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The royally appointed beds are adorned with gold and crystal accents and covered with custom linens.
The princesses left their personal photos for your enjoyment including portraits of their favorite beaus. Of course every princess needs access to her own private fireworks display. This is accomplished with a fiber optic headboard lighting up the night sky with the push of a button.
Even the lighting and curtains are royal in appearance. Disney was also cautious (and wise) enough to make sure the "cool" factor outweighs the "girl factor" making these rooms appeal to both the little girls and the little boys.
In true Disney fashion, the beauty extends beyond the room and spills over into the courtyard and gardens.


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Hold down Control (PC) or Command (Mac) key + mouseclick to select more than one option
|Avg. Dinner Entrée
|Greater than $25
|$18.01 - $25
|$12.01 - $18
|$7.01 - $12
|Less than $7
Posted by Melissa on 03/19/2009
Would you like to be charged three times for your meal? If so, Pongsri is the place for you because that is exactly what happened to me. I could tell the waiter was up to no good when he ignored the fact that my lunch friend had already paid his portion of the bill and tried to slip my friend's order onto my bill. I caught the error and after speaking to the waiter at length, he finally realized that my friend's portion was indeed already paid. When the new check came, it looked ok since it only had my order. That afternoon, I checked with my bank and saw that the waiter had charged my card 3 separate times. only one charge had the amount of my meal. Infact for a $22 lunch, including my friend's lunch, the 3 charges totaled almost $50! Right away I went back to the restaurant to speak with the manager and have the wrong charges taken off of my bill. the manager turned out to be the waiter who had served me! He looked the other way like I wasn't even there while I tried to explain what had happened. When the manager saw I was really upset, he begged me not to report the incident to the bank and that he would "look into it." Do you really think I trust him after what happened? Yeah right.
Posted by John on 01/09/2009
This is simply the best Thai restaurant in Manhattan. The food is excellent and the majority of it is cooked to your particular spice rating ( from mild up to Thai hot & Spicy ). On my last visit I tried the "Jewels On The Beach". I have never seen so much seafood in one meal, Mussells, Squid, Giant Prawns and Amazingly huge Scallops, all cooked to perfection. The food is excellent, the staff are pleasant and attentive, in short this is a MUST visit restaurant if you are in Manhattan.
Posted by Anonymous on 11/14/2008
I've been coming here for years and have never been disappointed. the staff is very attentive and takes the time to remember their repeat customers. I just got back from lunch and all i have to say is YUMMY!
Posted by Anonymous on 10/29/2008
the food is good for the price especially the lunch specials but the service is very bad, so don't expect a great customer service experience when you go there !
Posted by hatedit on 09/30/2008
if you go in for takeout, expect the woman in the back, when she gets around to acknowledging you, to ask you with a straight face if you would mind waiting a half an hour for your food. when you explain that that makes no sense, she tells you can go. the managers don't seem to understand that this is a terrible policy for retaining customers, they are so overstuffed with people and getting them in and out. sometimes when you call on the phone, the lady asks you if you would mind waiting an hour for your order. it's up to you, the food's sort of lousy, but it's better than most thai in the area.
Posted by Liz on 09/16/2008
Worked across the street from here for four yrs. The service is usually not good the servers don't listen to you because they want you in & out. The food is ok for the $, but not an enjoyable experience overall.
Posted by Chyna on 06/06/2008
I just feel the food could have had more zest. I like Thai becuase of the use of basil and cilantro in their foods. My spicy rice consisted of just eggs, chicken and rice sprinkled with a few scallions. It had no taste whatsoever. It's the first time I had to use Duck and Soy sauce to give Thai food flavor. Very sad. : - ( I was looking forward to a GREAT THAI LUNCH.

subset: commoncrawl


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Photos and Review by Oyster.com Investigators
This comfortable chain hotel gives you a true Seattle harbor experience -- Puget Sound and mountains included
Seattle is all about the water, which is why it makes perfect sense to want to stay at a waterfront hotel; and this eight-floor Marriott certainly affords that opportunity. Despite the harbor-centric location -- particularly attractive to cruise-ship travelers -- the hotel has a strong business base as well: It boasts large function rooms, which are frequently booked for Seattle philanthropic gatherings, and sits across the street from the 10,000-square-foot Bell Harbor Conference Center, which draws an even bigger corporate crowd. Unless you have a specific reason for wanting to stay closer to the heart of downtown (for shopping, say, or you desire a more luxurious hotel, like the Fairmont, Four Seasons, or Alexis), the Seattle Waterfront Marriott is fine choice that capitalizes on what is, undoubtedly, one of the city's proudest features.
The quintessential Seattle scene -- with a bit of a climb to some local attractions
Water, water everywhere could be the tagline for the Marriott, which is perched across the street from the boardwalk. The property is literally steps away from the Aquarium, cruise-ship terminals, Sculpture Park, antique warehouses, Argosy harbor tours, and a plethora of seafood restaurants (like the iconic Crab Pot, where -- in true Seattle style -- fresh seafood is literally strewn all over your table). But be forewarned: Unlike the Edgewater Hotel down the street, which literally hangs over the water, the Marriott is located next to the railroad tracks, across a busy, four-lane road, and below the Alaskan Way Viaduct, a local freeway overpass, which can be noisy. To get up to the Pike Place Market, be prepared to climb the eight-story hillside stairs from Alaskan Way up to First Avenue, or hire a taxi for about $5. (Note: You can also take a security-patrolled elevator up to First Avenue -- it's located right next to the hotel -- but it attracts a bit of an unsavory crowd at night, so probably not a good idea to go it solo.)
345 waterfront guestrooms and 13 suites; some with the best views in town
If you're booking the Marriott Waterfront, presumably you're doing so because you want a great view of Puget Sound. And one would think that you couldn't go wrong, given the fact that this property sits on Alaskan Way, literally across the street from the water. But beware that the hotel is shaped like the letter M; unless you end up at one of the front "points," your view of the water will be partial at best, and (as a front-desk staffer himself admitted) "barely" at worst. Another caveat: The hotel advertises balcony rooms (again, on the assumption that you'll want to take advantage of the spectacular views), but they are uniformly tiny, so you'll probably spend limited time out there. That said, the perfectly pleasant, perfectly neutral rooms (beige, beige, beige) are comfortable, if a little small, and rather pricey, considering their non-luxury status. Without question, you're paying for location.
An indoor/outdoor pool and a solid fitness center
There are very few Seattle hotels this close to the water, so if you want to enjoy everything this scenic city has to offer -- with an emphasis on harbor attractions and cruise access – the Marriott is a great pick. But note that not all of the rooms capitalize on the water views, balconies are small, and the five-minute trek to Pike Place Market is all uphill.
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A City Council committee approved extending hours on weeknights from 6 p.m. to 10 p.m. yesterday. The full council is expected to approve the ordinance next month.
Restaurant and bar owners have complained that their businesses are suffering because too many metered parking spaces are taken by downtown workers.
They claim that extending the meter enforcement time will lead to more turnover and open up spaces.
Safety Director James Draper says he knows of no other major city in the country that requires meters to be paid after 6 p.m.
He says enforcing the new hours will require more manpower from the traffic bureau.
The Associated Press


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yankton - Page 4
South Dakota Democrats Commit to Prudent Convention Atmosphere in Yankton this Weekend
This Dog May Have A Bite Worse Than Its Bark. A Yankton Girl Suffers Bites And Cuts After Attack.
Yankton Murder Suspect in Custody
New Movies in Sioux Falls Theaters. Legos, Vampires and Clooney.
Yankton Restaurant Fails 2 Health Inspections
Yankton's Construction Value Plummets in 2013
New Movies in Sioux Falls Theaters
Yankton Attorney Making Run for US Senate
Prisoner Back in Custody After Standoff
YANKTON, S.D. (AP) — A 26-year-old state prison inmate who failed to return to a minimum-security unit in Yankton is in custody after a standoff in Sioux Falls.


