gut flora in the inflamed colon of DSS-treated wt mice revealed that concentrations of commensal E. coli increased significantly (P<0.001) by four orders of magnitude, respectively (Figure 5A). Populations of Bacteroides/ Prevotella spp., enterococci, clostridia and lactobacilli were not significantly altered in the inflamed colon (Figures 5A and 5B). Thus, cultural analyses confirmed that the development of colitis is accompanied by shifts in the luminal E. coli population.
Identification of gut flora changes associated with the severity of acute intestinal inflammation
The fact that macroscopic signs and inflammatory parameters of acute intestinal inflammation were reduced in TLR2-/-, TLR4-/-, and TLR2/4-/- mice prompted us to identify distinct gut bacterial populations associated with colitis severity (Figure 4B and Figure 5). A molecular analysis of the colon microflora composition in DSS-treated TLR2/4-/- animals by DGGE revealed that the intensities of DNA-bands of Enterobacteriaceae were weaker when compared to wt animals (compare Figures 4A and B). Furthermore, TLR2/4-/- mice did not display an increased intensity of the DNA band containing a 16S rRNA gene fragment from so far undescribed clostridia (Figure 4B) observed in DSS-treated wt animals (Figure 4A). Most strikingly, a detailed culture-based comparative analysis of the intestinal flora demonstrated that E. coli concentrations increased to a lesser degree in DSS-treated TLR2- and TLR4-deficient animals as compared to wt mice (P<0.01), indicating that increased colitis severity is associated with higher E. coli loads (Figure 5A). In TLR2/4-/- mice, the increase in the E. coli numbers was also strongly alleviated, if compared to wt mice (P<0.001), and these mice displayed only an approximately 10-fold rise in E. coli after colitis induction (Figure 5A). Moreover, DSS-treated TLR2/4-/- mice contained significantly lower luminal loads of Bacteroides/Prevotella spp. and enterococci as compared to wt mice (P<0.01), whereas all other flora changes in the respective TLR-deficient mice did not significantly differ from those observed in wt controls (Figure 5). Biochemical analyses revealed that the Bacteroides population consisted of B. ovatus, B. merdae, B. uniformis, B. vulgatus, and B. thetaiotaomicron. Prevotella spp. were represented by P. oralis and P. buccae. Enterococcus spp. included E. faecalis, E. faecium, and E. gallinarum.
The first global and comprehensive analysis of the colon microflora in the DSS-induced colitis model revealed that acute barrier-damage in the colon is accompanied by accumulation of commensal E. coli. Because intestinal overgrowth occurs in different intestinal injuries [25], these flora shifts are most possibly caused by a breakdown of the mucosal physiology. Together with the finding that the lack of TLRs 2 and/or 4 per se had no impact on the composition of the intestinal microflora in healthy mice (Figure 3), the lower abundance of E. coli in TLR-deficient mice with less macroscopic disease symptoms indicates that E. coli can serve as a sensitive biomarker for colitis severity. This is in line with the earlier finding that commensal E. coli accumulated drastically during ileitis in our C57BL/10 mice and displayed a strong pro-inflammatory potential to trigger small intestinal inflammation via TLR4 [8], [14]. Similarly, abundant numbers of E. coli were associated with inflammation in the colon of IL2-/- mice [26]. Contributions of E. coli and other gut bacteria to the aggravation of colitis were shown earlier in mono-associated germ-free IL10-/- and IL2-/- mice [27]-[29] and by the curative effects of antimicrobial therapy [15], [30], [31]. Nevertheless, mechanisms by which accumulating E. coli may modulate DSS-induced acute colitis are still not known in detail. The reduced macroscopic signs of colitis displayed by the DSS-treated TLR2-/-, TLR4-/-, and TLR2/4-/- mice point towards important roles of LPS and TLR2 ligands (such as lipopeptides) in acute inflammatory processes in the colon. In the C57BL/10 mice analyzed here, both ligands seem to potentiate inflammation by TLR-mediated recruitment of neutrophils to inflamed tissue sites. The fact that FOXP3-positive cells were significantly decreased in DSS-treated TLR2-/-, TLR4-/-, and TLR2/4-/- mice suggests that TLR ligands foster the recruitment and/or proliferation of regulatory T-cells, which can serve as markers for acute intestinal inflammation in this animal model. This is consistent with similar observations in IBD, where inflamed tissue areas contained higher numbers of FOXP3-positive T-cells [24]. Taken together and in line with recent findings [18]-[21], our results underline the important role of gut bacterial sensing by TLRs in maintaining the intricate balance between mucosal immunity and intestinal inflammation.
