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Value Pricing the NFL Quarterback
This was a little something I was kicking around in my head for some time and finally got around to doing. This is a way to attempt to put a composite score to an NFL QB using a number of different efficiency measures and then plotting it against their reported salary, in essence created a Value Mapping of todays NFL QBs. I'll try and explain as best I can here what I did, and if you have any questions on it just drop me a line either here or via email.
Please note that all of the contract numbers used are based on various reports of the contracts yearly value. Since I do not have access to any official records this is the best I can do, though I believe most QB's have their numbers reported very accurately in the media.
The Criteria
In order to qualify for the listing the player had to have 2 qualifying seasons in the last 3 years with a qualifying season being defined as one in which a player has at least 100 pass attempts and participates in 25% of the teams offensive snaps in the same season
The Metrics
There are a number of different stats that attempt to put quantitative scores to a QB performance. Readers of my site know I keep my own stats, which are comparisons to schedule averages, but I maintain those on a team by team basis except for certain Jets where I try to keep them on a player basis. So that makes those pretty much useless here, so I did not attempt to include them in the evaluation.
The most widely know stat is the QB rating (QBR). QBR has been around forever and involves a mathematical formula that comes up with a rating that can reach as high as 158.3. The highest single season QBR belongs to Aaron Rodgers who hit a 122.3 this season. Similar to the stats I keep there is no consideration given to the situation and all results are weighed the same. Unlike my stats there is no consideration given to quality of opposition. More often than not you will hear sports people on TV using the QBR as a definitive mark for a passer.
Defense Adjusted Value Over Average (DVOA) is one of Football Outsiders metrics that measure the value of a number of players, QB included. DVOA is an attempt to place a value on a QB based on situational play. Their baseline is the league average in a situation (down and distance) and then they adjust the success criteria based on the opponent they are playing. Essentially they award a point for a play that picks up a minimum amount of yardage based on down and distance with bonus points awarded for amount of yards thrown beyond the necessary yardage as well as red zone play. They also award negative points for negative plays, such as interceptions. The DVOA then compares the players score to the average expectation. I believe the highest ever DVOA belonged to Peyton Manning in 2004 with a score of 60.6%. FO is often featured on ESPNs website for fans looking for more indepth statistical coverage.
Pro Football Focus has their own grading system, though they have yet to name anything so I will just refer to it as PFF. PFF grades a player on 3 criteria- pass, run, and penalties- and adds them up to come up with an overall grade for a player. Like DVOA it is more of a situational based grading scale with points being awarded between -2 and 2 for a play. They normalize the stats based on an average expectation which they set when they began their site. PFF has caught some steam in the last two years with bloggers and some mainstream reporters. I think the simplicity in their grading will help it gain more traction in the coming years, but for now it is a "pay per view" database which limits their exposure. Drew Brees' 60.2 from 2011 was the best season for a QB that they have recorded.
Percent of Team Yards (POTY) is something I decided to do for this study to give players credit for playing time, staying healthy, and general importance to the offensive scheme in which they have played. For example most of the efficiency stats can be skewed in the favor of players who see the field for a minimum amount of plays or are offensive caretakers. Though their numbers should, in theory, hold up given more opportunities over the course of 16 games that rarely would happen in the real world. There is a reason why the player is on the bench for most of the snaps year after year. That has to be taken into account when putting a value on a QB. For example Joe Flacco grades lower in almost every metric than Mike Vick, but Flacco accounts for about 53% of his teams offense the last 3 years while Vick, who spent one full season on the bench and multiple games hurt, only accounts for 27%. POTY gives the healthy player keeping a job a chance to narrow the gap between those who don't have the opportunity to screw up as often.
The Methodology
For each category I used the stats for the 2009, 2010, and 2011 NFL seasons and averaged the score across those three years. For QBR, DVOA, and PFF if a player did not have a qualifying season I did not count it in the average (i.e. Matt Stafford's 2010 season did not count in the averages due to the 25% requirement). For POTY I do count those seasons in which the player did not qualify. Why? Because injuries or poor practice play need to be factored in. It's not fair for a player like Peyton Manning to not be penalized when Drew Brees never misses a game. The only exception was for the two retired players on the list of Brett Favre and David Garrard and the 2010 rookies. Since the retired guys were no longer in the NFL in 2011 I did not count any stats for their former teams. 2010 rookies did not have any 2009 stats so that would be unfair to penalize them.
Now I did consider doing a weighted average (50% on 2011, 35% 2010 and 15% 2009), but for a first trial run ended up going with this. Admittedly that is probably a stronger way to look at the players, but I had done my POTY across the three years rather than for each individual year when I started to compile data, so this was simpler for me.
I wanted to normalize the scores with a grade of 0 so I did that by taking each stat and taking the lowest score in each category and bringing it either up or down to 0. For DVOA that required adding 28.5 points to ever score to bring Derek Anderson from a -28.5 to a 0. PFF's low man was Mark Sanchez at -19.9. Derek Anderson was again the man, this time for QBR, with a 54, so that led to a subtraction of 54 from each score. Finally Bruce Gradkowski led to a -15.4 point adjustment in the POTY category. This doesn't change the differential between players, it just makes things a little neater to plot.
Each category was given equal weight and the totals simply added up to determine a composite score for the player. In the future I may try something with percentage to average comparisons rather than overall totals.
The Results
The top 5 should come as no surprise- Rodgers, Brees, Brady, Rivers, and Roethlisberger. Peyton Manning ranked 6th as he was hit hard by the non play in 2011, but even if we took that season out he was still slightly behind Rivers. In recent years he just has not been as productive as the top guys. To me the most surprising result was David Garrard at 14. He's not great by any means, but a steady performer in each category. Vince Young at 18 was also a surprise, but he plays well in spurts and then heads to the bench.
The real duds are the 2009 and 2010 NFL draft class. Freeman, Bradford, McCoy, Sanchez and Stafford ranked 28, 29, 30, 31, and 32. In Stafford's case he would benefit greatly from a weighted system since he played so much better this season so he may be the guy to justify the contract. The others all have big uphill battles to remain as starters.
Here are the adjusted figures and total score for each player.
Adjusted QB Scoring Matrix
DVOA | PFF | QBR | PTOY | Total Score | |
Aaron Rodgers | 64.80 | 55.40 | 54.90 | 60.76 | 235.86 |
Drew Brees | 63.43 | 60.00 | 49.70 | 57.94 | 231.07 |
Tom Brady | 74.67 | 42.30 | 50.27 | 56.64 | 223.88 |
Phillip Rivers | 62.63 | 50.57 | 44.30 | 59.23 | 216.73 |
Ben Roethlisberger | 57.13 | 41.63 | 41.87 | 53.04 | 193.67 |
Peyton Manning | 60.10 | 48.85 | 41.90 | 40.57 | 191.42 |
Matt Schaub | 56.17 | 38.50 | 41.80 | 48.66 | 185.13 |
Eli Manning | 46.93 | 36.80 | 36.43 | 56.95 | 177.12 |
Matt Ryan | 50.23 | 40.77 | 34.03 | 49.83 | 174.87 |
Tony Romo | 57.40 | 30.00 | 44.33 | 41.95 | 173.68 |
Joe Flacco | 39.97 | 25.93 | 33.80 | 52.88 | 152.58 |
Brett Favre | 39.70 | 30.10 | 34.55 | 45.07 | 149.42 |
Mike Vick | 47.50 | 29.60 | 38.55 | 26.90 | 142.55 |
David Garrard | 28.57 | 31.30 | 33.15 | 48.48 | 141.50 |
Carson Palmer | 40.37 | 25.73 | 28.17 | 45.75 | 140.02 |
Kyle Orton | 38.20 | 13.93 | 30.03 | 42.85 | 125.01 |
Jay Cutler | 23.60 | 16.33 | 28.93 | 51.02 | 119.89 |
Vince Young | 50.75 | 21.25 | 36.70 | 11.18 | 119.88 |
Alex Smith | 25.03 | 21.77 | 30.77 | 40.25 | 117.82 |
Donovan McNabb | 32.27 | 18.03 | 30.30 | 35.22 | 115.82 |
Matt Moore | 38.80 | 22.50 | 38.80 | 15.52 | 115.62 |
Jason Campbell | 35.67 | 15.27 | 31.03 | 30.49 | 112.46 |
Matt Hasselbeck | 20.53 | 14.37 | 22.90 | 49.26 | 107.06 |
Chad Henne | 34.70 | 19.50 | 21.30 | 30.83 | 106.33 |
Josh Freeman | 24.03 | 10.23 | 22.77 | 48.66 | 105.69 |
Ryan Fitzpatrick | 21.90 | 13.13 | 22.87 | 44.20 | 102.10 |
Matt Cassel | 19.13 | 11.23 | 25.83 | 37.51 | 93.71 |
Sam Bradford | 14.55 | 13.05 | 19.50 | 45.99 | 93.09 |
Colt McCoy | 26.25 | 9.95 | 20.55 | 34.86 | 91.61 |
Mark Sanchez | 26.50 | 0.00 | 18.17 | 45.05 | 89.71 |
Matt Stafford | 23.15 | 7.80 | 25.10 | 33.13 | 89.18 |
Shaun Hill | 19.20 | 23.05 | 26.45 | 8.03 | 76.73 |
Kerry Collins | 21.55 | 16.15 | 19.85 | 8.30 | 65.85 |
Kevin Kolb | 20.60 | 10.35 | 24.60 | 8.00 | 63.55 |
Bruce Gradkowski | 21.00 | 18.60 | 19.45 | 0.00 | 59.05 |
Derek Anderson | 0.00 | 1.90 | 0.00 | 4.84 | 6.74 |
The Value Map
Finally I have a plot of value vs price. I used Excel to plot an exponential fit in there just as a point of reference. This just gives a very rough guideline of players who are likely overvalued or undervalued. Below the line means a team probably got a good deal and above means they are overpaid for production. The contract is the based on the latest contract the player signed.
I split the graph up into 25 point boxes to help compare values better. What you have to do is look up and down each section to see players that have had about the same value over the three year period. For example Sanchez, Bradford, Stafford, McCoy, Cassel, and Shaun Hill have all given about the same on the field aggregate performance. Bradford is horrible value right now. Colt McCoy gives about the same results for a fraction of the price. As you move to the right the value of the player increases so all things equal the more to the right the better the value.
The worst value is Kevin Kolb. His level of play is more or less equivalent to a player who should earn about $3.75 million a year. He makes $12.4 million. He's always hurt and does not play particularly well when healthy. He is Exhibit A of why you stay away from backup QBs that create interest off a handful of games. Matt Cassel is Exhibit B. The success though is Matt Schaub who is tremendous value basically giving you the same results you get from guys who cost around $15 million a season. You can bet that is the guy Matt Flynn will be compared to in free agency when he negotiates his deal with someone.
I still will never understand the Ryan Fitzpatrick signing by the Bills. He ranks right along with all those journeymen making under $5 million a year, which is what Fitzpatrick is, yet the Bills paid him close to $10 million. Drew Brees and Aaron Rodgers right now are the best values out there. It says something about signing guys early and taking a chance. Brees should emerge as the highest paid QB in the NFL since his contract is up, by a few $100,000 more a year than Brady and Manning. There is no way for the Saints to argue otherwise. It just seems like a slam dunk. Rodgers in under contract until 2014. In theory he should be the first $19 million dollar QB, but I can't see the Packers just tearing up the current deal and increasing his salary by that much no matter how good he is. That team is set for the next 3 years because his cap will never exceed $11 million. That's great planning and a great deal of luck too!
Based on the graphing I would think that the players most in danger of being asked to take a paycut next year are Kolb, Sanchez, and Carson Palmer. All are due significant money and carry decent size cap hits. Bradford still has one more year of leeway and Stafford's big 2011 makes him safe. Cassel may be saved because his actual cash payout is low, though Kyle Orton is better value and may choose to stay there and replace him.
I think Jay Cutler and Vick are interesting cases. Both got deals far in excess of performance, Cutler probably moreso than Vick since Vick is dragged down much more by being a backup one season. Cutler's cap is $9.6 million next year and most of his money has already been paid so he is no longer overpaid, its just a firm knock on the deal he signed. Vick is overpaid and will make $12.5 million guaranteed next season. It is going to be a big year for him because his salary jumps to $15.5 million the following season and there is no full guarantee on that money. Right now he only has $3 million guaranteed for injury only. The Eagles are masters at the cap and Vick won't be back at that figure if the same performance occurs.
Again if there are any questions or info you want to pass along drop me an email.