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RAY BROOK - The Adirondack Park Agency is now at work revising three proposed legislative bills in the hope they will gain support in the state Assembly and be introduced in the state Senate during its fall session.
The bills were first proposed by the agency during the summer session, and failed to gain Assembly sponsorship after local representatives weren't comfortable with them.
Local Assemblywoman Teresa Sayward said this week that the bills just weren't in the shape legislators wanted and revisions would be required to garner Assembly sponsorship.
"We just thought it would be best to move them as a package instead of in pieces," she said.
The Affordable Housing Bill and the Municipal Planning Fund bills gained the support of local governments in principal, but minor revisions were apparently required to gain overall approval.
APA spokesman Keith McKeever says the agency is making substantive changes based on the recommendations of local government officials.
"We are hoping we will get a sponsor in the Assembly and the bills in the Senate will be moved," he said.
The Affordable Housing Bill would allow four structures to be built in low- and moderate-intensity zones that under existing APA regulations would only accommodate one - as long as the property is relatively close to a "town center."
An early version of the Bill cited that APA approval of such development would hinge on the structures sharing a single septic system. But Local officials argued that the shared septic system would be highly cost prohibitive, and the APA subsequently axed the requirement, and reduced the required distance from navigable waters from 1/4 mile to a tenth of a mile.
The revised bill gained state Senate sponsorship from powerful downstate Democrat Carl Kruger.
"Now under this new bill, due to provisions made with local government and AATV, if the site has adequate soils for individual septic we will no longer require a shared septic system," McKeever said. "It will be more of a case-by-case and site-by-site determination."
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Reed: 'I'm embarrassed for the whole city'
Reed: 'I'm embarrassed for the whole city'
Even though the offense failed the defense in Sunday's 34-17 loss to the Denver Broncos by giving away points and failing to convert on third downs, safety Ed Reed took the Ravens' third consecutive loss hard.
Broncos quarterback Peyton Manning only threw for 204 yards, with 51 coming on his only TD throw to Eric Decker in the third quarter for a 24-3 lead. Ravens QB Joe Flacco had two turnovers that turned into 10 points as his team went down 17-0 at the half thanks to a 98-yard interception return by Chris Harris.
The Ravens, who have lost three games in a row with two coming at home, started 0-for-9 on third downs and didn't get a first down until 21 minutes had elapsed in the game.
Still, said Reed: "I'm embarrassed as a player to come out and perform the way we have. You have weeks like that. We're not the only team that lost today. We still have two more games but as a Ravens Nation, as a player, I'm embarrassed for the whole city."
A victory would've clinched the AFC North for the Ravens (9-5), who have to wait until the New York Giants come to M&T Bank Stadium next week. The Giants were shut out 34-0 by the Atlanta Falcons.
Reed credited the kicking unit of punter Sam Koch, long snapper Morgan Cox and kicker Justin Tucker. And that was it.
"We didn't play a great game," Reed said. "The best three players today that only came to work were Morgan, Sam and Tucker."


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January 24, 2011
BENTON TOWNSHIP, MI – It will be raining cats, dogs, and laughs at the Lake Michigan College Mendel Center Mainstage at 3 p.m. and 7 p.m. on Sunday, February 19, when Gregory Popovich and his Comedy Pet Theater perform.
Simply said, this show is a comedy act that includes 15 house cats, 10 dogs, four geese, eight doves, two parrots and a juggler that do astonishing tricks.
Popovich, the human star, started out following in his family footsteps as a master juggler and international star of the Moscow Circus for 15 years. Settling in the U.S., he began to look for new things to add to his act. Knowing that adding one more ball or ring would not impress his audience, he added a house cat. Audiences loved watching the furry critter on stage. Cats doing stunts and tricks is extraordinary and impresses cat lovers and non-cat lovers. Adding dogs and birds to the act gave Popovich a winning formula.
Popovich rescued his furry co-performers from Las Vegas animal shelters and taught them to be stars. Comedy Pet Theater, voted the Best Family Attraction in Las Vegas, is now a mainstay at the Planet Hollywood Hotel and Casino. Opening in the '90s, it quickly became a favorite "must see" act for visitors and stars. The animal, juggling and comedy act has appeared on Animal Planet, The Tonight Show with Jay Leno and The Late Show with David Letterman. The show's stars, Gregory, Rex and Sebastian, also have made their own TV miniseries.
Penn Jillette, of the Penn & Teller duo, probably best describes the appreciation of Popovich's ability to get house cats to perform on cue, "Its genius. It's like getting rocks to dance."
There will be a Special Animal House Party with a kid friendly buffet starting at 5 p.m. Buffet tickets are $5 for children under 12, and $10 for adults.
Tickets for the Comedy Pet Theater performance and Special Animal House Party are available by calling (269) 927-1221. Students (kindergarten through college) and senior adults (60 and over) receive a 10 percent discount off single ticket prices. Special group rates are available to parties of 20 or more. These groups receive 15 percent savings on ticket prices. For further information about group rates and special arrangements, call the group coordinator at (269) 927-8109 or e-mail questions to email@example.com.
The Popovich Comedy Pet Theater performance is sponsored by 97.5 Y Country.
The 1,517-seat Mendel Center Mainstage offers state-of-the-art acoustics and comfortable seating in elegant surroundings. Other amenities include free, lighted parking; handicap accessibility (inside and out); an array of special services; and friendly ushers and support personnel.
The Mendel Center is within a 30-minute drive of Niles and within a 40-minute drive of Kalamazoo or South Bend. Located on the Napier Avenue campus of Lake Michigan College, the Mendel Center is one mile east of I-94 on Napier Avenue (Exit 30) in Benton Township, Michigan.
1 (800) 252-1562 or (269) 927-1000


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The Armed Man - A Mass for Peace
Sunday 28 Sep 2014, 3.00pm
Royal Albert Hall, London
Malcolm Goldring conductor
Gounod, 'Judex', Mors et Vitabiography
Beethoven, Symphony No. 5biography | programme note
A chorus of 600 young voices marks the 100th anniversary of the outbreak of the First World War.
This Sing UK project will bring together young people from the UK, France, Belgium and Germany; the Philharmonia Orchestra, conducted by Malcolm Goldring; and four international soloists in a landmark performance of Karl Jenkins' The Armed Man.
This performance will be the first of a number of Sing UK events between 2014 and 2018 marking the important centenary years of the First World War.
- Beethoven - Symphony No. 5


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Now where was I? It's been so long since I've posted... I can't remember.
Oh yes, New York. I know you were all eagerly awaiting this next post. Heh. Because I did some craaaaazy stuff after the cook-off in the two hours I had before I left. Wild, wild stuff.
After the cook-off I was lucky enough to meet one of my readers, Tina, and her sister. Tina, I'm sorry, I can't remember your sister's name! Bahhh! I'm so mad at myself. I think it might start with a D?
Anyway, Tina and her sister were visiting the city, and I got to meet them. They were both very, very nice, and we're all going to start a bakery someday. This was definitely one of the highlights of my trip! I've never met anyone that reads my blog. I feel honored. I can't believe you all actually visit here and read this crap. I'm not exactly a great writer. Or photographer.
So I was very hungry after the cook-off because I hadn't eaten anything all day, and it was lunchtime. My friend, Sue, told me about this place called Shake Shack, located in Madison Square Park (right where the cook-off was held!). It's a modern day "roadside burger" stand serving burgers, hot dogs, fries, frozen custard and beer. It sounded realllly good, and I was right in the area, so I wandered over to check it out.
There was this huge line. I mean, huge. I was starving, so there was no way I could wait in line. They had this shorter line where you could stand and wait for frozen custard, only, so that's what I did. I wanted to hate this place, and the frozen custard, because of their ridiculously long line, but when I tasted my vanilla frozen custard, all was forgotten. SO GOOD! Oh-so-good. Creamy, smooth, delicious. I NEED MORE.
Frozen custard wasn't going to cut it; I needed real food to eat. I was hungry for a burger and fries, because I had my heart set on stupid Shake Shack (thanks a lot, Sue), and I was lucky enough to stumble across New York Burger Co.