The results obtained here add important information in as much as bacterial TLR2 ligands may contribute to colitis pathology. In this context it is interesting to note that so far non-cultured Gram-positive bacteria of the Clostridium group increased during colitis (as shown by DGGE). Furthermore, the inflamed colon of DSS-treated TLR2/4-/- animals displaying reduced disease symptoms contained significantly lower concentrations of Bacteroides/Prevotella spp. and enterococci, as compared to wt-controls. However, since DGGE is not a quantitative technique and because the enterococcus concentrations showed only a tendency to increase during colitis, the potential impact of these observations remains speculative.
In conclusion, DSS-induced colitis is accompanied by a population shift towards E. coli, which have the potential to trigger TLR-dependent accumulation of neutrophils and T-cells. This microflora shift towards pro-inflammatory bacteria may help to explain why blockage of TLR-signaling was successfully used to suppress acute intestinal inflammation [32]. Thus, DSS-induced barrier damage seems to be a valuable model to further identify bacterial factors involved in maintaining intestinal homeostasis and to test therapeutic interventions based upon anti-TLR strategies.
Materials and Methods
Mice, colitis induction and determination of clinical scores
C57BL/10ScSn wt, TLR2-/-, TLR4-/-, and TLR2-/-/TLR4-/- mice were bred as described [8], [14]. Experiments were conducted according to the German animal protection laws. For colitis induction, mice were treated with 3.5% (wt/vol) DSS (40.000 kDa, MP Biomedicals, Illkirch, France) in drinking water ad libitum for seven days. Prior to sacrifice, mice received water without DSS for 24 hours. The intake of the DSS-solution was controlled and mice were weighed daily. Total clinical scores with a maximum of 12 were assessed daily by combined data of weightloss, occurance of blood in stool (Haemoccult™, Beckman Coulter / PCD, Krefeld, Germany), and stool consistence, as described [33].
Sampling procedures and histologic scoring
Mice were sacrificed with Halothan™ (Eurim-Pharm, Mülheim, Germany) on day eight after induction of colitis. Colon samples were removed under sterile conditions. Histopathology was investigated in paraffin-embedded HE-stained tissue sections. A published standardized histologic score [33] ranging from 0 to 6 was used for blinded evaluation of the inflammatory processes in the colon.
For immunostaining, 4 µm sections of formalin-fixed, paraffin-embedded tissue were cut, deparaffinized, and subjected to a heat-induced epitope retrieval step. Slides were rinsed in cool running water, washed in Tris-buffered saline (pH 7.4) before incubation with primary antibodies against CD3 (N1580, Dako, Glostrup, Denmark, dilution 1:10), myeloperoxidase (MPO7, A0398, Dako, 1:10000), and Foxp3 (FJK-16s, eBioscience, 1:100) for 30 min. For detection, biotinylated donkey anti-rat (Dianova, Hamburg, Germany) or rabbit anti-rat (Dako) secondary antibodies were used followed by application of the streptavidinAP kit (K5005, Dako) or the EnVision peroxidase kit (K 4010, Dako). Alkaline phosphatase was revealed by Fast Red as chromogen and Peroxidase was developed with a highly sensitive diaminobenzidine (DAB) chromogenic substrate for approximately 10 minutes. Negative controls were performed by omitting the primary antibody. For each animal, the average number of positive stained cells within at least five independent high power fields (HPF, 400×magnification) were determined microscopically and subjected to statistical analysis as indicated.