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General Motors will be holding a conference call to review and discuss its U.S. sales results. The conference call will start at approximately 11:00 a.m. ET on Friday, January 3, 2014. The call will begin with a brief review of U.S. sales results followed by a question and answer session for security analysts and media.
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General Board / Re: How much you can disclose during an interview about previous legal work?
« on: June 03, 2008, 09:43:53 PM »
I agree with Steve, strongly disagree with Lampshade. Check out your employer's confidentiality policy. I bet they expect you to be pretty tight-lipped, so I would refrain from saying anything about specific clients or anything else that might reveal too much. Blabbing about clients might even hurt your prospects; it would show you can't keep your mouth shut.


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'To Lift a Nation' Dedicated in Emmitsburg, Maryland
EMMITSBURG, MD - In the shadow of a huge statue, Billy Eisengrein posed for pictures and signed autographs Monday morning.
The FDNY firefighter, one of three who raised the flag in the ruins of the World Trade Center on Sept. 11, 2001, spoke a few minutes with everyone who approached. He said it was the least he could do.
Eisengrein sat anonymously in the crowd of more than 500 Monday morning for the dedication of the monument - To Lift a Nation -- that depicts the historic moment.
He and the others have stayed out of the spotlight, fearing the attention would be on them, not their brothers who perished during the most successful rescue effort on record.
"We've all wanted to remain anonymous," he said. "It's not about us."
Eisengrein said he, Daniel McWilliams and George Johnson didn't know that someone was taking pictures when they raised the flag in the WTC rubble. "We didn't know at the time it would make such a difference..."
A day or so later, someone told him that his picture was in the paper. "I thought it was no big deal. I had been in the paper before. Then, they told me it was huge and nearly the whole front page."
"Now, I'm glad someone captured that moment in time."
Eisengrein said he is pleased the monument has been placed on the grounds of the National Fire Academy in close proximity to the National Fallen Firefighters' Memorial.
"This is perfect, very fitting."
Bob Carlo, whose son, FDNY Firefighter Michael Carlo, was killed in the tower collapse described the monument as awesome and "a wonderful tribute."
Carlo's voice cracked with emotion as he thanked people for supporting not only his family, but others who lost loved ones in the terrorist attacks.
"...I speak for my family, my son and his 342 brothers. I'm sure they are smiling down on us right now."
FDNY Deputy Chief John Jonas looked around, and remarked that the brilliant Sept. 11 sky was shining down on the monument, a "powerful image that represents courage and heroism."
He said the events were an awakening to America about what the fire service does on a daily basis. The deputy chief spoke briefly about what he experienced at the WTC that day.
"I witnessed it in their faces. It was as if the calvary had arrived...It was comforting to me when I was trapped in the north tower to know that they were coming to save me and my men..."
IAFC Second Vice President Larry Grorud said the monument will help lift the spirit of the American people, just as the gesture did in 2001.
Norman Hoeft, representing the National Volunteer Fire Council, said the Lift a Nation monument will compliment the memorial park. He congratulated those involved for chosing the site.
Kim Corpany, associate sculptor, said it was gratifying to see the project unveiled. But, more importantly, to see what it means to nation's firefighters.
She said all the long hours were well worth it.
Sculptor Stan Watts said he, as all Americans, was moved the instant he saw the photograph. When his wife suggested the project, he first thought it was an endeavor he didn't want to tackle.
"Sometimes, your projects chose you," he said.
He recalled meeting the three firefighters and their attorney. To his dismay, they asked him not to do it. Watts told them it was not for them. "It's for us and for generations to come..."
FEMA Director R. David Paulison said the three firefighters raising the flag sent a powerful message to everyone - Never Give Up."


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The practitioners of politics -- and those who write and speak about it -- claim that these matters are secondary to "pocketbook issues." I was told this week, "Nobody in America cares about that 'constitutional stuff' right now with all that's gone wrong with our economy." If that's true, we're in more serious trouble than my 401(k).
Perhaps I have spent too much of my life with young Americans who sacrificed the comforts of home and the company of loved ones to take on the responsibility of protecting the rest of us. They didn't sign up to fight for gold or colonial conquest or "the economy." The soldiers, sailors, airmen, guardsmen and Marines I have been covering for Fox News Channel in Mesopotamia, Afghanistan, the Persian Gulf and the Philippine archipelago volunteered to defend us and protect our liberty from those who had done us grievous harm.
They raised their right hands and took an oath to "support and defend the Constitution of the United States." They understand what it means to "bear true faith and allegiance." Most of them have seen parts of the world where there is no freedom, and they know that freedom is an idea worth fighting for, preferably at a great distance from home.
Thanks to the courage and sacrifice of young Americans in uniform and those who preceded them, foreign adversaries do not immediately threaten our liberty. But freedom certainly is at risk here at home if our elected leaders and appointed judges believe that our essential freedoms are "political rights." If that is true, then politicians and the judges they appoint can abridge, alter or eliminate them.
The extraordinary dedication, commitment and tenacity of American men and women in uniform serving the cause of freedom inspire me. Their bravery and perseverance on battlefields around the world should remind us all that freedom is fragile and must be defended to flourish. The Bill of Rights, including the Second Amendment, did not come to us gratis or without obligation.
We are blessed in America that we can fend for freedom with ballots instead of bullets. Our charge is to elect those who will deliver those freedoms intact and undiminished to those who follow us, as my son and I now follow in the footsteps of Joe Foss.
Oliver North is a nationally syndicated columnist, the host of War Stories on the Fox News Channel, the author of the new novel Heroes Proved and the co-founder of Freedom Alliance, an organization that provides college scholarships to the children of U.S. military personnel killed or permanently disabled in the line of duty. Join Oliver North in Israel by going to www.olivernorthisrael.com.
Due to the overwhelming enthusiasm of our readers it has become necessary to transfer our commenting system to a more scalable system in order handle the content.