Now let's pause here and refect on my life a bit. I was a vegetarian for many years. Even when I started eating meat again, I wouldn't eat burgers. Especially medium-rare burgers... because I watched an episode on ecoli, on 20/20, when I was a child, and it scarred me... not for life, apparently, as I eat them medium rare-medium now.
Within the last year-or-two, I have developed a passion for a really good burger. New York Burger Co. had a selection of interesting burger choices. Hello?? The Chicago Burger sounds amazing. This place has also won a lot of awards, so I was smitten. I ordered a mini-cheeseburger with sweet potato fries. And because one deep-fried side wasn't enough for me, I ordered onion rings. And a variety of different sauces (I could drink the chipotle-honey). Everything was delicious! I have no complaints. Only that I couldn't finish my deep-fried sides.
And... that was pretty much my day. I stopped at this deli/bakery, picked out a variety of cookies, and sat in Madison square park and nibbled at them while doing some people-watching. They were all just okay. Tasted kind of like they had been sitting around in a deli/bakery for a couple of days.. aborbing all kinds of meat smells. But I ate them anyway, ha. Well, some of them. I brought some home for my family to try. I even brought black and white cookies back to my darling boyfriend and sister.
Here's my first rainbow cookie! I hope they're usually better than this. This one tasted greasy and old. And a little like pastrami.
Then I walked to my hotel, got my stuff and headed for the airport. You see how short this trip was? That's probably good, because this was a massive, massive post, and it only covered a few hours. I'm sorry.
Of course I need to give you the recipe I made at the cook-off! I almost forgot. So this is a very good recipe, even though it didn't win. I made these again the other day, and received rave reviews. So give them a try sometime. It's a moist cake doused with toffee sauce, vanilla ice cream, and a walnut-oatmeal praline (aka - granola).
Cooking spray
1/3 cup water
1/3 cup chopped dates (sugar coated kind)
1/2 teaspoon baking soda
1/2 cup all-purpose flour
1/2 teaspoon baking powder
1/8 teaspoon salt
2/3 cup Quaker Old Fashioned Oats
1/4 cup unsalted butter, softened
3 tablespoons granulated sugar
1 large egg
1 teaspoon vanilla extract
Toffee Sauce
3 tablespoons unsalted butter, softened
1/2 cup firmly packed brown sugar
1/2 cup milk
Salted Walnut-Oatmeal Praline
2 tablespoons unsalted butter, softened
1/4 cup firmly packed brown sugar
1/4 teaspoon ground cinnamon
1/4 teaspoon salt
1/4 cup finely chopped walnuts
1/4 cup Quaker Old Fashioned Oats
Vanilla ice cream, if desired
Preheat oven to 350 degrees F. Spray 4 muffin cups with cooking spray.
Combine water, dates and baking soda in a small saucepan over medium heat; bring to a boil, whisking occasionally. Remove pan from heat and set aside.
In a medium sized mixing bowl, whisk together flour, baking powder, salt and 2/3 cup oats until combined.
In large mixing bowl, using a mixer on medium speed, beat together 1/4 cup butter and granulated sugar until creamy. Beat in egg and vanilla until combined; beat in date mixture until combined. Reduce mixer speed to low and beat in flour mixture until just combined; divide batter into prepared muffin cups. Bake for 14-15 minutes or until light golden brown - do not overbake. Run a knife around outer edges and invert onto a wire rack to cool 5 minutes. Slice about 1/4-inch off of the tops of cakes. Top with half of the toffee sauce* and let the cakes absorb the sauce for a minute. Flip the cakes over, plate, and top with remaining sauce, ice cream and praline**.
*To make the toffee sauce: melt 3 tablespoons butter in a small saucepan over medium heat; whisk in 1/2 cup brown sugar until well combined, and sugar starts to melt- about 2-3 minutes. Whisk in milk and bring mixture to a boil; simmer sauce, whisking frequently, over medium-low heat, until ready to serve. Basically, you just let this sauce simmer away while the cakes are baking.
**To make the Salted Walnut-Oatmeal Praline: melt 2 tablespoons butter in a small saucepan over medium heat; whisk in 1/4 cup brown sugar and cook for 2 minutes or until sugar starts to bubble. Stir in cinnamon, 1/4 teaspoon salt, walnuts and 1/4 cup oats until combined. Cook mixture 3-4 minutes, stirring frequently, until golden brown and fragrant; scrape mixture into a large mass over waxed paper, and smooth and flatten evenly with a rubber spatula. When cool, break into pieces.
Makes 4 servings


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Sounds crazy: The U.S. Senate recently voted by unanimous consent to remove the word "lunatic" from federal law.
The goal?Reducing the stigma of mental illness.
That worthy cause was cited by North Dakota Democrat Kent Conrad and Idaho Republican Mike Crapo, Senate sponsors of the "21st Century Language Act." Conrad's case that "lunatic" must go: "Federal law should reflect the 21st century understanding of mental illness and disease. The continued use of this pejorative term has no place in the U.S. Code.''
The Mental Health Liaison Group wrote in support of the bill: "Deleting these terms from usage in the U.S. Code is a simple means of demonstrating respect for individuals living with mental health conditions and will have no effect on the underlying federal laws."
Well sure, "demonstrating respect for individuals living with mental health conditions" seems like a sweet idea.
After all, we all at least occasionally feel like we're about to jump the mentally balanced track.
Err ... don't we?And just as what is and isn't acceptable attire changes, so does what is and isn't acceptable wording. For instance, while some vile 21st Century lyrics wouldn't have been tolerated in 1966, a record that reached No. 3 on the Billboard charts that year poked fun at the mentally ill under the title "They're Coming To Take Me Away, Ha-Haaa!"
Trivia test: Who recorded that hit single? (answer at column's end)
Forty-six years later, the U.S. Senate is coming to take the word "lunatic" away from the U.S. Code — though none of those wacky House members have introduced their own bill to do the same thing yet. But not even federal lawmakers can eliminate the existence of people who can accurately — albeit harshly by today's sensibility standards — be described as lunatics.
Some folks can even be correctly branded homicidal maniacs. Charles Manson comes to mind.
So does a confessed wholesale killer who inflicted his human slaughter more than four decades after Manson's:
Anders Breivik shot 69 people to death last July at a summer camp in Norway in what he later called a blow against the menace of multiculturalism. Breivik also called himself "Europe's most perfect knight since World War II."
Yet he was judged fit to stand trial due to mental health experts' revised assessment that he was not psychotic during those attacks. Instead, they ultimately deemed him an "extreme narcissist."
Does that mean it's still OK to call somebody a narcissist?
Does the modern zeal for "demonstrating respect for individuals living with mental health conditions" require us to avoid hurting that mass-murdering Norwegian nut case's feelings?
Regardless of how you answer that, what you saw in your last ink-blot test at your shrink's office or which prescription drugs are now moderating your moods, just make sure that you don't call Heather Webber "crazy."
OK, so that's kind of a crazy warning considering that Heather's a soap-opera character, not a real person.
But she is a really scary resident of Port Charles, the setting of ABC's "General Hospital." Released a while back from a lunatic asylum — oops, mental health facility — due to the naivete of her son Dr. Steve Webber, Heather has somehow remained on the loose despite being clearly tetched in the head.
And that sicko psycho Heather becomes downright unhinged when anybody calls her — or anybody she likes — "crazy."
Ponder the sad fate of Dr. Maggie Wurth, Steve's ex-girlfriend and accomplice in pulling the plug on a brain-dead arch-criminal to save an innocent patient who needed his heart.
Heather, freshly sprung from the nervous hospital, was acting blatantly "mental" when Maggie first met her. Unaware that Heather was deranged, or that she was Steve's mom, Maggie told her she sounded crazy.
Bad move. That made Heather, already quite mad in the insane sense, extremely mad in the angry sense.
So Heather poisoned Maggie's cup of tea — and made it look like suicide.