Analysis of the colon microflora
Molecular detection, biochemical identification, and cultural analyses of intestinal bacterial communities were performed as described [8], [14], [34]. Briefly, luminal feces samples were removed for molecular analyses from the distal colon, resuspended in PBS, and centrifuged (16,000×g/10 min/4°C). Total DNA, isolated by phenol extraction as described [8], served as template for PCR amplification of bacterial 16S rRNA genes with consensus primers TPU1 (5′-AGAGTTTGATCMTGGC TCAG-3′, nt 8-27 in the E. coli 16S rRNA gene) / RTU8 (5′-AAGGAGGTGATCCANCCRCA-3′, nt 1541-1522 in the E. coli 16S rRNA gene). Gene libraries of the amplicons were constructed and analyzed as described [34]. For high-resolution DGGE, which yielded the highest numbers of individual bands from a given sample, the variable region V3 in bacterial 16S rRNA genes was amplified from total gut content DNA with GC clamp (underlined) primer HDA-1-GC (5′-GCCCGGGGCGCGCCCCGGGCGGGGCGGGGGC ACGGGGGGACTCCTACGGGAGGCAGCAGT-3′, nt 339-360 in the E. coli 16S rRNA gene) and primer HDA-2 (5′- GTATTACCGCGGCTGCTGGCAC-3′, nt 539-518 in the E. coli 16S rRNA gene).
Determination of IFN-gamma concentrations
MLNs were removed and incubated in 24-flat-bottom well culture plates (Nunc, Wiesbaden, Germany) containing 500 µl serum-free RPMI medium supplemented with penicillin/ streptomycin for 18 h at 37°C. IFN-gamma concentrations in supernatants were determined by ELISA as described [8], [14].
The authors thank Michaela Wattrodt, Jutta Imlau, Fränzi Creutzburg, Diana Woellner, Simone Spieckermann, Francoise Burri, and Gernot Reifenberger for excellent technical assistance. We also thank Dr. Jutta Wagner and Dr. Matthias Heimesaat for critical discussions.
Author Contributions
Conceived and designed the experiments: MF RS MH MB OL SB BS UG. Performed the experiments: MH SB AF AK JN DF HJ. Analyzed the data: RS MH OL HL SB AF BS AK JN DF HJ CL AB UG. Contributed reagents/materials/analysis tools: MF MH HL AF BS AK CL AB. Wrote the paper: RS MH MB OL SB AF BS CL UG.
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text:
Walter Hill turns Akira Kurosawa's samurai classic Yojimbo into a gangster Western with Bruce Willis as a hired gun who plays off rival bootlegging mobs against one another in a Texas bordertown. It's all good, unclean, gang war fun... until the drifter's double-dealing catches up with him. Chilling henchman Christopher Walken and sneaky sheriff Bruce Dern fit perfectly into Hill's no-nonsense mix of bullets and bravado. Look out too for comedy queen Leslie Mann in an early straight role.
Walter Hill
Bruce Willis
David Patrick Kelly
William Sanderson
Christopher Walken
Bruce Dern
Alexandra Powers
With one of the slimmest storylines ever put on screen, this Prohibition-era, blow-them-away gangster saga provides a rare old shoot-fest.
Throaty Bruce Willis takes on whispering Christopher Walken in the story of a hired gun who drives into a small Texas town to find most of the locals have fled, leaving two trigger-happy gangs to fight a private war over bootleg liquor.
Willis takes first one side, then the other, until he's beaten to a pulp for his double-dealing pains. There's lots of body-blasting action and it's all smartly done, though more akin to the spirit of the spaghetti Western than the Japanese samurai film on which it's actually based.
The dialogue's difficult to hear, but the gun battles speak for themselves and the early 1930s costumes, especially bathed in brown filters, look exactly right.
Nice supporting performance by Bruce Dern, whose character is less predictable than you might expect.


text:
Muslim pilgrims cast stones at a pillar, symbolizing the stoning of Satan, in a ritual called "Jamarat," the last rite of the annual hajj, in Mina near the Saudi holy city of Mecca, Saudi Arabia, Nov. 6, 2011, according to the Associated Press. The annual Islamic pilgrimage draws 2.5 million visitors each year, making it the largest yearly gathering of people in the world.
Here are other photos of Muslim pilgrims traveling to Mecca.


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History will record that on Tuesday, Dec. 3, 2013, the U.S. House of Representatives Committee on the Judiciary met to consider the impeachment of Barack Hussein Obama.
They didn't use that word, of course. Republican leaders frown on such labeling because it makes the House majority look, well, crazy.