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Sea Eagles
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STATE of Origin is done and dusted for 2014. Here are tbe best images from the final game.
48Dally M: JT fires again but who's on top?
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The Unsung FIRST Heroes Award Committee, after honoring the regional winners, is now pleased to honor the national winners of the Woodie Flowers Award. Congratulations to the past national winners. Please take a few moments to read about the accomplishments and events that these honorees have made possible.
The Unsung FIRST Heroes Award would also like to honor Paul Copioli, this year's national winner. Paul, a mentor for Team #217, the ThunderChickens, is the second consecutive national winner of the Woodie Flowers Award that was previously honored with an Unsung FIRST Heroes Award. The UFH committee is proud of this statistic, and congratulates Paul on his accomplishments. We will be honoring the Woodie Flowers Award winners until May 15th, whereupon we will be resuming regular UFH activities. Thank you to Woodie Flowers, Liz Calef, Mike Bastoni, Ken Patton, Kyle Hughes, Bill Beatty, Dave Verbrugge, Andy Baker, Dave Kelso, and now, Paul Copioli: you are a wealth of inspiration for the FIRST community. We commend you. Amanda Morrison and the Unsung FIRST Heroes Award Committee |
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The Rise of the Mega-RegionRichard FloridaMartin Prosperity Institute, Rotman School of Management, University of Toronto; New York University (NYU) Tim GuldenGeorge Mason University - Center for Social Complexity; George Mason University - Department of Computational Social Science Charlotta MellanderJonkoping University November 2008 Cambridge Journal of Regions, Economy and Society, Vol. 1, Issue 3, pp. 459-476, 2008 Abstract: This paper develops new data on mega-regions. It takes issue with theories of globalization which argue that global economic activity is being more widely decentralized-'the world is flat'. We use a global dataset of night-time light emissions to produce an objectively consistent set of mega-regions for the globe. We draw on high-resolution population data to estimate the population of each of these regions. We then process the light data in combination with national gross domestic product (GDP) to produce rough but useful regional estimates of economic activity. We also present estimates of technological and scientific innovation. Keywords: mega-region, globalization, urbanization, night-time lights, O18, R10 Date posted: March 17, 2009Suggested CitationContact Information
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03-26-2014, 06:11 AM | #2 (permalink) |
Zombie Queen Moderator
Join Date: Jun 2003
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I believe it is a matter of personal choice
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03-26-2014, 06:26 AM | #4 (permalink) |
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It entirely depends on what you want. For me, the command sit (sitz) or down (platz) means don't move until I give you another command. However, both of my dogs also know a stay command (each dog has a different command).
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03-26-2014, 07:42 AM | #5 (permalink) |
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I agree it's a personal choice, both dogs know what the sit or down command entails but there is a seperate "stay" command which is not attached to a certain position which they've learned which essentially means "freeze in whatever position you are in now and don't move until released"
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03-26-2014, 08:23 AM | #6 (permalink) |
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I like the implied sit/stay as long as I don't move. If I get up and move to a different place then I tell them to stay. If I am standing there and say sit or down I expect them to stay in that position until I give a release word or start to move.
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03-26-2014, 09:01 AM | #7 (permalink) |
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The reason I use a stay is dogs usually see a sit down or stand as an action and not a position. Thats why you have to teach a down from a sit a down from a stand and down in motion as separate actions. Doesn't really matter that much though but its the reason behind my preference.
03-26-2014, 09:13 AM | #8 (permalink) |
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I do not use a stay command. A sit, down or stand etc means "get into commanded position until another command is given".
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03-26-2014, 09:15 AM | #9 (permalink) |
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I don't teach a 'stay'. My last command is to be held until I either give another command or I give a release.
I do teach a 'wait'. Meaning, wait before you go through the door or wait inside your kennel after I open the door until I release. I want my dogs to be clear on 'wait', there is no gray area. This command may stop them from crossing the street, or running to meet my husband's pickup (while it's still moving) when he comes home. Again, this just works best for me. Honestly, there are times when I'll say "Lay down and you better not move!" My dogs get what I'm implying......
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03-26-2014, 09:17 AM | #10 (permalink) |
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I agree with Packen. Sit, down, and stand imply "stay in that position until you get another command or release word."
I do have a "wait" command but this is used by itself not paired with a position. Like say my dog is hiking off leash and gets ahead of me, I say "wait" and he waits until I catch up. Or, if I'm feeding dogs and don't want everyone knocking me around and diving in, I say "wait" and they have to stay where they are until released. I don't care if it's sit, down, or stand, just hold still.
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Forums → Art, Music, and Writing
Posted Oct 1, '09 at 5:36pm
27 posts
It was ttly vise.Now, vise, you`ve had that sword stuck up your rear for quite a while, haven`t you? I`d imagine that would cause a large build up of... Matter in your rectum. Now, this buildup would, I imagine,probably be released in a rapid, explosive few secods. Perhaps you really weren`t waiting to get your helm at all. Perhaps you were near Flippo`s bakery,trying to remove the object from your body. Perhaps the following release of waste was what destroyed the bakery.
Posted Oct 1, '09 at 5:38pm
4,696 posts
Who is to say that it wasn't Snelly or Flipper?They both seem somewhat.... ditzy. Maybe it was all a horrible accident caused by the two.
Posted Oct 1, '09 at 5:49pm
10,086 posts
You have lots of gun ammo, but no explosives?Do you have any automatic weapons? Like a Gatling gun or an assault rifle?
Posted Oct 1, '09 at 6:34pm
5,718 posts
Well lets see...who is to say the contestants who are not here might not have all had something to do with this incident? Whether on purpose or not. No one can account for any of them.
Posted Oct 1, '09 at 6:39pm
2,353 posts
Leon says: Means to commit a crime is not evidence. I know many who have weapons to fight evil, hunt for food or simply protect themselves from people like me.This is an amusing diversion, but we have neither evidence nor means of acquiring it. I grow tired of this deadlock. Someone did it. He was instructed to not give up his identity no matter what. If he admits guilt, it will save us a lot of trouble, but at his expense, and through no fault of his own. Would you admit guilt, even if it isn't your fault, to save the innocent? I probably wouldn't. Maybe the guilty party is a better man than me. Maybe not.
Posted Oct 1, '09 at 6:41pm
5,809 posts
Gatling gun? Clunky and not so useful in CQC, only good if you have back up.Assault Rifle? Yes, I have an assault rifle. But I think it's gathering dust. I really should clean it...It got jammed one day and I never got around to fixing it.
Posted Oct 1, '09 at 6:44pm
Quick question where was the phoenix when this happened. If a flaming bird flew through or into the building it could be mistaken as a flaming bomb of some sort couldn't it?
Posted Oct 1, '09 at 6:56pm
1,748 posts
Well just to clarify if it was the phoenix who did this, it might not have been her fault. I mean she can't just flame off right?
Posted Oct 1, '09 at 7:04pm
Posted Oct 1, '09 at 7:13pm
Well if we are going to be pointing blades i think it was Vise. I find him to be a very strange person.
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Available for Emily Nash Smith:
Emily Nash Smith (1897 - 1983)Emily Nash Smith was born in Tipton, Indiana in 1897. Educated as a schoolteacher, in 1920 she married fellow Tipton resident Thearl W. Smith. Two years later they moved to Omena, Michigan and purchased what is now known as Overlook Farm. Emily continued to teach and turned her farmhouse into a restaurant during the summer where she became well known for her Sunday chicken dinners. Always enterprising and creati (showing 500 of 2010 characters).


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Yagyu Shinkage Ryu Kenjutsu DVD (Nihon Kobudo Series)
Yagyu Shinkage Ryu is a classical Japanese kenjutsu school (odachi, kodachi, nitto) and was the official kenjutsu style of the Tokugawa shogunate; derived from Shinkage Ryu. The school was founded circa 1568 by Yagyu Sekishusai Munemori (1527-1606), a student of Kamiizumi Ise no Kami (Shinkage Ryu). The life of his son Yagyu Munemori (1571-1646), teacher of the shogun Tokugawa Ieyasu, has been the subject of numerous films. The fukuro shinai (shinai in a leather bag) is unique for this ryu. Current headmaster is Yagyu Nobuharu.