Sure, that sounds crazy, too.But so does the U.S. Senate, which hasn't passed a federal budget in three years, taking the time to pass a bill erasing "lunatic" from U.S. law.
As for readers who detect lunacy in checking into "General Hospital" to make a point (but which one?), please:
Demonstrate respect for individuals living vicariously in Port Charles.
Trivia answer: Napoleon XIV.Frank Wooten is assistant editor of The Post and Courier. His email is firstname.lastname@example.com.
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aggregation explicitly? Second, if the conditions are satisfied, and one computes a COLI for a representative agent, what relationship does this COLI bear to the COLIs of the underlying consumers?
We begin with a definition. The representative consumer of consumer theory is not defined to be representative of tastes or of levels of living but of behavior. The economic theory of consumer behavior works with a single person who is assumed to be greedy (always wants more), to make consistent choices, and to do the best to satisfy his or her desires within a fixed budget at a fixed set of prices. As a result of doing the best he or she can, each person will have demand functions that relate the amount demanded of each good to income and to the prices of all the goods. Because different people have different tastes and live in different socioeconomic and physical environments, these demand functions will generally differ from person to person, even if they have the same level of income and face the same prices. For the economy as a whole, one can sum (or average) the demand functions of each person to get the aggregate (or average) demand for each good in the economy as a function of prices and the incomes of each person in society. The representative consumer exists if this aggregate can be thought of as coming from a single consumer whose behavior replicates the aggregate of all consumers. Note again that this definition is in terms of behavior, not tastes or welfare.
In general, this construction cannot work, and for a very obvious reason. According to the theory of individual behavior, demand is a function of income and all the prices. But aggregate demand is a function of all the incomes and all the prices. The distribution of income between people matters for the aggregate but has no part in the theory of individual behavior. The representative consumer demands goods according to her representative income and the prices, and there is generally no way in which all the possible effects of the distribution of income can be captured through a single representative income. So the representative consumer cannot exist in general.
There are special cases where the distribution of income has no effect on aggregate demands: when each consumer spends his or her marginal dollar in exactly the same way. If so, taking a dollar from A will shrink A's demands for goods in exactly the same way as giving the dollar to B will expand B's demands for goods. As a result, the total demand for each good in the economy depends only on total income, not on who owns that income. Total income will work as representative income, and the representative agent exists.
How realistic is this condition? For it to hold exactly is clearly absurd; no one would seriously claim that everyone in the economy spends an additional dollar in exactly the same way so that, at the margin, all consumers are identical. A more serious question is whether, at the level of aggregation in the CPI (about


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Black accent chairs will take your room from boring to brilliant
In any room in your home there's that one statement piece of furniture that chair, that bookshelf, that piece of art work that takes your room from boring to brilliant. In many rooms that statement piece is also your favorite thing in the room. Now, while we all love a great piece of wall art, wouldn't you rather be able to curl up in statement piece and read a good book and sip on some Merlot?
Chic, functional, and comfortable
Black accent chairs are not only chic, they're functional too. It's important that when you pick out your black accent chair that you choose it for more than just looks. You want to be able to sit in this chair and feel comfortable and for more than just a minute.
Many people who purchase furniture only sit on the piece they're intending to buy for about one minute. Anything can be comfortable for one minute, so make sure to sit in your black accent chair for three to five minutes to really get a feel for how it makes you feel. Because honestly, it does you no good to have a stunning statement piece that one will ever want to sit on.
Black accent chairs we know you'll love:
Armen Living Hampton Wingback Chair: You will love this classic wingback chair with a modern twist. Its seat is extra large, and its arm-less design makes it perfect for curling up in with a good book. This modern wingback accent chair would look stunning in your study, bedroom, or living room.
Black Swirl Upholstered Accent Chair: You'll never want to get out of this modern black swirl chair. While not the classic black accent chair its modern whimsical white swirl pattern will make it the statement chair in your room. With its arching back, tapered arms, and wood legs in a dark finish your accent chair will make you the envy of the block.
Baxton Studios Fiore Black Accent Chair: If you love all things modern you need this chair. This sleek and sophisticated chair has transparent legs that strongly contrast with its faux black leather seat and back.
If you find a black accent chair you love let us know with comments or pictures below!


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Sunday, February 3, 2013 - Saturday, February 16, 2013
8:00 pm - 10:15 pm
This event occurs every week on the following day(s): Friday Saturday Sunday
Cost: Tickets: $20 Adults, $15 Seniors/18 & Under
Sponsored by: Prince George's Little Theatre
In Moon Over Buffalo, a second-rate and dysfunctional theater company gets the chance of a lifetime when famed director Frank Capra plans to catch a matinee performance. Will the leading man sober up in time for curtain? Will his wife, the company's leading lady, run away with her agent? Will the company decide to present Private Lives or Cyrano or a disturbing mixture of both? Join us for this comedic valentine to theater hams everywhere & find out!
Event Contact Info:


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Call of Duty remains one of the most successful video game franchises, and most recognizable game brands, in the history of the medium.
The latest, Call of Duty: Ghosts, launches on PS3, Xbox 360, Wii U, and PC this Tuesday. It launches ten days later on the PlayStation 4 and the following week on Xbox One.
And while it will no doubt sell millions of units just like the past few games, it finds itself in a bit of a peculiar situation this year: Right at the heart of the controversy surrounding the PS4 and Xbox One.
To make a long story short, the upcoming consoles from Sony and Microsoft have been the hot news item of the year, ever since the reveal of the PS4 in February and the pre-E3 reveal of the Xbox One.
The controversy has shifted form over the intervening months. It began with Microsoft's peculiar used games policies, which gave publishers rights over whether or not games could be sold second-hand or not, and continued with the news that the Xbox One would require a daily internet login to function.
That was heightened by the NSA's spying program revelations and news that Microsoft, among many other US tech companies, had given the government access to their data. As quickly as these policies and surprises landed, Microsoft started to change them, but in many ways the game was already lost. Sony had momentum while Microsoft played catch-up.
Now the controversy has morphed once again. While the hardware for both systems hasn't been fully analyzed (since they're not out yet) the PS4 has generally been seen as the more powerful of the two units. And here's where Call of Duty: Ghosts comes to into play.
Recently Infinity Ward's Mark Rubin revealed that the Xbox One version of the game would run at 720p (upscaled to 1080p) and the PS4 version would run at a native 1080p. This followed similar revelations about Battlefield 4 as well as the fact that upcoming shooter Titanfall (made by former Call of Duty developers) would also run at 720p on the Xbox One.
In other words, many people who believed that the next-gen systems would be roughly on par power-wise and that games would make the natural, evolutionary leap to 1080p are starting to worry, at least about the Xbox One.
Now, I've said before that I think this is less of an issue than many people are making it out to be. Don't get me wrong, I think it's a very important thing to take into consideration when purchasing a next-gen video game console.
Knowing the difference between competing options is integral to making a smart purchase. The fact that the PS4 is currently outputting at a higher resolution certainly seems to indicate that it's a stronger system (though we don't know all the details yet) and that, along with the price-gap of $100 (in Sony's favor,) are both going to factor into many peoples' decision. As well they should. Being a smart consumer is important—far more important than being angry at a corporation.
On the other hand, a lot of console gamers probably won't care.
I know people are aghast when I say this, but the vast majority of people playing games aren't forum posters at NeoGaf or reddit; the vast majority of gamers aren't regular commenters on video game blogs and don't spend their time reading about video games. It's like in politics: Political junkies latch onto every detail in the news, read all the blogs, write passionate (or abusive) comments, and assume that everyone else is just like them and cares just as much.
But that's not the case, and it's not the case with people who purchase consoles either. You don't buy a PS4 because it has higher resolution if you're a big Halo fan. You don't buy an Xbox One because it comes with a Kinect if you're a big Uncharted fan.
Over at Cinema Blend, William Usher—whose work I often admire—argues that the gaming media is defending Microsoft by downplaying the resolution differences. I disagree.
I think the gaming media understands the intended audience for different gaming platforms.