It is, Rep. Steve King (R-Iowa) said from the dais, "the word that we don't like to say in this committee, and I'm not about to utter here in this particular hearing."


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If Fast Johnny'S ability is cancelled by the opposing character and if Fast Johnny loses his/her fight, the Damage inflicted on his/her owner will be reduced by 4 points up to a minimum of 1. If the winning character's Damage points are lower than or equal to 1, then the ability has no effect.
Junkz's Attack points are increased by 8 points. (Remember: Power * Pillz = Attack)
Clint City, night.


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Could Kashkari be the next governor?
Could Neel Kashkari defeat Jerry Brown and be elected governor of California?
Many have written him off. But I think, if he plays his cards right, and with a little luck, he could pull it off. I may be long odds, but I think he has a shot.
First, Jerry Brown has some serious vulnerabilities. He has a record of being soft on crime: the Rose Bird Court, prison realignment and his liberal appointment of Goodwin Liu to the court. This alienates law enforcement and even many city and county Democrats, who are taking the brut of prison "reform."
Second, the water tunnels issue has even liberal Democrats, Democrat environmentalists and practically all of Northern California up in arms. Not to mention the train to nowhere, poorly conceived and badly managed and executed.
Third, it is an off term election year. Low turnout favors Republicans.
And finally, there is the Tim Donnelly vote. What would activate them to vote? The gun rights issue! If Kashkari would agree to veto any restrictive gun legislation, it might motivate enough Donnelly supporter to hold their noses and vote for him. Donnelly had 16-17 percent of the vote, Kashkari 19 percent, that adds up to about 35 percent. Brown polled 52 percent, about a 17 percent difference. Influencing about 9 percent of voters to change their minds or to vote is within striking distance. Republicans are more motivated than Democrats. it's worth a shot. Contemplating three Brown appointments to the California Supreme Court just might turn the tine against Brown, if, and it is a big if, Kashkari plays his cards just right.
Paul Schecter, Vacaville


text: Cairoli, Herlings Clinch World Motocross Titles Cycle News Staff | September 9, 2012Antonio Cairoli clinches his sixth World title.With still one round left on the 2012 FIM World Motocross Championship calendar, Red Bull KTM's Antonio Cairoli and Jeffrey Herlings clinched the MX1 and MX2 titles, respectively, in Italy today at the Grand Prix of Europe at Faenza. Both Cairoli and Herlings won their classes by sweeping both motos.For Cairoli, the 2012 has been a record-breaking season, as he is now third on the all-time Grand Prix victories winners list, behind Joel Smets and Stefan Everts, and his sixth World title equals him with Joel Robert. Only Stefan Everts has more with 10 World titles.As opposed to last year, Cairoli started the 2012 season with the red plate on his KTM already after the first Grand Prix and he did not lose it until the MXGP of Sweden, where he suffered two DNFs. The Italian said today that the MXGP of Sweden was like a turning point in his season:"After Sweden something changed," he said. "I am usually careful with my riding and my riding style involves running a good pace without too many risks. After Uddevalla and those results, I said 'I'm going for the win every moto and we'll see what happens.' It turned out good! Maybe in 2007 I had similar results but this is better."Cairoli won 11 of the last 12 motos, and today he won his 53rd MXGP with a double victory for the eighth time from his 10 wins this season.The Italian has become one the most successful riders in the MX1 class since the inception of the series in 2004. He dedicated his sixth World title to his mother, who passed away on this day last year, and he said that he was wishing to have a perfect day to dedicate it to her. In fact, the day finished even better for Cairoli when he was surprised by his own father, who gave him the trophy on the podium for being the winner of the MXGP of Europe.With this new World title, the 26 year old from Patti has handed KTM its third FIM MX1 World title in a row on the 350cc machine. In addition, KTM has claimed again both MX1 and MX2 World titles for the third time in a row, the first one in 2010 with Marvin Musquin and Cairoli. Last year it was with Ken Roczen.Herlings, meanwhile, obtained his maiden FIM MX2 World title in Faenza after winning the Grand Prix of Europe. The young rider from Geldrop is the first Dutch rider to win a World