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ActiveWake is your online Wakeboard Shop offering free shipping on every wakeboard and no sales tax. Wakeboarding has never been better with huge tech advancements coming from the top brands like Liquid Force, Hyperlite, Ronix, Byerly and Slingshot.
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on Jul 07, 2002 at 11:53 UTC ( #179958=monkdiscuss: print w/ replies, xml ) | Need Help?? |
I've put together an experimental perlmonks search engine that is now up and running. It searches node titles not the node contents and currently only contains data from the past few months. Even with those limitations, I hope it will help fill the gap we currently have searching this site.
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The majority of colorectal cancer (CRC) cases develop through the adenoma-carcinoma pathway. If an increase in DNA repair expression is detected in both early adenomas and carcinomas it may indicate that low repair capacity in the normal mucosa is a risk factor for adenoma formation.
We have examined mRNA expression of two DNA repair genes, ERCC1 and OGG1 as well as the putative apoptosis controlling gene RAI, in normal tissues and lesions from 36 cases with adenomas (mild/moderat n = 21 and severe n = 15, dysplasia) and 9 with carcinomas.
Comparing expression levels of ERCC1, OGG1 and RAI between normal tissue and all lesions combined yielded higher expression levels in lesions, 3.3-fold higher (P = 0.005), 5.6-fold higher(P < 3·10-5) and 7.7-fold higher (P = 0.0005), respectively. The levels of ERCC1, OGG1 and RAI expressions when comparing lesions, did not differ between adenomas and CRC cases, P = 0.836, P = 0.341 and P = 0.909, respectively. When comparing expression levels in normal tissue, the levels for OGG1 and RAI from CRC cases were significantly lower compared to the cases with adenomas, P = 0.012 and P = 0.011, respectively.
Our results suggest that increased expression of defense genes is an early event in the progression of colorectal adenomas to carcinomas.
Most colorectal cancers (CRC) develop through multiple mutations in the normal colonic mucosa, and evolve through the adenoma-carcinoma sequence [1,2]. Various endogenous and exogenous agents from environmental exposures are constantly damaging DNA, and in combination with low DNA repair capacity this have been interpreted as increasing the likelihood of cancer development [3-7].
The range of different DNA lesions is broad and there are different repair pathways depending on the nature of the damage. Nucleotide excision repair (NER) will repair bulky adducts [8] while base excision repair (BER) is responsible for the repair of base damage and single strand breaks [9]. Only a few studies have to our knowledge studied DNA repair expression of nucleotide excision repair (NER) and base excision repair (BER) genes in CRC. Even less is known about the level and significance of DNA repair expression during the formation of adenomas and the transition period in the adenoma-carcinoma sequence. Previous studies have indicated that the NER gene excision repair cross-complementation group1 (ERCC1) and BER gene 8-oxoguanine glycosylase 1 (OGG1) may be inducible [10] and they have also been shown to correlate with enhanced DNA repair activities [11-15]. DNA repair mechanisms are complex and involve several genes. OGG1 and ERCC1 are among the few for which it has been shown that mRNA levels and repair activity correlate. The ERCC1 gene encodes a subunit of the nucleotide excision repair complex required for the incision step of NER [16,17]. Several factors indicate that the ERCC1 mRNA levels can be used as a proxy for DNA repair capacity. The mRNA levels of ERCC1 may correlate with DNA repair capacity in various tissues [11-13,15], and also predict the response to chemotherapy (high ERCC1 levels have been associated with tumor growth and lower levels have been associated with improved disease response) [15,18-21]. In addition, inter-individual variation of ERCC1 mRNA levels is much larger than the intra-individual variation [22], indicating that the mRNA level of ERCC1 may be used as a biomarker for NER.
The enzymes responsible for the BER process which repair damaged bases, abasic sites and single-strand breaks are initiated by specific DNA glycosylases. The DNA glycosylase OGG1 removes 8-oxo-guanine (8-oxoG) directly from damaged DNA [23,24]. Kondo et al concluded that there is a correlation between 8-OHdG levels and hOGG1 expression in CRC tissue [14]. Kondo et al also concluded that colorectal carcinoma cells but not adenoma cells are exposed to more oxidative stress than corresponding normal tissue [25]. Previous studies have shown that oxidative stress is generally proportional to OGG1 mRNA expression and activity [10,26,27]. To the best of our knowledge, it has not been investigated if increased OGG1 expression is an early or late event in the adenoma-carcinoma sequence. It is therefore of interest to study and compare the expression of OGG1 in adenoma and carcinoma tissues.
There are several responses to DNA damage including induction of apoptose to eliminate damaged cells. The putative apoptosis controlling gene RAI was included to determine if the expression of RAI was coordinated with the expression of ERCC1. Both genes are located on chromosome 19q13.2. The RelA associated inhibitor (RAI) gene, encodes an inhibitor of the RelA subunit of the transcription factor NF-κB [28]. The inclusion of this gene is more explorative but previous studies suggest that RAI is involved in carcinogenesis [29]. High levels of RAI seem to promote apoptosis while low levels of RAI may inhibit apoptosis, although the literature is not clear on this issue [28,30]. This is to the best of our knowledge the first study to investigate if increased RAI expression is an early or late event in the adenoma-carcinoma sequence.
In this study we have measured mRNA levels of ERCC1, OGG1 and RAI in patients with colorectal adenomas and carcinomas (normal colonic mucosa and lesions).
The main focus was to investigate if increased expression of DNA repair genes is an early or late event in the adenoma-carcinoma sequence. By studying repair genes in the various stages of the adenoma-carcinoma sequence, we may gain new information on the significance of repair capacity in normal and neoplastic tissues during transition.
The KAM biobank (Kolorektal cancer, Arv og Miljø) is based on the screening group of the Norwegian Colorectal Cancer Prevention study (The NORCCAP study) in the county of Telemark [31]. The ID number for the NORCCAP study at clinicaltrials.gov is I NCT00119912 [32]. The KAM biobank has previously been described by Hansen et al. [33]. In the present study we have selected and analyzed cases with adenocarcinomas (9) and cases with adenomas (36). The sampling pool of cases contains tissue (normal colonic mucosa and lesion) from 180 CRC cases and 242 adenoma cases. The cases are matched for age and gender. The adenocarcinomas were collected prior to chemo- or radiotherapy treatment. The tumor histology of the adenomas was examined independently by two specialist histopathologists in order to determine the tumor stage as either mild/moderate (n = 21) or severe (n = 15) dysplasia (tumor cellularity 60–80%). They reached the same conclusion in all cases. All cases completed a questionnaire containing information on a family history of cancer and the included cases had no known personal history of cancer. The KAM cohort consists of an ethnic homogeneous group of Norwegian origin. The KAM study is approved by the Regional Ethics Committee and The Data Inspectorate.
Total RNA was purified from normal colonic mucosa and lesions as recommended by the manufacturers using NucleoSpin DNA II kit (Macherey Nagel). The tissue had been snap frozen in liquid N2 before RNA purification. RNA purification included a DNAse treatment. The cDNA synthesis was performed on ca. 200 ng RNA in a final volume of 10 μl using Gold RT-PCR kit (Applied Biosystems, Nærum, Denmark).
Quantitative PCR was performed on ABI 7500 sequence detection system (Applied Biosystems, Nærum, Denmark) in universal mastermix (Applied Biosystems, Nærum, Denmark) using 100 nM Taqman probe and 200 nM primers for ERCC1 and for OGG1, 100 nM probe and 600 nM primers for RAI. ERCC1, OGG1 and RAI primers and probes were obtained from TAG Copenhagen, Copenhagen, Denmark. The OGG1 probe recognizes all splice forms of OGG1. The expression was normalized to 18S rRNA. 18S primers and probes were commercially available from Applied Biosystems, Nærum, Denmark.
The quantification of mRNA levels has been described previously [22,34]. The probes and primers have been validated, and the PCR was shown to be quantitative over a range of 130-fold dilution for ERCC1 and OGG1 and over a 32-fold range for RAI. mRNA measurements were excluded if the 18S content was below the detection level of the individual mRNA defined by the validation experiments. ERCC1, OGG1, RAI mRNA and 18S levels were quantified in triplicate in separate wells. The average mRNA level of the specific mRNAs was then normalized to the average 18S level. The average standard deviation on triplicates was 15 %. The standard deviations on repeated measurements of the same sample (the control) in separate experiments were 34%, 21% and 25% for ERCC1, OGG1 and RAI, respectively, indicating the day-to-day variation of the assay. Independent PCR reactions of the same samples yielded a correlation coefficient of 0.97. Negative controls (where the RNA was not converted to cDNA) and positive controls were included in all sets.
For comparison of different mRNA expression levels between normal tissue and lesions in cases we used paired t-test. When comparing expression levels in normal colonic mucosa from all cases, and lesions in all the cases separately, a one-way ANOVA test was used. P values < 0.05 were considered significant for all statistical tests. For trend analysis of normal colonic mucosa in OGG1 and RAI we used logistic regression after dividing cases in mild/moderate dysplasia (1), severe dysplasia (2) and CRC (3). MiniTab Statistical Software, Release 13.1 Xtra (Minitab Inc.) was used for statistical calculations.
The distributions of age and gender are described in Table 1. Cases are divided into three groups according to diagnosed degree of dysplasia; adenomas (mild/moderate or severe dysplasia) and carcinomas. mRNA expression in normal colonic mucosa and all lesions for the three genes, ERCC1, OGG1 and RAI are displayed separately in Figure 1 (A, B, C), and mean values are displayed in Table 2.
Table 1. Distribution of age and gender.
Figure 1. mRNA expression of ERCC1, OGG1 and RAI in lesions. mRNA levels were normalized to the 18S mRNA level. The classification of lesions are; M/M: adenoma with mild or moderate dysplasia; S: adenomas with severe dysplasia; C: adenocarcinomas. Open squares designate the expression level in normal colonic mucosa while crossbars designate the expression in lesions. A: ERCC1, B: OGG1, C: RAI. * designate statistically significant different mRNA levels in normal colonic mucosa compared with lesions in the same persons (p < 0.05).
Table 2. Mean normalized ERCC1, OGG1 and RAI mRNA levels in normal colonic mucosa and lesions.
For all three genes, ERCC1, OGG1 and RAI, a comparison of expression levels between normal colonic mucosa and lesions in all cases combined (adenomas and CRC) yielded significantly higher expression levels in lesions, 3.3-fold P = 0.005, 5.6-fold P < 3*10-5 and 7.7-fold P = 0.0005, respectively. When comparing expression levels between normal colonic mucosa and lesions separately for each case group (mild/moderate dysplasia, severe dysplasia and CRC), we detected significantly higher expression levels for ERCC1 and RAI in cases with severe degree of dysplasia and for OGG1 we detected significantly higher expression levels in cases with severe degrees of dysplasia and CRC (Table 2).
When comparing expression levels of ERCC1 in lesions only, we detected no difference between the adenoma and CRC case groups, P = 0.836. This was also true for normal tissue, P = 0.291, (Fig 1A).
The level of OGG1 expression when comparing lesions did not differ between adenoma and CRC cases P = 0.34, (Fig 1B), but for normal colonic mucosa the OGG1 expression in CRC patients was statistically significantly lower than in normal colonic mucosa from adenoma cases with mild/moderate dysplasia, P = 0.012, (Fig 1B). A trend of lowered mRNA expression with increasing degree of dysplasia was also observed in normal colonic mucosa, P = 0.003.
The level of RAI expression when comparing lesions did not differ between adenoma and CRC cases, P = 0.909, (Fig 1C). The level of expression in normal colonic mucosa was however significantly lower in CRC cases compared to adenoma cases with mild/moderate dysplasia, P = 0.043, (Fig 1C). A trend of lowered mRNA expression with increasing degree of dysplasia was also observed in normal colonic mucosa, P = 0.011.
In this study we have measured mRNA levels of ERCC1, OGG1 and RAI in patients with colorectal adenomas and carcinomas (normal colonic mucosa and lesions). We have compared expression levels between corresponding normal colonic mucosa and lesions in both adenoma and CRC cases. In order to see if an increase in expression is an early or late event in the adenoma-carcinoma sequence we have also compared expression levels between case groups in normal colonic mucosa and lesions separately.
ERCC1 expression was statistically significantly higher in lesions than in the corresponding normal tissue when all cases were combined. For OGG1 and RAI, a similar increase in mRNA levels in lesions compared to the corresponding normal colonic mucosa was detected. Previous studies have shown that the mRNA levels of ERCC1 [11-13,15,35] and OGG1 [10,14,27] correlate with the DNA-repair capacity in various tissues. The increased mRNA level detected in lesions in this study may therefore be interpreted as enhanced DNA repair activity.
Low expression of DNA repair genes in lymphocytes have previously been shown in patients with breast cancer, lung cancer and cancer of the head and neck [4-7]. This has been interpreted as low DNA repair gene expression is a risk factor for cancer. For both OGG1 and RAI we found that the expression was lower in normal colonic mucosa from CRC patients than in normal colonic mucosa from persons with mild/moderate dysplasia. This lowered mRNA level can either be interpreted as a risk factor for adenoma and CRC development but it can also be a consequence of the same.