Usher makes a simple mistake. He likens the discussion of the Xbox One and PS4 to the discussions we see each year over PC graphics cards:
The last I checked, if a benchmark for a GPU from Nvidia trumps AMD at stable frames at twice the resolution, it's not even a debate about longevity or efficiency, we simply acknowledge that AMD lost in the benchmarks and it's a weaker card. Period.
I can't even begin to fathom if there were benchmarks for a card that cost $100 more and performed – in some cases – at half the performance level of the competition, what the articles would look like. Heck, there was definitely a lot of hoopla over the 7990 vs the Titan, and most enthusiasts made it known that the price to performance difference was not negligible.
You have to understand something about GPUs. They're benchmarked by multiple websites all the time. New graphics cards at the low, mid, high, and ultra-high end come out each year or so and they're compared endlessly. Even just a handful of extra frames-per-second is a huge deal to the hardcore enthusiast crowd.
Cards with nVidia and AMD chips on board are made by multiple vendors, and even the same exact chip is compared across these vendors and pored over by PC builders whose love of gaming is often rivaled by the love of the gear that goes into their boxes.
Such is not the case with consoles. The reason people play on one console over another is almost never about power.
Indeed, consoles are the antitheses of this sort of gear obsession. They aren't customizable. You don't upgrade them each year. You don't overclock the CPU or run two GPUs side-by-side. You just plug and play, end of story. And the type of gamer (on average) who is drawn to consoles is also the type that doesn't get off on extensive research into the fastest available motherboard, RAM, CPU, and GPU. You don't equip your PS4 with water-cooling.
This isn't to say that price-to-performance isn't a factor.
I'd simply argue that the resolution difference is not nearly as big a deal as the price difference to the target demographic. You can disagree with that, but you need to remember that if you're reading this and feel compelled to comment, then you probably aren't the target demographic.
Even if you are a console gamer, or one of the many people claiming to have cancelled their Xbox One pre-order, etc. you need to realize that you still probably aren't the average console gamer. The very fact that you're out pre-ordering suggests you're more of an enthusiast than many gamers, and that you pay closer attention to the news and to every little detail. And perhaps every little pixel, too.
But consoles don't live or die on power alone. Price is a factor, but probably also not the biggest one. This simply isn't a discussion of the relative prowess of two annual graphics cards. Not even close.
That's why I said that if you really care about this, you should just build yourself a gaming PC. Not because it shouldn't be a factor in your decision-making, but because consoles are less about sheer horsepower and more about convenience and exclusive games.
Even all the little extras like social media integration, Kinect, and so forth won't save or doom these systems. It's all about the games. Which system has the best games? Which system has the best online service? For games like Call of Duty: Ghosts, the online experience is crucial. And for all of that we'll need to wait and see.
P.S. Please refrain from silly complaints that I'm "defending Microsoft" or that this is a "paid article" from Microsoft. That sort of childish nonsense is irritating and boring at this point. I've already said that the PS4 is my console of choice. Though I'll certainly be getting both and expect there will be things I like and dislike about each.
Ghosts launches Tuesday. Here's a pretty funny live-action trailer to usher the game in—starring, sort of, Megan Fox:
Follow me on Twitter or Facebook. Read my Forbes blog here.
Also on Forbes:


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|These IRlox mutant mice have loxP sites flanking exon 4 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 4 in the cre expressing tissue(s). These "floxed" mice may be useful in studying insulin receptor function in several different tissues (including pancreas, liver, and skeletal muscle), as well as diabetes and glucose regulation.
Type Congenic; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Mating System Homozygote x Homozygote (Female x Male) 16-FEB-11 Species laboratory mouse Generation N11+F11 (08-MAY-15)
Generation Definitions
Donating Investigator C. Ronald Kahn, Joslin Diabetes Center
Mice homozygous for this IRlox allele are viable and fertile. These mutant mice have loxP sites flanking exon 4 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 4 in the cre expressing tissue(s). These "floxed" mice may be useful in studying insulin receptor function in several different tissues (including pancreas, liver, and skeletal muscle), as well as diabetes and glucose regulation.
For example, when crossed to a strain expressing Cre recombinase in the central and peripheral nervous system (see Stock No. 003771), this mutant mouse strain may be useful in studies of glucose homeostasis.
When crossed to a strain expressing Cre recombinase in skeletal and cardiac muscle (see Stock No. 006475), this mutant mouse strain may be useful in studies of diabetes.
When crossed to a strain expressing Cre recombinase in the liver (see Stock No. 003574), this mutant mouse strain may be useful in studies of insulin resistance.
When crossed to a strain expressing Cre recombinase in pancreatic beta cells (see Stock No. 003573), this mutant mouse strain may be useful in studies of diabetes.
A targeting vector was designed to insert a loxP-flanked neomycin cassette downstream of exon 4, as well as a single loxP site 80 bp downstream of exon 4 of the targeted gene. The construct was electroporated into the 129S4/SvJae-derived J1 embryonic stem (ES) cells. ES cell were transiently transfected with a Cre-recombinase plasmid to delete the selection cassette, leaving single loxP sites upstream and downstream of exon 4. Correctly targeted ES cells were injected into C57BL/6J blastocysts, which were injected into pseudopregnant CD-1 foster females. The resulting mutant mice (IRlox) were backcrossed to C57BL/6J inbred mice. At some point, mice were bred to Mck-Cre transgenic mice (FVB genetic background, see Stock No. 006405). The double mutants were backcrossed for 10 generations to C57BL/6 mice and then selected for the IRlox (and against the transgene) prior to arrival at The Jackson Laboratory.
A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background.
|Considerations for Choosing Controls
Strains carrying other alleles of Insr
002939 B6.129S4-Insrtm1Dac/J 002426 B6;129S4-Insrtm1Dac/JView Strains carrying other alleles of Insr (2 strains)
Introduction to Cre-lox technology
View Related Disease (OMIM) TermsRelated Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.Diabetes Mellitus, Insulin-Resistant, with Acanthosis Nigricans (INSR)
Donohue Syndrome (INSR)
Hyperinsulinemic Hypoglycemia, Familial, 5; HHF5 (INSR)
Pineal Hyperplasia, Insulin-Resistant Diabetes Mellitus, and Somatic Abnormalities (INSR)
View Mammalian Phenotype TermsMammalian Phenotype Terms provided by MGIassigned by genotype
The following phenotype relates to a compound genotype created using this strain.
Contact JAX® Services email@example.com for customized breeding options.