title since 1993 with Pedro Tragter.Jeffrey Herlings wins his first MX2 World title at Faenza.Herlings has had a very consistent season, with only a few problems in the muddy races like the one in Brazil and the DNF he had in Latvia. A part from that, the 17-year-old had an outstanding season. So far he has obtained eight pole positions from the 15 possible, he has won 18 motos out of 30, and he has been on the top of the podium in nine occasions."I had many ups and downs during the whole season, but I managed to find the way to get through everything and win the title," he said. "I am really happy to have had my team behind me because they have been really supportive all the time."It has been more than 20 years since a Dutch rider won a World title," he added, "so it is amazing feeling, like I am really writing history now. In the last few years I have managed to put the motocross back in the front covers and on TV in the Netherlands, so I hope to do good for my country and put the sport in the place it deserves."With this MX2 World title, Herlings has contributed to keep KTM's winning streak in the MX2 class, and KTM has now up to five FIM MX2 World titles in a row since Tyla Rattray won in 2008. Comments


text:
Ted Baker Abadi Endurance Sterling Shirt for Men in Blue
Coes ID: H00090BLUnow £45.00 was £69.00
Style Notes
The Abadi Shirt, from Ted Baker's Endurance range, is a stylish formal shirt for men which is perfect for work-to-weekend wear and features a retro geometric jacquard print, and contrasting printed internal trims. The contrast pattern on the underside of the cuff adds a subtle pop of colour
Ted Baker's Menswear Collection Double cuff with silver cufflinks (included) Tailored fit No pocket Classic collar Jacquard pattern Standard placket Mother of Pearl effect, branded buttons Contrast internal trims 100% Cotton Please see care label for washing instructions
Product Delivery
Postage and packaging charges are as follows:
UK (including Channel Islands) – Standard Delivery is Free on orders over £50 & £2.50 on orders below £50. Express Delivery is Free on orders over £100 or £5 for orders below £100.
General Returns Policy
Because we offer free delivery to UK addresses and minimal postage charges to other destinations, we are unable to supply a free return option, unless goods are defective, or we have made an error in dispatch.
For any further information please visit our Returns page.
Any Questions? - Either contact us via email firstname.lastname@example.com, or telephone us on 01473 256061 between 9 am - 6 pm Tuesday to Saturday
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text:
via press release:
|More than 200 Total Hours of Formula One™ and IZOD IndyCar Series Programming to Air Across NBC and NBC Sports Network
F1's Rolex Australian Grand Prix Drops Flag on Coverage This Sunday at 1:30 a.m. ET on NBC Sports Network
"Mimosas from Monaco" — Biggest Day in Racing Begins with Live Coverage of Monaco Grand Prix on Sunday, May 26 at 7:30 a.m. ET on NBC
NBC Sports Network to Televise Record 13 IZOD IndyCar Races in 2013
IndyCar Booth Features New Look
Motorsports Media Conference Call Set for Wednesday
|NEW YORK – March 11, 2013 – The NBC Sports Group will present its most extensive and comprehensive motorsports coverage ever in 2013, with more than 200 programming hours of Formula One™ and IZOD IndyCar races, practices, qualifying, pre- and post-race studio shows, and behind-the-scenes programs. Coverage will air across NBC, NBC Sports Network, and NBC Sports Live Extra, the NBC Sports Group's live streaming platform, via TV Everywhere. Additionally, two F1™ races will air on CNBC, NBCUniversal's business channel.
Formula One, which makes its NBC Sports Group debut this week on NBC Sports Network with the Rolex Australian Grand Prix, will air four races live on NBC, 13 on NBC Sports Network, and two on CNBC. The famed Monaco Grand Prix will air live on broadcast television at 7:30 a.m. ET on Sunday, May 26 on NBC.
NBC Sports Network, which has been the exclusive cable home for the IZOD IndyCar Series since 2009, will televise more Indy races this season than ever before. The addition of two "doubleheaders" to the schedule will result in NBC Sports Network televising 13 races this season, plus 12 Indy Lights races.
Programming for both open-wheel circuits will include significant shoulder content that is consistent with their unique brands. In addition, NBC Sports Digital will dedicate more motorsports coverage than ever. It will cover the entire racing industry with the recently launched MotorSportsTalk on NBCSports.com, and, later this year, it will live stream both circuits on NBC Sports Live Extra via TV Everywhere.