When comparing different lesions in the adenoma-carcinoma sequence, we detected no significant difference in expression. This was true for all three genes, ERCC1, OGG1 and RAI. This may indicate that increased expression of DNA repair is an early event in the adenoma-carcinoma sequence. The result for RAI may be an indication that RAI and ERCC1 are coordinated as they both are located on chromosome 19q13.2. The NER gene XPD is also located on chromosome 19q13.2 and a previous study by Vogel et al concluded that ERCC1 and XPD mRNA quantities were highly correlated [13]. The RAI mRNA is many-fold induced during apoptosis and the induction is essential to apoptosis (Magdalena Laska et al, manuscript in preparation). Increased RAI expression has previously been observed in acute leukaemia cells [36]. We and others have found that RAI mRNA is also often increased in cancer cells (Bergamaschi et al [30] and this paper). We interpret this increase as an attempt on the part of the cancer cells to activate the apoptotic pathway. However, that attempt is presumably abortive as the cancer cells continue to multiply. Possibly, the well-known derangement of the intracellular control in cancer cells may have destroyed other essential factors and/or the downstream response.
Higher expression of DNA repair genes in lesions compared with normal colonic mucosa may indicate chemoresistance. The difference in expression levels between normal colonic mucosa and lesions for both ERCC1 and OGG1 could mean that lesions in general have a higher DNA repair capacity and therefore is less sensitive to DNA damaging agents such as chemotherapy. Shirota et al showed that CRC patients with low levels of intratumoral mRNA ERCC1 expression had significantly better survival than patients with high expression, when treated with 5-FU and oxaliplatin as second- or third-line chemotherapy [21].
Hereditary cancer predisposition syndromes have provided insight to the importance of DNA repair, but there are only limited data on inter-individual variation in DNA repair and susceptibility to sporadic cancer. Vogel et al detected an inter-individual mRNA variation for ERCC1 and OGG1 that was 5–10 fold in healthy volunteers [22], and a study by Paz-Elillzur et al concluded that low OGG1 activity was associated with an increased risk of lung cancer [37]. However, in the only prospective study of mRNA levels of DNA repair genes and RAI, low expressions of ERCC1, XPD or RAI were not associated with increased risk of lung cancer [38]. In a study by Hansen et al [39] the OGG1 Ser326Cys polymorphism, which has a reduced glycosylase activity [40], was not associated with an increased risk of colorectal adenomas or carcinomas.
In conclusion, mRNA levels of ERCC1 and OGG1 were up-regulated in both colorectal adenomas and carcinomas compared to corresponding normal colonic mucosa, indicating that increased expression of defense genes is an early event in the progression of colorectal adenomas to CRC. There are some issues that must be considered when evaluating our findings. The number of cases is relatively small, therefore there is a possibility that the reported findings are due to chance. Larger prospective studies would be required to clarify this issue.
Competing interests
The author(s) declare that they have no competing interests.
Authors' contributions
MS prepared samples for analysis and contributed with the data analysis. She prepared the first draft of the paper.
CFS prepared samples for analysis and contributed with the data analysis. She also contributed to the manuscript.
ILH participated in collection and quality control of the questionnaires.
UBV, HW and BAN performed quantification of RAI and OGG1
EHK brought the idea of the KAM study and organized it.
All authors discussed the results, contributed to interpretation of the results and the final manuscript.
Anne-Karin Jensen is thanked for her excellent technical assistance. We will also like to thank Lotte Vogel for making the figures used in this paper. This study was supported by the Norwegian Cancer Society (Grant numbers 51024/001 and E01-0851001), Telemark University College (Grant number 22069), the Norwegian Colorectal Cancer Prevention (NORCCAP) study (Grants from the Norwegian Cancer Society and the Department of Health and Social Affairs), with the aid of EXTRA funds from the Norwegian Foundation for Health and Rehabilitation (2001/2/0110), Eastern Norway Regional Health Authority, the Danish Research Agency (Grant numbers 22-02-0356 and 2052-03-0016) and DRAGE, a grant from Danish Ministry of Health, Research Centre for Environmental Health's Fund.
Kinzler KW, Vogelstein B: Lessons from hereditary colorectal cancer.
Cell 1996, 87(2):159-170. PubMed Abstract | Publisher Full Text
Fearon ER, Vogelstein B: A genetic model for colorectal tumorigenesis.
Cell 1990, 61(5):759-767. PubMed Abstract | Publisher Full Text
Dybdahl M, Frentz G, Vogel U, Wallin H, Nexo BA: Low DNA repair is a risk factor in skin carcinogenesis: a study of basal cell carcinoma in psoriasis patients.
Mutat Res 1999, 433(1):15-22. PubMed Abstract
Wei Q, Matanoski GM, Farmer ER, Hedayati MA, Grossman L: DNA repair capacity for ultraviolet light-induced damage is reduced in peripheral lymphocytes from patients with basal cell carcinoma.
J Invest Dermatol 1995, 104(6):933-936. PubMed Abstract | Publisher Full Text
Wei Q, Cheng L, Hong WK, Spitz MR: Reduced DNA repair capacity in lung cancer patients.
Cancer Res 1996, 56(18):4103-4107. PubMed Abstract
Cheng L, Eicher SA, Guo Z, Hong WK, Spitz MR, Wei Q: Reduced DNA repair capacity in head and neck cancer patients.
Cancer Epidemiol Biomarkers Prev 1998, 7(6):465-468. PubMed Abstract
Shi Q, Wang LE, Bondy ML, Brewster A, Singletary SE, Wei Q: Reduced DNA repair of benzo[a]pyrene diol epoxide-induced adducts and common XPD polymorphisms in breast cancer patients.
Carcinogenesis 2004, 25(9):1695-1700. PubMed Abstract | Publisher Full Text
Benhamou S, Sarasin A: Variability in nucleotide excision repair and cancer risk: a review.
Mutat Res 2000, 462(2–3):149-158. PubMed Abstract | Publisher Full Text
Wilson DM 3rd, Thompson LH: Life without DNA repair.
Proc Natl Acad Sci USA 1997, 94(24):12754-12757. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Tsurudome Y, Hirano T, Yamato H, Tanaka I, Sagai M, Hirano H, Nagata N, Itoh H, Kasai H: Changes in levels of 8-hydroxyguanine in DNA, its repair and OGG1 mRNA in rat lungs after intratracheal administration of diesel exhaust particles.
Carcinogenesis 1999, 20(8):1573-1576. PubMed Abstract | Publisher Full Text
Cheng L, Guan Y, Li L, Legerski RJ, Einspahr J, Bangert J, Alberts DS, Wei Q: Expression in normal human tissues of five nucleotide excision repair genes measured simultaneously by multiplex reverse transcription-polymerase chain reaction.
Cancer Epidemiol Biomarkers Prev 1999, 8(9):801-807. PubMed Abstract | Publisher Full Text
Dabholkar M, Bostick-Bruton F, Weber C, Egwuagu C, Bohr VA, Reed E: Expression of excision repair genes in non-malignant bone marrow from cancer patients.
Mutat Res 1993, 293(2):151-160. PubMed Abstract
Vogel U, Dybdahl M, Frentz G, Nexo BA: DNA repair capacity: inconsistency between effect of over-expression of five NER genes and the correlation to mRNA levels in primary lymphocytes.
Mutat Res 2000, 461(3):197-210. PubMed Abstract | Publisher Full Text
Kondo S, Toyokuni S, Tanaka T, Hiai H, Onodera H, Kasai H, Imamura M: Overexpression of the hOGG1 gene and high 8-hydroxy-2'-deoxyguanosine (8-OHdG) lyase activity in human colorectal carcinoma: regulation mechanism of the 8-OHdG level in DNA.
Clin Cancer Res 2000, 6(4):1394-1400. PubMed Abstract | Publisher Full Text
Li Q, Yu JJ, Mu C, Yunmbam MK, Slavsky D, Cross CL, Bostick-Bruton F, Reed E: Association between the level of ERCC-1 expression and the repair of cisplatin-induced DNA damage in human ovarian cancer cells.
Anticancer Res 2000, 20(2A):645-652. PubMed Abstract
van Duin M, de Wit J, Odijk H, Westerveld A, Yasui A, Koken HM, Hoeijmakers JH, Bootsma D: Molecular characterization of the human excision repair gene ERCC-1: cDNA cloning and amino acid homology with the yeast DNA repair gene RAD10.
Cell 1986, 44(6):913-923. PubMed Abstract | Publisher Full Text
Wood RD: Nucleotide excision repair in mammalian cells.
J Biol Chem 1997, 272(38):23465-23468. PubMed Abstract | Publisher Full Text
Metzger R, Leichman CG, Danenberg KD, Danenberg PV, Lenz HJ, Hayashi K, Groshen S, Salonga D, Cohen H, Laine L, et al.: ERCC1 mRNA levels complement thymidylate synthase mRNA levels in predicting response and survival for gastric cancer patients receiving combination cisplatin and fluorouracil chemotherapy.
J Clin Oncol 1998, 16(1):309-316. PubMed Abstract | Publisher Full Text
Lord RV, Brabender J, Gandara D, Alberola V, Camps C, Domine M, Cardenal F, Sanchez JM, Gumerlock PH, Taron M, et al.: Low ERCC1 expression correlates with prolonged survival after cisplatin plus gemcitabine chemotherapy in non-small cell lung cancer.
Clin Cancer Res 2002, 8(7):2286-2291. PubMed Abstract | Publisher Full Text
Rosell R, Taron M, Ariza A, Barnadas A, Mate JL, Reguart N, Margel M, Felip E, Mendez P, Garcia-Campelo R: Molecular predictors of response to chemotherapy in lung cancer.
Semin Oncol 2004, 31(1 Suppl 1):20-27. PubMed Abstract | Publisher Full Text
Shirota Y, Stoehlmacher J, Brabender J, Xiong YP, Uetake H, Danenberg KD, Groshen S, Tsao-Wei DD, Danenberg PV, Lenz HJ: ERCC1 and thymidylate synthase mRNA levels predict survival for colorectal cancer patients receiving combination oxaliplatin and fluorouracil chemotherapy.
J Clin Oncol 2001, 19(23):4298-4304. PubMed Abstract | Publisher Full Text
Vogel U, Moller P, Dragsted L, Loft S, Pedersen A, Sandstrom B: Inter-individual variation, seasonal variation and close correlation of OGG1 and ERCC1 mRNA levels in full blood from healthy volunteers.
Carcinogenesis 2002, 23(9):1505-1509. PubMed Abstract | Publisher Full Text
Radicella JP, Dherin C, Desmaze C, Fox MS, Boiteux S: Cloning and characterization of hOGG1, a human homolog of the OGG1 gene of Saccharomyces cerevisiae.
Proc Natl Acad Sci USA 1997, 94(15):8010-8015. PubMed Abstract | Publisher Full Text | PubMed Central Full Text
Aburatani H, Hippo Y, Ishida T, Takashima R, Matsuba C, Kodama T, Takao M, Yasui A, Yamamoto K, Asano M: Cloning and characterization of mammalian 8-hydroxyguanine-specific DNA glycosylase/apurinic, apyrimidinic lyase, a functional mutM homologue.
Cancer Res 1997, 57(11):2151-2156. PubMed Abstract
Kondo S, Toyokuni S, Iwasa Y, Tanaka T, Onodera H, Hiai H, Imamura M: Persistent oxidative stress in human colorectal carcinoma, but not in adenoma.
Free Radic Biol Med 1999, 27(3–4):401-410. PubMed Abstract | Publisher Full Text
Bancroft LK, Lupton JR, Davidson LA, Taddeo SS, Murphy ME, Carroll RJ, Chapkin RS: Dietary fish oil reduces oxidative DNA damage in rat colonocytes.
Free Radic Biol Med 2003, 35(2):149-159. PubMed Abstract | Publisher Full Text
Kim HN, Morimoto Y, Tsuda T, Ootsuyama Y, Hirohashi M, Hirano T, Tanaka I, Lim Y, Yun IG, Kasai H: Changes in DNA 8-hydroxyguanine levels, 8-hydroxyguanine repair activity, and hOGG1 and hMTH1 mRNA expression in human lung alveolar epithelial cells induced by crocidolite asbestos.
Carcinogenesis 2001, 22(2):265-269. PubMed Abstract | Publisher Full Text
Yang JP, Hori M, Sanda T, Okamoto T: Identification of a novel inhibitor of nuclear factor-kappaB, RelA-associated inhibitor.
J Biol Chem 1999, 274(22):15662-15670. PubMed Abstract | Publisher Full Text
Yin J, Rockenbauer E, Hedayati M, Jacobsen NR, Vogel U, Grossman L, Bolund L, Nexo BA: Multiple single nucleotide polymorphisms on human chromosome 19q13.2-3 associate with risk of Basal cell carcinoma.
Cancer Epidemiol Biomarkers Prev 2002, 11(11):1449-1453. PubMed Abstract | Publisher Full Text
Bergamaschi D, Samuels Y, O'Neil NJ, Trigiante G, Crook T, Hsieh JK, O'Connor DJ, Zhong S, Campargue I, Tomlinson ML, et al.: iASPP oncoprotein is a key inhibitor of p53 conserved from worm to human.
Nat Genet 2003, 33(2):162-167. PubMed Abstract | Publisher Full Text
Gondal G, Grotmol T, Hofstad B, Bretthauer M, Eide TJ, Hoff G: The Norwegian Colorectal Cancer Prevention (NORCCAP) screening study: baseline findings and implementations for clinical work-up in age groups 50–64 years.
Scand J Gastroenterol 2003, 38(6):635-642. PubMed Abstract | Publisher Full Text
Hansen R, Saebo M, Skjelbred CF, Nexo BA, Hagen PC, Bock G, Bowitz Lothe IM, Johnson E, Aase S, Hansteen IL, et al.: GPX Pro198Leu and OGG1 Ser326Cys polymorphisms and risk of development of colorectal adenomas and colorectal cancer.
Cancer Lett 2005, 229(1):85-91. PubMed Abstract | Publisher Full Text
Vogel U, Nexo BA, Tjonneland A, Wallin H, Hertel O, Raaschou-Nielsen O: ERCC1, XPD and RAI mRNA levels in lymphocytes are not associated with lung cancer risk in a prospective study of Danes.
Mutat Res 2006, 593(1–2):88-96. PubMed Abstract | Publisher Full Text
Wei Q, Xu X, Cheng L, Legerski RJ, Ali-Osman F: Simultaneous amplification of four DNA repair genes and beta-actin in human lymphocytes by multiplex reverse transcriptase-PCR.
Cancer Res 1995, 55(21):5025-5029. PubMed Abstract
Zhang X, Wang M, Zhou C, Chen S, Wang J: The expression of iASPP in acute leukemias.
Leuk Res 2005, 29(2):179-183. PubMed Abstract | Publisher Full Text
Paz-Elizur T, Krupsky M, Blumenstein S, Elinger D, Schechtman E, Livneh Z: DNA repair activity for oxidative damage and risk of lung cancer.
J Natl Cancer Inst 2003, 95(17):1312-1319. PubMed Abstract | Publisher Full Text
Vogel U, Nexo BA, Tjonneland A, Wallin H, Hertel O, Raaschou-Nielsen O: ERCC1, XPD and RAI mRNA levels in lymphocytes are not associated with lung cancer risk in a prospective study of Danes.
Mutat Res 2005. PubMed Abstract | Publisher Full Text
Hansen R, Saebo M, Skjelbred CF, Nexo BA, Hagen PC, Bock G, Bowitz Lothe IM, Johnson E, Aase S, Hansteen IL, et al.: GPX Pro198Leu and OGG1 Ser326Cys polymorphisms and risk of development of colorectal adenomas and colorectal cancer.
Cancer Lett 2005. PubMed Abstract | Publisher Full Text
Yamane A, Kohno T, Ito K, Sunaga N, Aoki K, Yoshimura K, Murakami H, Nojima Y, Yokota J: Differential ability of polymorphic OGG1 proteins to suppress mutagenesis induced by 8-hydroxyguanine in human cell in vivo.
Carcinogenesis 2004, 25(9):1689-1694. PubMed Abstract | Publisher Full Text
Pre-publication history
The pre-publication history for this paper can be accessed here:


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Narrow your search
The latest flagship in Sony's line of sleek, waterproof Android smartphones has been announced by the company on its Japanese website.
CNET's Daniel Terdiman wrangles up tech and geek culture in Texas, Oklahoma, Kansas, and more.
Worldly looks and top-notch specs make the impressive, metal Samsung Galaxy S6 the Android phone to beat for 2015.
Technically Incorrect: Google may have all sorts of problems in Europe, but it's trying to make a contribution too.
When HBO launched its online streaming service, "Game of Thrones" fans welcomed the chance to stream the show direct from the source. Now, they're being told their accounts will be deactivated.
The Apple Watch is the most ambitious, well-constructed smartwatch ever seen, but first-gen shortfalls make it feel more like a fashionable toy than a necessary tool.
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Apple Watch all alone: what can it do? Not a lot -- it's mainly an iPhone accessory -- but there are some key things that it can handle on its own.
With data retention now in the law books and rights holders given the green light to chase individual pirates, VPNs are more popular than ever with Australians looking to cover their tracks online.
The company had previously let users view their search history, but this is the first time it's providing a download tool.
Samsung's striking, high-end Galaxy S6 Edge has the beauty, brains and brawn to take down the iPhone 6 and all the Android competition.
After a bootleg version leaked late Thursday, Warner Bros. officially releases a dark and gritty trailer for next year's 'Batman v Superman.'