Insrtm1Khn/Insrtm1Dac Tg(Ckmm-cre)5Khn/0involves: 129S4/SvJae * C57BL/6J * FVB (conditional)
- homeostasis/metabolism phenotype
- hyperglycemia
- in the fed state, incomplete penetrance (MGI Ref ID J:51266)
- increased circulating insulin level (MGI Ref ID J:51266)
Insrtm1Khn/Insrtm1Khn Tg(Alb-cre)21Mgn/0involves: 129S4/SvJae * C57BL/6J * DBA/2 * FVB (conditional)
- homeostasis/metabolism phenotype
- abnormal circulating serum albumin level
- at 6 months, mutant mice display a 50% reduction in serum albumin levels (MGI Ref ID J:63878)
- abnormal glucose homeostasis
- at 2 months, male mutants fail to suppress hepatic glucose output in response to insulin administration, despite intact insulin signaling in adipose tissue and nearly normal insulin signaling in muscle (MGI Ref ID J:63878)
- abnormal insulin clearance
- in addition to increased insulin secretion, 11-week-old male mutants show a 75% reduction in the C-peptide:insulin ratio, indicating decreased insulin clearance (MGI Ref ID J:63878)
- hyperglycemia
- at 2 months, male mutants exhibit significantly elevated blood glucose in the fed state, despite a 20-fold increase in insulin levels relative to control mice; in contrast, glucagon levels remain unaffected (MGI Ref ID J:63878)
- at 2 months, male mutants also display a mild hyperglycemia in the fasted state, despite a 7-fold increase in serum insulin levels (MGI Ref ID J:63878)
- unexpectedly, as mutant mice age, the elevated fasting blood glucose levels progressively decline; by 6 months of age, mutants exhibit fasting hypoglycemia rather than hyperglycemia (MGI Ref ID J:63878)
- impaired glucose tolerance
- increased circulating insulin level
- at 2 months, male mutants exhibit an extreme increase in serum insulin levels (20-fold in fed state; 7-fold in fasted state) (MGI Ref ID J:63878)
- increased insulin secretion
- at 6 months, female mutants show a have 5- to 6-fold increase in pancreatic insulin content measured in acid-ethanol extracts (MGI Ref ID J:63878)
- insulin resistance
- at 2 months, random-fed male mutants are severely resistant to the blood glucose-lowering effects of exogenously administered insulin (MGI Ref ID J:63878)
- abnormal lipid homeostasis (MGI Ref ID J:63878)
- decreased circulating free fatty acid level
- at 2 months, male mutants show a 40-50% reduction in the levels of serum free fatty acids (MGI Ref ID J:63878)
- decreased circulating triglyceride level
- at 2 months, male mutants show a 40-50% reduction in the levels of serum triglycerides (MGI Ref ID J:63878)
- increased bile salt level
- mutant gallbladders show a notable increase in bile volume (MGI Ref ID J:92861)
- increased circulating alkaline phosphatase level
- at 6 months, mutant mice show a 50% increase in alkaline phosphatase levels, suggesting biliary tract dysfunction (MGI Ref ID J:63878)
- increased circulating aspartate transaminase level
- liver/biliary system phenotype
- abnormal liver morphology
- at 2 months, mutant livers appear a little darker in color, with areas of focal dysplasia and reduced glycogen storage in the parenchyma; no steatosis is observed (MGI Ref ID J:63878)
- at 6- to 12-months of age, mutant livers display multiple hyperplastic pale nodules scattered throughout all lobes (MGI Ref ID J:63878)
- by 12 months, the normal lobular structure is disrupted; hyperplastic nodules consist of highly vacuolated cells that compress the adjacent normal tissue, in the absence of fibrosis (MGI Ref ID J:63878)
- abnormal hepatocyte morphology
- at 6 months, mutant hepatocytes exhibit a moderate increase in lipid accumulation; only a few electron-dense glycogen granules are observed (MGI Ref ID J:63878)
- small liver
- at 2 months, mutant livers are 40% smaller than those of age- and gender-matched controls; liver size decreases significantly with increasing age (MGI Ref ID J:63878)
- abnormal liver physiology
- insulin resistance in liver results in elevated expression of PEPCK, the rate-limiting enzyme for gluconeogenesis, and reduced expression of glucokinase and liver pyruvate kinase, two enzymes critical for glucose utilization (MGI Ref ID J:63878)
- the mutant liver appears to be chronically geared toward glucose production; early insulin signaling events, such as IRS-1 and IRS-2 phosphorylation, are lost (MGI Ref ID J:63878)
- enlarged gallbladder
- at 6- to 12-months of age, mutant gall bladders appear enlarged (MGI Ref ID J:63878)
- endocrine/exocrine gland phenotype
- enlarged gallbladder
- at 6- to 12-months of age, mutant gall bladders appear enlarged (MGI Ref ID J:63878)
- increased insulin secretion
- at 6 months, female mutants show a have 5- to 6-fold increase in pancreatic insulin content measured in acid-ethanol extracts (MGI Ref ID J:63878)
- increased pancreatic beta cell mass
- pancreatic islet hyperplasia
- at 6 months, mutant mice show an adaptive islet hyperplastic response to insulin resistance (MGI Ref ID J:92861)
- cellular phenotype
- increased mitochondria size
- at 6 months, mutant hepatocytes exhibit giant mitochondria (MGI Ref ID J:63878)
- growth/size/body region phenotype
- postnatal growth retardation
Insrtm1Khn/Insrtm1Khn Tg(Alb-cre)21Mgn/0involves: 129S4/SvJae * C57BL/6 * DBA/2 (conditional)
- homeostasis/metabolism phenotype
- decreased circulating glucose level
- at 10 to 12 months of age (MGI Ref ID J:121640)
- hyperglycemia
- while mice display normoglycemia during the first 3 weeks of life, at 4 weeks mice develop hypoglycemia that lasts until week 6 (MGI Ref ID J:121640)
- impaired glucose tolerance (MGI Ref ID J:121640)
- increased circulating insulin level (MGI Ref ID J:121640)
- insulin resistance (MGI Ref ID J:121640)
- endocrine/exocrine gland phenotype
- increased pancreatic beta cell mass
- at 2 weeks beta cell mass is increased 2-fold and at 6 weeks 4-fold compared to in wild-type mice due to increased mitosis of beta cells (MGI Ref ID J:121640)
- at 10 to 12 months of age, mice exhibit a 27-fold increase in beta cell mass due to an 8-fold increase in proliferating beta cells with a slight increase in apoptosis (MGI Ref ID J:121640)
Insrtm1Khn/Insrtm1Khn Tg(Alb-cre)21Mgn/0 Tg(Ins2-cre)25Mgn/0involves: 129S4/SvJae * C57BL/6 * DBA/2 (conditional)
- mortality/aging
- premature death
- 82% of mice die by 6 weeks of age with some mice surviving a few weeks longer (MGI Ref ID J:121640)
- homeostasis/metabolism phenotype
- decreased insulin secretion (MGI Ref ID J:121640)
- hyperglycemia
- impaired glucose tolerance (MGI Ref ID J:121640)
- increased circulating insulin level (MGI Ref ID J:121640)
- insulin resistance (MGI Ref ID J:121640)
- endocrine/exocrine gland phenotype
- decreased insulin secretion (MGI Ref ID J:121640)
- renal/urinary system phenotype
- polyuria
- during terminal stages (MGI Ref ID J:121640)
- behavior/neurological phenotype
- polydipsia
- during terminal stages (MGI Ref ID J:121640)
- digestive/alimentary phenotype
- *normal* digestive/alimentary phenotype
- unlike mice null for Insr in beta cells mice, islet cell mass is not increased despite similar levels of elevated insulin levels (MGI Ref ID J:121640)
- growth/size/body region phenotype
- decreased body weight
- mice develop severe diabetes and loss 30% of their body weight in terminal stages (MGI Ref ID J:121640)
Insrtm1Khn/Insrtm1Khn Tg(Ckmm-cre)5Khn/0involves: 129S4/SvJae * C57BL/6J * FVB (conditional)