The 2013 Formula One World Championship schedule includes all 19 races in 19 countries from March through November, including 13 on NBC Sports Network, four on NBC and two on CNBC.
COMMENTATORS: As previously announced, NBC Sports Group's F1 announce booth will feature lead race announcer Leigh Diffey, who will call both F1 and the IZOD IndyCar Series this year, veteran analyst and former racecar driver David Hobbs, and analyst Steve Matchett, a former race mechanic for the Benetton F1 team, including two years with seven-time Formula One world champion Michael Schumacher.
Rounding out the team is Will Buxton, an F1 insider and former journalist, who will serve as the team's on-site reporter. Respected by fans and critics alike, Diffey, Hobbs, Matchett and Buxton bring continuity to each telecast, as all four worked together for several years previously on SPEED's coverage of the circuit.
ON-SITE: It is estimated that Buxton will travel more than 115,000 miles this season while covering all 19 races in 19 countries.
MIMOSAS FROM MONACO: Sunday, May 26 can arguably be called 'the biggest day in racing' as it features three of sport's most famous races from three different circuits — the Monaco Grand Prix (Formula One), the Indy 500 (IndyCar) and the Coca-Cola 600 (NASCAR).
This year, the day will begin with live coverage of the famed Monaco Grand Prix on broadcast television when NBC airs the race at 7:30 a.m. ET. The entire NBC Sports F1 studio team will join Buxton on site to capture the unique glitz-and-glamor atmosphere of the Monaco Grand Prix.
NBC GRAND PRIXES: NBC will provide F1 with unprecedented exposure this year as it airs four races in 2013. In addition to Monaco, races scheduled to air on NBC are the Canadian Grand Prix (Montreal) on Sunday, June 9, the United States Grand Prix (Austin, Texas) on Sunday, November 17, and the final race of the season, the Brazilian Grand Prix on Sunday, Nov 24. The NBC Sports F1 studio team will also be on site for live coverage of the Montreal and Austin races.
Due to scheduling conflicts, CNBC, NBCUniversal's fully-distributed business channel, will air the Grand Prixes from the United Kingdom and Germany.
F1 EXTRA: NBC Sports Network's post-race show, F1 Extra, will air live after every NBC Sports Network and CNBC race, as well as the Monaco NBC race. Post-race coverage for Canada, USA and Brazil will air on NBC. The 30-minute wrap-up show will be handled by the F1 team of Diffey, Hobbs, Matchett and Buxton.
F1 36: Three-time defending Formula One champion Sebastian Vettel will be the first driver profiled in the first-ever episode of F1 36, airing Friday, March 29 at 7 p.m. ET. F1 36 is the latest in the NBC Sports Group's original behind-the-scenes 36 series, which gives viewers an all-access pass into the life of world-class athletes. For each episode, cameras will follow a F1 driver for 36 hours, providing a behind-the-scenes look at their on- and off-track activities. The all-access 36 series, which is produced by IMS Productions, also includes NHL 36, Fight Night 36, IndyCar 36 and MLS 36.
PRACTICE, QUALIFYING & RE-AIRS: NBC Sports Network will offer extensive coverage of F1 practice and qualifying throughout the season. The network will also offer a re-air of the race, often in the early afternoon, allowing viewers to enjoy coverage during a more traditional sports-viewing time period.
ROLEX AUSTRALIAN GRAND PRIX: The first race of the season will air live from Australia on Sunday, March 17 on NBC Sports Network at 1:30 a.m. ET. The race will re-air at 1 p.m. ET. F1 action gets underway Friday, March 15 at 12 a.m. ET with the first practice session.
Following is this week's coverage schedule for the Rolex Australian Grand Prix on NBC Sports Network:
A week after Formula One coverage begins, NBC Sports Network will start the 2013 IZOD IndyCar Series on Sunday, March 24 in St. Petersburg, Fla. This year, the network will air a record 13 races live, the most in the channel's four-year history as the cable home of IndyCar (up from nine in 2012). The increase is largely due to the innovative addition of two doubleheaders — in Toronto and Houston — which provide two races over two days from one location.