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"Chomp it up!"
We listened to this as a family with 10 and 8 y/o kids on a road trip to florida! This was the PERFECT book to listen to on the way to florida! Hiaasen knows so much about florida's natural fauna and animals, we learned a bunch about the everglades. The kid characters are strong, but not over the top. There are some tough issues, mainly a child character being physically abused by her father, but it is handled well. Also, very good narrator! We love Hoot by Hiaasen aswell!
"my daughter loves this book"
my 10y/o has listened to this many times and each time tells me how good it is.
"ugh, may not be able to finish it"
Boring, taking forever to get to any real plot. Trying to decide if I will even listen to the last part.
"story of recovering from depression"
The narrator mispronounces the name of the game Kubb. He calls it "cub", the name of the game rhymes with tube. This distracted me from an otherwise interesting story.


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Desert View (NPS Campground)
Grand Canyon National Park,
Phone: (928) 638-7888
Visit Campground Website
Sites: 50
Recent Rate: $9 9/2014
Latitude: 36.039225213858
Longitude: -111.829396759644
These reviews are the opinion of an RVParkReviews' member and not the views of RVParkReviews.com
Date of Stay: September, 2014 - $9.00
Like all NPS parks, this one is 'dry camping'. Water hydrants strategically placed in park. Length limit of 30' on RV, no big rigs in here. First come first serve, park fills up fast. We were in Spot 42 (?) with good view of desert. Crowded but some spaces on the outside of the loop have privacy. Some people have no concept of 'quiet hours'.... rental rvs and generators...... ugh! we would camp here again We camped at Desert View (NPS Campground) in a Travel Trailer.
Date of Stay: September, 2012 - $12.00
This is a National Park Service campground. There are NO hookups; it is boondocking at its finest. If you want to get away from the bedlam at the Grand Canyon Village area, this is the place. We stayed in site #22, in the back of the loop. Bring leveling boards or be prepared to use your leveling system if you have one. Absolute quiet, all you hear are the ravens and the wind. Short bike ride or walk to the canyon rim and the watch tower. No facilities at the campground other than restrooms and water spigots throughout the park. No dump station; you need to go to Mather campground (26 miles) to dump. If you love peace and quiet, this is your paradise; if you want hustle and bustle and hookups, go to Trailer Village. Not reservable; first come, first served, but we had no problem finding a site in September. We loved this place and will definitely return. We camped at Desert View (NPS Campground) in a Motorhome.
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WHS Basketball Games Postponed |
Written by Mike Kelly | ||||
Monday, 10 February 2014 14:41 | ||||
Watauga High Athletic Director Tom Wright has announced that the basketball teams will not be making the trip down to Hickory tonight as was originally scheduled. The games, according to Wright, will be made up at the next available playing date---most likely Tuesday night---weather permitting. Watauga Middle School Athletic Director Jim Godwin has annouced that the middle school semifinal basketball games scheduled to be played at Lentz-Eggers Gym tonight have been postponed due to inclement weather. The games have been rescheduled for tomorrow night at their scheduled times.
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New HC, new hope! Join Date: Feb 2004 Location: I'm in LA, trick!
Posts: 8,700
| Times Dispatch - Gibbs, Parcells enjoy job satisfaction at 64 http://tinyurl.com/bm6js Sorry, it's late. ASHBURN The hours are long, the scrutiny is constant and the lows are lower than most people experience in their daily existence. But the highs? Ah, the highs. The highs are higher than the tallest building. And Joe Gibbs, 64, coach of the Washington Redskins, and Bill Parcells, 64, coach of the Dallas Cowboys, are glad to be where they are. "I told our guys, 'I hope you have something in your life when you're 64 years old that gets you excited as this gets me'," Parcells said. |
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December 15th, 2012 · Leave a Comment
Life isn't a blur anymore after cornea transplant surgery
Life had literally been a blur for 87-year-old Maxine Kaehler for the past 18 years as three age-related eye conditions gradually worsened vision in both of her eyes. Her vision deteriorated so much that by 2008 she could not drive, or read the newspaper or a restaurant menu.
In May 2008, Maxine had a partial-thickness cornea transplant on her right eye to treat Fuchs' endothelial dystrophy. The results were almost instantaneous.
"After the transplant, I realized there were words on the buttons on my microwave, and then I looked at my dishwasher and noticed the same thing. I couldn't believe it. I was just pushing random buttons before because I couldn't read what was written on them," says Maxine with a laugh.
If you know Maxine, you know that seeing little details are important to her daily routine as a retiree. Some of her favorite hobbies include embroidering, playing cards with friends and cooking. Read the rest of this entry »
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Tags: cornea transplant, James Garrity M. D., Maxine Kaehler, Matthew Clark PhD
August 23rd, 2012 · Leave a Comment
Rare Arthritis No Match for Woman Determined to Save Her Eyesight
By Jason Pratt
(written by Raquel Rivas - Mayo Clinic in Florida)
When most of us think about eye problems, we think about a trip to the eye doctor for a new eyeglass prescription. But for Sandy Blue, a rare eye condition posed a mystery that almost left her blind.
Blue, then 44, first noticed red streaks in her eyes as she got ready for work one morning in 2008. She thought she was just tired, but her eyes got progressively worse. Eventually, "the white part of the eyes went red like apples. " She saw a local eye specialist in Savannah, Georgia, and was treated with antibiotics for eye redness and pain that spread to her ears.
"I saw eight different ophthalmologists over the next six months," recalls Blue. Different eye drops did not help, and her eyes became "cranberry sauce red" and painful.
August 10th, 2012 · Leave a Comment
Teamwork makes the routine extraordinary
There was no doubting the value of the team approach on the early morning of Tuesday, May 22, 2012 in the Ambulatory Surgery Center at Mayo Clinic in Arizona.
In what was otherwise a fairly routine procedure — cataract removal — this time required the assistance of the ophthalmologic surgeon, nurses, a cardiologist and a cardiac device specialist. The center of attention was the patient — 62-year-old James Billingsley, a Vietnam veteran with Type II diabetes, a hearing issue, a bad heart and cataracts.
The Mayo team had two important goals — safety and quality of life for Billingsley. Billingsley, thanks to a ventricular support device (VAD) to support his failing heart, had been granted "extra innings" in a life that includes a supportive family, friends and a passion for performing as part of the honor guard for commemorations such as Memorial Day.
Dave Patel, M.D., chair of Ophthalmology, was strongly motivated to improve Billingsley's sight so he could enjoy life. But Billingsley's surgery did not fall in the category of routine. Cataracts needed to be removed from both of his eyes, and Patel decided to do a double cataract surgery so Billingsley would not have to go through the procedure twice.
Billingsley's heart needed to be monitored, and safety was top priority. So a team converged to closely monitor blood pressure levels and intravenous meds. "This double cataract surgery on a patient with a VAD could not be done elsewhere in a traditional eye center because of the potential risks," Patel says. "Here, at Mayo Clinic, we have all the specialists coming together as a team for the safety of the patient in this special circumstance."
The surgery was a success. One day later, when Billingsley returned for a follow-up appointment, his spirits were high and his sight had already improved. In fact, one eye registered 20/20 and the other eye was almost as good. "It made a big difference. Now I can read, I can watch TV and it doesn't feel like I'm looking through dirty glass. Dr. Patel did an excellent job."
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Tags: Arizona, cataract surgery, cataracts, Dave Patel, James Billingsley, Matthew Clark PhD, mcimg, mcvid, patient story, teamwork
November 8th, 2011 · Leave a Comment
Mackenzie's vision: Coordinated care, rapid treatment restore child's eyesight
When Mackenzie Chicos, an active 8-year-old from Owatonna, Minn., woke up for school one morning seeing spots in her left eye, her family didn't suspect that anything could be seriously wrong.
It was — and her vision was at risk.
On that day in September 2010, Mackenzie went to school as usual. She mentioned the spotty vision to her teacher, who sent her to see the school nurse. The nurse performed a vision test, which was normal, and sent Mackenzie home with a note alerting her parents about the eye screening.
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Tags: M.D., Mackenzie Chicos, Mayo Clinic Health System in Owatonna, Miguel Mulet
August 6th, 2009 · Leave a Comment
Doctors at Mayo Clinic in Florida and Minnesota are using a new technique to stabilize glaucoma and preserve vision.
Glaucoma is an eye disease that slowly damages the vision. A leading cause of blindness, it occurs when the eye's natural drainage system fails to work properly. Fluid builds up inside the eye leading to elevated pressure that can permanently damage the optic nerve. Read the rest of this entry »
View full entry · Comment on this
Tags: glaucoma, Trabectome


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Red Velvet Whoopie Pies
Cookie- 8 tablespoons (1 stick) unsalted butter, at room temperature
- 1 cup granulated sugar
- 1 large egg, at room temperature
- 1 teaspoon pure vanilla extract
- 1 ounce red food coloring (about 2 tablespoons)
- 2 cups sweet rice flour blend
- 2 tablespoons unsweetened cocoa powder
- 1/2 teaspoon kosher or fine sea salt
- 1/2 cup buttermilk
- 1/2 teaspoon apple cider vinegar
- 1/2 teaspoon baking soda
- 6 ounces cream cheese, at room temperature
- 3 tablespoons unsalted butter, at room temperature
- Pinch of kosher or fine sea salt
- 1 teaspoon pure vanilla extract
- 3 cups confectioners' sugar
Preheat the oven to 375 degrees. Line baking sheets with parchment paper or silicone baking mats.
In the bowl of an electric mixer fitted with the paddle attachment, cream the butter and sugar together until light and fluffy, about 3 minutes. Add the egg and mix well, scraping down the sides of the bowl with a large spatula. Add the vanilla and food coloring and mix well.
In a separate large mixing bowl, whisk together the sweet rice flour blend, cocoa powder, and salt. With the mixer on low, add half the flour blend mixture, then the buttermilk, and finally the rest of the flour blend mixture to the butter mixture and mix well.
In a small bowl stir the vinegar and baking soda together and then stir into the batter. Using a large spatula, scrape down the bottom and sides of the mixing bowl and make sure all the ingredients are incorporated. Drop the batter onto the prepared baking sheets using a small ice cream scoop or large tablespoon.
Bake the cookies for 7 to 9 minutes, or until the edges are set and the cookies are firm but springy to the touch. Cool on the baking sheets for 5 minutes, then transfer to a wire rack to cool completely. While the cookies are cooling, make the filling.
In the bowl of an electric mixer fitted with the paddle attachment on medium speed, cream together the cream cheese, butter, salt, and vanilla until smooth. Turn the mixer off. Sift in the confectioners' sugar and starting with the mixer on low speed and slowly increasing the speed to medium, mix well.
With your hand, brush the crumbs off the bottom (flat side) of a cookie, spread with a generous amount of filling, then top with another cookie, flat side down on the filling. Repeat with remaining cookies and filling.
The cookies should be stored in the refrigerator but are best eaten un-chilled, so take them out of the refrigerator 10 t0 15 minutes prior to serving.
Source Information
Reprinted with permission from Simply…Gluten-free Desserts by Carol Kicinski, © 2011 Thomas Dunne Books
Epicurious.com © Condé Nast Digital, Inc. All rights reserved.