- adipose tissue phenotype
- abnormal fat pad morphology
- larger than normal fat depots in fat pads, including the perianal, subcutaneous and perigonadal fat pads (MGI Ref ID J:51266)
- homeostasis/metabolism phenotype
- *normal* homeostasis/metabolism phenotype
Insrtm1Khn/Insrtm1Khn Tg(Ckmm-cre)5Khn/0involves: 129S4/SvJae * C57BL/6 * FVB (conditional)
- cardiovascular system phenotype
- *normal* cardiovascular system phenotype
- heart function and morphology is normal (MGI Ref ID J:118987)
- growth/size/body region phenotype
- *normal* growth/size/body region phenotype
- mice exhibit normal growth rates (MGI Ref ID J:118987)
- homeostasis/metabolism phenotype
- *normal* homeostasis/metabolism phenotype
- mice exhibit normal glucose homeostasis (MGI Ref ID J:118987)
Insrtm1Khn/Insrtm1Khn Tg(Ins2-cre)25Mgn/0involves: 129S4/SvJae * C57BL/6 * DBA/2 (conditional)
- mortality/aging
- increased sensitivity to induced morbidity/mortality
- when fed a high fat diet, 30% of mice die by 16 weeks (MGI Ref ID J:121640)
- premature death
- some mice die due to severe hyperglycemia (MGI Ref ID J:121640)
- homeostasis/metabolism phenotype
- decreased insulin secretion (MGI Ref ID J:121640)
- hyperglycemia
- mice exhibit an increase in serum glucose level on a regular diet and a severe increase when fed a high fat diet (MGI Ref ID J:121640)
- impaired glucose tolerance
- endocrine/exocrine gland phenotype
- decreased insulin secretion (MGI Ref ID J:121640)
- decreased pancreatic beta cell mass
- mice exhibit decreased beta cell mass when fed a normal or high fat diet (MGI Ref ID J:121640)
Insrtm1Khn/Insrtm1Khn Tg(Nes-cre)1Kln/0involves: 129S4/SvJae * C57BL/6J * SJL (conditional)
- adipose tissue phenotype
- increased white adipose tissue amount
- behavior/neurological phenotype
- polyphagia
- endocrine/exocrine gland phenotype
- abnormal seminiferous tubule morphology
- Leydig cell hypoplasia (MGI Ref ID J:64790)
- decreased corpora lutea number (MGI Ref ID J:64790)
- impaired ovarian folliculogenesis
- reduced number of antral follicles (MGI Ref ID J:64790)
- growth/size/body region phenotype
- increased body weight
- homeostasis/metabolism phenotype
- decreased circulating luteinizing hormone level
- increased circulating insulin level
- increased circulating leptin level
- increased circulating triglyceride level
- both males and females exhibit a 30% increase in circulating triglycerides (MGI Ref ID J:64790)
- insulin resistance
- females exhibit blunted response when injected with insulin and males performed similarly to controls (MGI Ref ID J:64790)
- nervous system phenotype
- *normal* nervous system phenotype
- brain weights and general brain histology appeared similar to controls (MGI Ref ID J:64790)
- reproductive system phenotype
- abnormal seminiferous tubule morphology
- Leydig cell hypoplasia (MGI Ref ID J:64790)
- abnormal spermatogenesis
- impaired (MGI Ref ID J:64790)
- oligozoospermia
- 30% reduced in epididymal sperm content (MGI Ref ID J:64790)
- decreased corpora lutea number (MGI Ref ID J:64790)
- impaired ovarian folliculogenesis
- reduced number of antral follicles (MGI Ref ID J:64790)
- reduced male fertility (MGI Ref ID J:64790)
Insrtm1Khn/Insrtm1Khn Tg(Nes-cre)1Kln/0involves: 129S4/SvJae * C57BL/6 * SJL (conditional)
- homeostasis/metabolism phenotype
- abnormal glucose homeostasis
- insulin-induced suppression of hepatic glucose productionas assessed with a euglycemic hyperinsulinemic clamp is attenuated (MGI Ref ID J:109359)View Research ApplicationsResearch ApplicationsThis mouse can be used to support research in many areas including:
Diabetes and Obesity Research
Insulin Receptors and Growth Factors
Research Tools
Cre-lox System
loxP-flanked Sequences
Diabetes and Obesity Research
|Allele Symbol
|Allele Name
|targeted mutation 1, Ronald Kahn
|Allele Type
|Targeted (Conditional ready (e.g. floxed), No functional change)
|Common Name(s)
|IR(lox); IRLox; IRflox; IRlox; Insrflox;
|Mutation Made By
|C. Ronald Kahn, Joslin Diabetes Center
|Strain of Origin
|Gene Symbol and Name
|Insr, insulin receptor
|Gene Common Name(s)
|4932439J01Rik; CD220; D630014A15Rik; HHF5; IR; IR-A; IR-B; RIKEN cDNA 4932439J01 gene; RIKEN cDNA D630014A15 gene;
|General Note
In conjunction with Tg(Mycha-cre)1Abel, this allele is knocked out specifically in cardiac muscle. The resulting mice are referred to as "Cardiac-specific insulin receptor knockout mice" or CIRKO.
In conjunction with Tg(Ckmm-cre)5Khn, this allele is disrupted specifically in skeletal muscle. The resulting mice are referred to as "Muscle-specific insulin receptor knockout mice" or MIRKO.
|Molecular Note
|Exon 4 was left flanked by single loxP sites after a downstream floxed neo cassette was removed via in vitro cre mediated recombination. Deletion of the resultant floxed fragment will result in a frameshift mutation that introduces a stop codon. Translation, if it were to occur, would putatively produce a truncated peptide consisting of 308 amino terminal residues and lacking the high affinity binding site, transmembrane domain, and kinase domain. [MGI Ref ID J:51266]
Genotyping ProtocolsGeneric Neo Melt Curve Analysis, MELT
Insrtm1Khn Alternate1, Standard PCR
Helpful LinksGenotyping resources and troubleshooting
Bruning JC; Michael MD; Winnay JN; Hayashi T; Horsch D; Accili D; Goodyear LJ; Kahn CR. 1998. A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 2(5):559-69. [PubMed: 9844629] [MGI Ref ID J:51266]
Insrtm1Khn related
Barger JL; Walford RL; Weindruch R. 2003. The retardation of aging by caloric restriction: its significance in the transgenic era. Exp Gerontol 38(11-12):1343-51. [PubMed: 14698815] [MGI Ref ID J:87701]
Bartels ED; Nielsen JM; Hellgren LI; Ploug T; Nielsen LB. 2009. Cardiac expression of microsomal triglyceride transfer protein is increased in obesity and serves to attenuate cardiac triglyceride accumulation. PLoS ONE 4(4):e5300. [PubMed: 19390571] [MGI Ref ID J:148263]
Baumgartl J; Baudler S; Scherner M; Babaev V; Makowski L; Suttles J; McDuffie M; Tobe K; Kadowaki T; Fazio S; Kahn CR; Hotamisligil GS; Krone W; Linton M; Bruning JC. 2006. Myeloid lineage cell-restricted insulin resistance protects apolipoproteinE-deficient mice against atherosclerosis. Cell Metab 3(4):247-56. [PubMed: 16581002] [MGI Ref ID J:129654]
Belke DD; Betuing S; Tuttle MJ; Graveleau C; Young ME; Pham M; Zhang D; Cooksey RC; McClain DA; Litwin SE; Taegtmeyer H; Severson D; Kahn CR; Abel ED. 2002. Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression. J Clin Invest 109(5):629-39. [PubMed: 11877471] [MGI Ref ID J:75348]
Biddinger SB; Haas JT; Yu BB; Bezy O; Jing E; Zhang W; Unterman TG; Carey MC; Kahn CR. 2008. Hepatic insulin resistance directly promotes formation of cholesterol gallstones. Nat Med 14(7):778-82. [PubMed: 18587407] [MGI Ref ID J:137829]
Biddinger SB; Hernandez-Ono A; Rask-Madsen C; Haas JT; Aleman JO; Suzuki R; Scapa EF; Agarwal C; Carey MC; Stephanopoulos G; Cohen DE; King GL; Ginsberg HN; Kahn CR. 2008. Hepatic insulin resistance is sufficient to produce dyslipidemia and susceptibility to atherosclerosis. Cell Metab 7(2):125-34. [PubMed: 18249172] [MGI Ref ID J:132137]
Biddinger SB; Miyazaki M; Boucher J; Ntambi JM; Kahn CR. 2006. Leptin suppresses stearoyl-CoA desaturase 1 by mechanisms independent of insulin and sterol regulatory element-binding protein-1c. Diabetes 55(7):2032-41. [PubMed: 16804073] [MGI Ref ID J:111873]