COMMENTATORS: NBC Sports Network's coverage will feature a new look this year. Lead race announcer Leigh Diffey, in his first year covering the IndyCar Series, will be joined by returning race analyst and former NASCAR driver Wally Dallenbach, Jr. (analyst), and newcomer to the booth, IndyCar driver Townsend Bell.
Jon Beekhuis, an analyst who has also served at the network since 2009, will now report from pit road. A former CART driver (1989-92) and 1988 Indy Lights Champion, Beekhuis will be inside the race action, reporting minute-to-minute on what happens on the track.
Veterans Marty Snider and Kevin Lee will return this season as pit reporters, and will be joined by Robin Miller, the network's IndyCar reporter.
RACES: NBC Sports Network's schedule includes 13 races in three different countries (U.S., Canada, and Brazil), the first and last races of the year, as well as the popular Toyota Grand Prix of Long Beach.
The season begins March 24 at Noon ET with the Honda Indy Grand Prix of St. Petersburg from St. Petersburg, Fla. Other race locations include: Barber, Ala., Long Beach, Calif., Sao Paulo, Brazil, Milwaukee, Wis., Mid-Ohio, Ohio, Sonoma, Calif., and Baltimore, Md.
QUALIFYING: NBC Sports Network will air 12 hours of Indianapolis 500 qualifying coverage. Also, on May 24 at 11 a.m. ET, NBC Sports Network will air five hours of live coverage of Carb Day, which includes the final practice for the Indy 500, the Indy Lights Freedom 100 and the Pit Stop Challenge.
The network will also air one-hour of qualifying coverage the day before each of its races. It will also replay race coverage the following day.
INDYCAR 36: NBC Sports Network will continue its all-access series IndyCar 36 in 2013. The first half-hour episode will feature Chip Ganassi driver Charlie Kimball on Saturday, May 4, at 6:30 p.m. ET. The original series is produced by IMS Productions and gives viewers an all-access pass into the life of a world-class driver in the middle of race season.
The cameras follow a driver for 36 hours during a race weekend providing a behind-the-scenes look at the on- and off-track activities of the stars of the IndyCar Series. The all-access 36 series includes NHL 36, Fight Night 36, F1 36, and MLS 36.
FIRESTONE INDY LIGHTS: NBC Sports Network will air 12 one-hour telecasts of Firestone Indy Lights beginning with the 1.8-mile street course St. Petersburg, Fla., on March 24 at 11 a.m. ET, on NBC Sports Network. Additionally, there will be two new venues added to the series; the 2.5-milie Pocono Raceway oval, and the 1.7-mile, 10-turn temporary street course at Reliant Park in Houston. All Indy Lights races will be featured on event weekends to run in conjunction with and complement the IZOD IndyCar Series.
Firestone Indy Lights is the premier ladder series for drivers and teams striving to compete in the IZOD IndyCar Series and the Indianapolis 500. Primarily run in conjunction with the IZOD IndyCar Series, the Firestone Indy Lights schedule features races on road courses/street circuits and ovals, including the famed 2.5-mile Indianapolis Motor Speedway.
NBC SPORTS NETWORK'S SEASON OPENER COVERAGE FROM ST. PETERSBURG (subject to change, all times ET):
MOTORSPORTSTALK: NBC Sports Digital has added MotorSportsTalk (@MotorSportsTalk) to the already established SportsTalk franchises on NBCSports.com. The site brings racing fans up-to-the-minute news, video and information on the Formula One, IZOD IndyCar Series, NASCAR Sprint Cup Series, and all other motorsports racing from around the world. The site will also serve as the destination for all news, analysis and video from NBC and NBC Sports Network productions of F1 and IndyCar, including contributions from on-air commentators.
MotorSportsTalk's content will be provided by top racing journalists and expert analysts, including:
To explore the site, please visit MotorSportsTalk.com.nbcsports.com or www.NBCSports.com.
SOCIAL: Follow @MotorsportsTalk, @F1onNBCSports and @NBCSN on Twitter and "like" Facebook.com/NBC Sports for the most up-to-date news, videos and commentary about Formula One and IndyCar on NBC Sports and NBC Sports Network.
NBC SPORTS LIVE EXTRA: Beginning later this year, NBC Sports Live Extra, the NBC Sports Group's live streaming platform, will live stream F1 and IndyCar races via TV Everywhere.