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New Clips & Stills from "Scooby-Doo! Mystery Incorporated" Ep "The Song of Mystery"
Toonzone News is proud to present the following new clips and stills from "The Song of Mystery," the newest upcoming episode of Scooby-Doo! Mystery Incorporated premiering on Monday, August 9, 2010, at 7:00 PM (Eastern/Pacific).
Click on any of the screenshots below to view in full high-definition resolution:
Previous Scooby-Doo! Mystery Incorporated video clips and stills:
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Described as one of the strongest and most distinctive foundation programmes in the country, you will develop the skills and portfolio required for most degree programmes in art and design. The various creative projects you undertake will allow you to experience a range of ideas, materials, processes and technologies, enabling you to then identify and explore your preferred degree with the support of experienced staff. At the end of the course you will have the opportunity to exhibit in the established annual degree show.
In Term 1 you will be introduced to a wide range of creative activities to develop your practical and conceptual skills, helping to make choices for your future area of study. Through various practical projects you will investigate ideas, materials, processes and technologies, which will give you an awareness of historical and theoretical contexts and develop your independent learning skills. You will also begin preparation for BA course entry.
In Term 2 you will move towards the specialisation that you wish to follow at degree level, and apply for your chosen degree place. Individual guidance is given from an experienced range of staff on the options best suited to your work and future ambitions.
In Term 3 you will produce an exhibition of your final major project alongside the BA Degree Show and complete preparation for BA course entry.
Continuous assessment, advice and feedback. Assessed final major project.
You can find further details about the curriculum in the Programme Specification Document
Our Degree Show web sites display a selection of work exhibited by our Foundation Diploma students at the end of year show.
Foundation graduates go on to study a wide range of BA (Hons) courses at Manchester School of Art and other institutions across the UK. Following completion of a degree programme our graduates then go to establish themselves within a wide range of professions in the art and design world. These include careers as creative consultants, artists, curators, gallery owners, textile designers, fashion designers, product and furniture designers, illustrators, retail buyers, theatre and set designers, graphic designers, art critics and journalists, photographers, film-makers, animators, stylists, interior designers and architects.
Our Alumni include:
Sarah Burton: Fashion Designer & Creative Director at Alexander McQueen, Dean Hughes: Artist & Head of Undergraduate Study at Edinburgh College of Art, Andy Soup: Film-maker, Animator & Music Video Production, Nick Sharratt: Children's Book Illustrator, David Hoyland: Director of Seventeen Gallery, Amy Thomas: Artist, Nabil El Nayal: Fashion Designer, Oliver East: Illustrator & Artist's Book publications, Bruce Bell: Construction Designer & Architect, Genevieve Bennett: Interior Textiles Designer & Colour Consultant, Mike Mercer-Brown: Graphic Designer, Paul Harfleet: Artist & Garden Designer, Zoe Hitchens: Art Director & Fashion Film Director, Charlie Lightening: Documentary Film Dircetor, Chantelle King: Tablet Designer at Vanity Fair Magazine, Nicolas Byrne, Painter, David Longshaw: Fashion Designer.
UCAS Tariff Points/Grades Required | 120 at A2 or equivalent (such as BTEC National at Level 3 or Advanced Diploma). |
Specific GCSE Requirements | GCSE grade C in English Language |
International Baccalaureate | 24 Points |
Applications are through the University application form and not through UCAS. The form can be downloaded via the link below.
After completing the application form, please e-mail to firstname.lastname@example.com or post to:
Art & Design Admissions Team
Manchester Metropolitan University
Business School & Student Hub
Lower Chatham Street
All Saints Campus
Manchester M15 6BH
Home/EU candidates who are applying for September 2015 entry should return their applications by 12 December 2014 to ensure an interview.
Download Foundation Diploma Application Form
If you are invited for an interview we will ask you to complete an entry project which you will need to bring along with a portfolio of your work. Further details.
Home/EU students who are under 19 years old on the 31st August in the year they start the course do not pay any fees.
The fees for 2015 entry are not confirmed yet, but in 2014/15 the fees were:
Students aged 19 - 23: £1,220
Students aged 24 or older: £5,420
Non-EU international students (all ages): £6,900
A £60 studio materials fee is also payable.


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Please Register or Log in to Remove this Advertisement! Nope! (How 'bout that. This may be the shortest post I've ever made) :p
I think what people forget about NFL contracts is that only the guaranteed up front money means anything to players. So for the right guaranteed money we could sign Cutler to a very nice CAP friendly deal.
That's what I would do too and that's what I think will end up happening unless Cutler accepts a "below market" deal. It's hard to justify paying Cutler a LT "market deal" given his age, injury history, turnover issues, and lack of postseason wins. Don't get me wrong, I want him to be here next year and think he's by far the best option to be the starter but I don't think a LT deal is justified (unless it comes at a discount) when you have the FT option to use. Use the lions share of resources rebuilding the defense, get Trestman a rookie QB he can groom (for better or worse who knows), and kick the can down the road one more season on this decision.


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AK-47 inventor Mikhail Kalashnikov in intensive care | |
Anonymous Coward User ID: 27352798 United States 12/25/2012 01:12 PM Report Abusive Post Report Copyright Violation | |
CE1 ***** User ID: 30781337 United States 12/25/2012 01:17 PM Report Abusive Post Report Copyright Violation | 93-year-old Mikhail Kalashnikov, the inventor of the world's most popular automatic rifle, has been admitted to a cardiology hospital in Izhevsk, in the Urals. The engineer's health is said to have worsened during a routine check up on December 20, with Kalashnikov residing in intensive care ever since. His son insists the inventor is just undergoing routine procedures. Quoting: =EkIm= [link to rt.com] I was probably born with some designing abilities. -Mikhail Kalashnikov - [link to www.searchquotes.com] |


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Through the use of human figure drawing and self-report, this study examines factors that impact the concept of masculinity and identity as understood by African-American males, ages 11-15, who are living in a residential treatment center. Four factors influencing their development are examined: (a) mass media in the forms of television, movies, video games and magazines; (b) the presence or absence of family members; (c) social and cultural elements; and (d) community and environmental factors.
This paper addresses the following questions: What have adolescent boys in residential treatment been socialized to believe are behaviors indicative of manhood? How do the boys' drawn representations of men and their responses on the corresponding report form reflect their experiences of the media, their family, their culture, their environment and their community?
Ellamonique Greene graduated with a BFA in Painting in 2001 from Bowling Green State University. Ellamonique also studied Renaissance painting in Atelier Neo Medici, France; taught African American art history at Arkansas Baptist College; served as an artist-in residence at the Hearne Fine Art Gallery; and served as an intern at Rush North Shore Medical Center and Lydia Home Association.
Thesis Advisor: Terry Sweig, Adjunct Assistant Professor, Art Therapy
Thesis Reader: Barbara Fish, Adjunct Assistant Professor, Art Therapy
Second Reader: Alesia Montgomery, Education Trainer, Girls and Boys Town National Headquarters
admissions | saic home | degrees | cont act info | calendar | grad catalog
Cody Feagan Glushtrom Gomez Kulak Lewis Martin Morrissey Mosinski Newman Rocchi STUDENTS 2004
Barzacchini Bulosan Gage Greene Hilliard Koh Kunkel Lucchese Nagasaka Parkinson Peterson Phillips Reed Robertson Roskelly Shaw Snell Weil


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Other Languages, Other services
Translator tools at imtranslator.net
No German Translation / Keine Deutsch Uebersetzung
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To: email@example.com unsubscribe walk subscribe ski lists subscribe bg-announce firstname.lastname@example.com
If your mailer sends mail in multiple parts using MIME formatted enclosures, probably sending duplicates in Ascii & HTML:
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If you have a solution for others such as "For Micro Stuff v 1..2.3, click in this order to set your auto responder properly" then please mail your advice to majordomo-owner
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It's your responsibility to force your provider to fix problems he/she caused. If they fail to fix your problem, unsubscribe your address (if you haven't already been forcibly un-subscribed), & subscribe yourself from a better address with a different domain.
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More info: http://www.berklix.org/help/majordomo/#grey_listing
Also Do not allow your mailer to screw up "Subject:" with a wild Germanic non compliant mess of eg
To: email@example.com help index demo-list
To: firstname.lastname@example.com get demo-list.archive.0304
To: firstname.lastname@example.com index sfd-org
To: firstname.lastname@example.com get sfd-org sfd-org.archive.1009
The Majordomo source doc/FAQ reads:
If you want to filter mail lists into seperate mail sub-directories:
Occasionally someone receives on an old address, but posts from a new address. This get bounced to the list owner as potential spam, (as from an unlisted sender). If the list owner knows the human sender, the list owner may choose to forward the mail, embedding headers so the sending human can see which old address they sent from, so the human can unsubscribe, & subscribe their new current address. Headers In Body
Mostly the problem ia a regular list member who has failed to coordinate his/her sender address with his subscription receiving address.
Some subscribers do not react when list owners ask them to re-subscribe their proper sender's address. They ignore the requests & continue posting from a non subscribed addresses. That wastes list owner's time with repeat forwardings (& they & list would be inconvenienced if list owner was away & not available to manually keep forwarding on time).
Options then are to silently delete bad postings (as some list owners do), until sender learns he/she Must fix his/her wrong subscription address, or sometimes to be a bit more lenient for a while, & forward with headers so senders realise:
List owners usually remember to strip the part of the header between the list server & their private routing as irrelevant. List owners may leave headers between wrongly subscribed list members & mail list server as relevant. Sometimes list owner might strip a bit more, but better to strip too little than too much: removing too many clues for sender as to where they sent from & what they need to fix their end.


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Safari Land
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