Bluher M; Kahn BB; Kahn CR. 2003. Extended longevity in mice lacking the insulin receptor in adipose tissue. Science 299(5606):572-4. [PubMed: 12543978] [MGI Ref ID J:82237]
Bluher M; Michael MD; Peroni OD; Ueki K; Carter N; Kahn BB; Kahn CR. 2002. Adipose tissue selective insulin receptor knockout protects against obesity and obesity-related glucose intolerance. Dev Cell 3(1):25-38. [PubMed: 12110165] [MGI Ref ID J:108968]
Bluher M; Patti ME; Gesta S; Kahn BB; Kahn CR. 2004. Intrinsic heterogeneity in adipose tissue of fat-specific insulin receptor knock-out mice is associated with differences in patterns of gene expression. J Biol Chem 279(30):31891-901. [PubMed: 15131119] [MGI Ref ID J:91903]
Bluher M; Wilson-Fritch L; Leszyk J; Laustsen PG; Corvera S; Kahn CR. 2004. Role of insulin action and cell size on protein expression patterns in adipocytes. J Biol Chem 279(30):31902-9. [PubMed: 15131120] [MGI Ref ID J:91902]
Boucher J; Charalambous M; Zarse K; Mori MA; Kleinridders A; Ristow M; Ferguson-Smith AC; Kahn CR. 2014. Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes. Proc Natl Acad Sci U S A 111(40):14512-7. [PubMed: 25246545] [MGI Ref ID J:216467]
Boucher J; Mori MA; Lee KY; Smyth G; Liew CW; Macotela Y; Rourk M; Bluher M; Russell SJ; Kahn CR. 2012. Impaired thermogenesis and adipose tissue development in mice with fat-specific disruption of insulin and IGF-1 signalling. Nat Commun 3:902. [PubMed: 22692545] [MGI Ref ID J:205635]
Boudina S; Bugger H; Sena S; O'Neill BT; Zaha VG; Ilkun O; Wright JJ; Mazumder PK; Palfreyman E; Tidwell TJ; Theobald H; Khalimonchuk O; Wayment B; Sheng X; Rodnick KJ; Centini R; Chen D; Litwin SE; Weimer BE; Abel ED. 2009. Contribution of impaired myocardial insulin signaling to mitochondrial dysfunction and oxidative stress in the heart. Circulation 119(9):1272-83. [PubMed: 19237663] [MGI Ref ID J:166005]
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Sotiropoulos KB; Clermont A; Yasuda Y; Rask-Madsen C; Mastumoto M; Takahashi J; Della Vecchia K; Kondo T; Aiello LP; King GL. 2006. Adipose-specific effect of rosiglitazone on vascular permeability and protein kinase C activation: novel mechanism for PPARgamma agonist's effects on edema and weight gain. FASEB J 20(8):1203-5. [PubMed: 16672634] [MGI Ref ID J:111347]
Swindell WR. 2009. Accelerated failure time models provide a useful statistical framework for aging research. Exp Gerontol 44(3):190-200. [PubMed: 19007875] [MGI Ref ID J:146582]
Symons JD; Hu P; Yang Y; Wang X; Zhang QJ; Wende AR; Sloan CL; Sena S; Abel ED; Litwin SE. 2011. Knockout of insulin receptors in cardiomyocytes attenuates coronary arterial dysfunction induced by pressure overload. Am J Physiol Heart Circ Physiol 300(1):H374-81. [PubMed: 20971769] [MGI Ref ID J:168410]
Tiwari S; Sharma N; Gill PS; Igarashi P; Kahn CR; Wade JB; Ecelbarger CM. 2008. Impaired sodium excretion and increased blood pressure in mice with targeted deletion of renal epithelial insulin receptor. Proc Natl Acad Sci U S A 105(17):6469-74. [PubMed: 18424559] [MGI Ref ID J:134541]
Ueki K; Okada T; Hu J; Liew CW; Assmann A; Dahlgren GM; Peters JL; Shackman JG; Zhang M; Artner I; Satin LS; Stein R; Holzenberger M; Kennedy RT; Kahn CR; Kulkarni RN. 2006. Total insulin and IGF-I resistance in pancreatic beta cells causes overt diabetes. Nat Genet 38(5):583-8. [PubMed: 16642022] [MGI Ref ID J:109011]
Ulanet DB; Ludwig DL; Kahn CR; Hanahan D. 2010. Insulin receptor functionally enhances multistage tumor progression and conveys intrinsic resistance to IGF-1R targeted therapy. Proc Natl Acad Sci U S A 107(24):10791-8. [PubMed: 20457905] [MGI Ref ID J:165059]
Vicent D; Ilany J; Kondo T; Naruse K; Fisher SJ; Kisanuki YY; Bursell S; Yanagisawa M; King GL; Kahn CR. 2003. The role of endothelial insulin signaling in the regulation of vascular tone and insulin resistance. J Clin Invest 111(9):1373-80. [PubMed: 12727929] [MGI Ref ID J:83275]
Vogt MC; Paeger L; Hess S; Steculorum SM; Awazawa M; Hampel B; Neupert S; Nicholls HT; Mauer J; Hausen AC; Predel R; Kloppenburg P; Horvath TL; Bruning JC. 2014. Neonatal insulin action impairs hypothalamic neurocircuit formation in response to maternal high-fat feeding. Cell 156(3):495-509. [PubMed: 24462248] [MGI Ref ID J:205557]
Welsh GI; Hale LJ; Eremina V; Jeansson M; Maezawa Y; Lennon R; Pons DA; Owen RJ; Satchell SC; Miles MJ; Caunt CJ; McArdle CA; Pavenstadt H; Tavare JM; Herzenberg AM; Kahn CR; Mathieson PW; Quaggin SE; Saleem MA; Coward RJ. 2010. Insulin signaling to the glomerular podocyte is critical for normal kidney function. Cell Metab 12(4):329-40. [PubMed: 20889126] [MGI Ref ID J:166544]
Wojtaszewski JF; Higaki Y; Hirshman MF; Michael MD; Dufresne SD; Kahn CR; Goodyear LJ. 1999. Exercise modulates postreceptor insulin signaling and glucose transport in muscle-specific insulin receptor knockout mice. J Clin Invest 104(9):1257-64. [PubMed: 10545524] [MGI Ref ID J:58296]
Wu S; Divall S; Wondisford F; Wolfe A. 2012. Reproductive tissues maintain insulin sensitivity in diet-induced obesity. Diabetes 61(1):114-23. [PubMed: 22076926] [MGI Ref ID J:191388]
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Yechoor VK; Patti ME; Ueki K; Laustsen PG; Saccone R; Rauniyar R; Kahn CR. 2004. Distinct pathways of insulin-regulated versus diabetes-regulated gene expression: an in vivo analysis in MIRKO mice. Proc Natl Acad Sci U S A 101(47):16525-30. [PubMed: 15546994] [MGI Ref ID J:123452]
Yoon JC; Puigserver P; Chen G; Donovan J; Wu Z; Rhee J; Adelmant G; Stafford J; Kahn CR; Granner DK; Newgard CB; Spiegelman BM. 2001. Control of hepatic gluconeogenesis through the transcriptional coactivator PGC-1. Nature 413(6852):131-8. [PubMed: 11557972] [MGI Ref ID J:120036]
Zabolotny JM; Haj FG; Kim YB; Kim HJ; Shulman GI; Kim JK; Neel BG; Kahn BB. 2004. Transgenic overexpression of protein-tyrosine phosphatase 1B in muscle causes insulin resistance, but overexpression with leukocyte antigen-related phosphatase does not additively impair insulin action. J Biol Chem 279(23):24844-51. [PubMed: 15031294] [MGI Ref ID J:122895]
Animal Health ReportsRoom Number AX10
Colony Maintenance
Breeding & Husbandry When maintaining a live colony, homozygous mice are bred. Mating System Homozygote x Homozygote (Female x Male) 16-FEB-11 Diet Information LabDiet® 5K52/5K67
|Pricing for USA, Canada and Mexico shipping destinations
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $239.00 Female or Male Homozygous for Insrtm1Khn
Price per Pair (US dollars $) Pair Genotype $478.00 Homozygous for Insrtm1Khn x Homozygous for Insrtm1Khn
Standard Supply
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.
|Pricing for International shipping destinations
Price per mouse (US dollars $) Gender Genotypes Provided Individual Mouse $310.70 Female or Male Homozygous for Insrtm1Khn
Price per Pair (US dollars $) Pair Genotype $621.40 Homozygous for Insrtm1Khn x Homozygous for Insrtm1Khn
Standard Supply
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.
|Considerations for Choosing Controls
|Control Pricing Information for Genetically Engineered Mutant Strains.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON's MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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