text: tag:blogger.com,1999:blog-142662752014-03-18T04:25:43.989+08:00See a lil bit of evil, Hear a lil bit of evil, Talk a lil bit of evilDchttp://email@example.com:blogger.com,1999:blog-14266275.post-5723387749039576062010-04-28T09:36:00.002+08:002010-04-28T09:46:59.731+08:00Back from PenangGood and bad news, Good news was, Penang was fun, eat sleep enjoy relax, run around the island.Bad news, came back home hear of my sis's house got broken into. SIEN. Hope the police can do something but highly doubt their capability. Last time my friend's house got broken into nothing was done other than come look see only.Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-55442458950014777512010-04-22T09:18:00.003+08:002010-04-22T09:20:12.238+08:00Glad to be going for a break this WeekendYay, going to Penang this weekend, hopefully it wouldn't be too hot, will take a leisurely drive up there, and have a free and easy time dozing around the island.Wanted to see how to train your dragon, but don't think can make it on time. Oh WellNote to self : Charge all camera batteries b4 going, clear all camera memory cards b4 going too ^^Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-90855612830020941052010-04-21T12:05:00.003+08:002010-04-21T12:13:10.601+08:00Haven't felt it this short beforeWahaha, don't think on the slanted side.Well i don't know why, but i have nose hairs growing thick and long, which is very irritating to my nostrils. Makes me sneeze and itch in the nose, People think i always dig my nose, but no, i was just scratching the itch.When they get too long, I have had this irritating painful habit of 'pulling' my nose hairs by gripping them with my fingers and giving Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-12417824441256437352010-04-12T16:35:00.000+08:002010-04-12T16:36:32.962+08:00Minor Minor Minor Tech ProblemsI wonder why these things happen, nobody can touch the servers other than us, but when we setup the servers, it all works fine, after afew weeks some things start to go awry. Drivers go missing on their own.X Files. Unknown reasonDchttp://email@example.com:blogger.com,1999:blog-14266275.post-58617860406217895332010-04-08T16:59:00.002+08:002010-04-08T17:01:11.054+08:00Cracking your head over quirky stuffHave you ever had something happen to you which you thought would not happen, but it happens anyhow, and that something actually shouldn't act like that, but it's acting that way which you have never encountered before.Well, today is one of those days which made me waste tons of time dwelling on these small little problems.No Solution yet, luckily it's just a PC still can format. ^^Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-72829913322304292602010-04-07T18:24:00.001+08:002010-04-07T18:24:43.097+08:00Hoping the plan falls into place properlyHere's to hope that everything gets running at the same time and falls into place perfectly, hope hope hopeDchttp://email@example.com:blogger.com,1999:blog-14266275.post-64729726515704677502010-04-06T16:02:00.003+08:002010-04-06T16:04:59.851+08:00Do you have one of these nosey relatives?It's funny how some people act to want to help, but doesn't go out of their way to help.Saying things like "if i hit the lottery tonite, then i can help so and so" in front of everyone is like trying to show off how compassionate they are. These people are so fake.If someone is down with critical illness, you don't come to tell them your insurance coverage is not good enough, you come to offer Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-11001404100935167362010-04-01T16:25:00.003+08:002010-04-01T16:32:50.963+08:00Tip Toe Tip Toe Tip ToeBeen working my arse off and it's been a good time, loads to work to do ^^Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-32931600503570725242008-08-27T08:56:00.002+08:002008-08-27T08:58:49.009+08:00And then there was a winAnd a win it was, although it doesn't matter to where i stay, but still it is a good thing for them to have won, the lesser of 2 evils?people just want a change, and the bigger powers are being sore losers, maybe because of being too well used to being fed and fat.oh well congrats to the PRDchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-34196414338542624082008-08-20T15:12:00.012+08:002008-08-21T09:46:14.129+08:00And then there was a trip, and a leak, and another leakTime after time, the shoddy workmanship of the apartment i'm staying in is starting to surface, firstly the fuse box, one of the fuses which don't usually fail, failed, it keep tripping and i thought that it was my computers which were giving the trouble.Well long story cut short, after removing one after another appliance from the sockets leading to the fuse box, it still trip, so concluded thatDchttp://email@example.com:blogger.com,1999:blog-14266275.post-60379745100523162232008-08-12T17:03:00.002+08:002008-08-12T17:07:39.634+08:0012 Boxes of Doughnuts pleaseWe just had a small company meeting, well not exactly small, i think around 50-60 ppl. Went out for an earlier lunch to tapao stuff for the meeting, and we went to get some vegetarian po-piah and karipap for the vegetarians in the company.Then we went to Big Apple Donuts, (I fancy them more than J-CO), wahahaha, they went in and told the counter staff, 12 dozen please, and the staff was like...Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-41179830778092472172008-08-11T09:47:00.002+08:002008-08-11T10:10:11.816+08:00I got rewarded for my loyaltyLOL, Ok, i'm sorry for taking so long to post another post, my friends/readers have been telling me, post la, waiting to read your posts.Here is what the title of this post is about, I went back to Malacca last Saturday, and before that i was telling my wife that i wanted to reload my TnG card at the Add Value lane at the Plus highway, well, wifey said that if there's alot of cars at that lane, Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-36710158679227628732008-07-15T16:25:00.003+08:002008-07-15T16:31:54.023+08:00Trying to get healthierI admit, i'm addicted to the internet, to computers and the works, the second i reach home, first thing i do is i turn on the computer, be it to surf facebook or play my online games.So i try to get it out of the system. Sometimes i go out with wifey shopping, be it grocery or other stuff, on Wednesdays i go for a badminton session with colleagues, "Great to sweat it out" never knew sweat can be Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-33125738664603132102008-07-03T11:37:00.004+08:002008-07-03T11:41:26.904+08:00Week 1 Lag, Week 2 Lag, Week 3 Lag and at Week 4 no more lag!!Stupid Maple Story, they have their third anniversary event in their server for 1 month and they totally lagged out all the players outside Singapore, their people did something to the routers with Starhub and it caused people not using Starhub to have frequent freeze and disconnections.I was put off, to the point of almost quitting, but then again, have some really nice friends in the game and Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-76814333828302696082008-07-03T11:31:00.002+08:002008-07-03T11:37:11.938+08:001 Month HiatusHmmm my updates tend to be sparse nowadays, maybe there was loads of things to do, maybe i just got lazy, i wonder if i will ever stop this procrasination :PAnyhow, about my last post, 1 finally got the vouchers 1 month after i won it, i think my mom received the mail yesterday, i forgot if it was registered mail or those courier mail. But they never told me how the prize will be sent to me, all Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-53270276600625498222008-05-30T10:53:00.002+08:002008-05-30T10:57:08.826+08:00Leaves and WinningsLeaves as in taking leave from your office for personal choresand Winnings as in winning some contest or something good.Bwahahah this is not the first time it happened, i was on leave yesterday, and was driving when i decided to try my luck with the local radio station Mix FM, to my surprise i got through even though i think i called in a little bit late. And after i gave my answer, i won a RM200Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-25574446232960758252008-05-14T13:25:00.002+08:002008-05-14T13:40:10.782+08:00Mothers Day & CatchupAhem ahem, i think it's a wee bit late, but anyhow Happy Belated Mother's day ^^ to all mothers out there.Oh ya, don't think i didn't celebrate it, because i did, celebrated it with my Mom In Law and my Mom one day after the other :) Lots of food and feasting.Anyhow, thinking back, i think i've had 3 long weekends adding this week to it would be 4, almost every Monday or Friday there would be Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-16159519588597717662008-04-23T11:54:00.002+08:002008-04-23T11:58:03.319+08:00Quest for saving more money..Suggestions please...How do people save money?Last time when your pay was 500, you managed to save 200When your pay was 1k you managed to save 150When your pay was 2k you saved 100?and now when your pay is 3 to 4k you say not enough of money....How to save?Any ideas?Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-62633951528362351802008-04-22T23:15:00.003+08:002008-11-14T00:21:27.576+08:00Cook Cook CookI've taken into cooking during weekends, first, i get to improve my culinary skills, second i save from eating outside.Usually wifey and i will go to Midvalley to shop for the fresh stuff on Friday nights so that i can store over the weekend for cooking whatever we fancy. The condiments are getting more and more and more.Mostly i make meals with chicken breast, since chicken is white meat, and Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-49109143009492361782008-04-03T08:52:00.005+08:002008-11-14T00:21:28.496+08:00Maple Story Exclusive WatchHehehe, i'm still playing Maple Story, after work go home, grind 1 or 2 hours or more if the mood hits me, then i level up and so on and so forth, Just another avenue to unwind from daily work and traffic stresses.Anyhow, being a supporter of the game, my wife and i buy their cash cards to show them support, these cards can be loaded in game to buy some virtual items which help out in the game.WeDchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-10682914121917030362008-03-26T16:54:00.002+08:002008-03-26T16:59:01.943+08:00Floored by Food PoisoningHappened over the weekend, wifey and i were enjoying our meal before going back to Melaka last weekend, we had our meal at Oldtown Kopitiam at Sri Petaling, was pleased with their service, but mana tau, kena food poisoning pulakWe both had the nasi lemak, and she took the white coffee cold, while i had a mocha blend.I usually can detect if the meal is not fresh, but this time it escaped me, my Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-56409297273742056112008-03-17T13:16:00.004+08:002008-03-17T13:20:29.040+08:00Can TNB do this?Blunder my eletricity bills. BAH!!!!First of all, somewhere last year, i got 2 bills for the same month, one is around RM64 and the other one is RM92. I was like duh, which is the right one?Now this month, the problem with them is, they come as they like, they come late by 10 days in one month, and early by a week for another month and thus cause my bills to fluctuate.I stay at an apartment, so Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-11502604501186635022008-03-17T11:52:00.002+08:002008-03-17T11:57:23.021+08:00Shielded eyesWhy oh why, i just got into a minor argument with my dad the other day, about the riot rumours which is floating around and he's saying this and that and what not and etc etc....I asked him where he got the information, he keep saying in an aggrieved voice that the TV news have just shown. I told him it's the main coalition's doing, and it's not all the bumi race which is protesting. He was Dchttp://firstname.lastname@example.com:blogger.com,1999:blog-14266275.post-4497201305152301172008-03-13T13:58:00.003+08:002008-03-13T14:01:48.715+08:00New CarYay, at last the new car has arrived, I am so excited, i told my wife sexcited because ehhh, ahem, our own personal communication line, bwahahahaha.Anyhow Honda City idsi- beautiful car, nice new colour, sparkle gray, and nice number too WRC XXXX !! World Rally Championship hehehehe, bought the number a day before and luckily it was still available.Will take some pics and post them up soon, ... Dchttp://email@example.com:blogger.com,1999:blog-14266275.post-24612871388809608942008-03-11T11:11:00.003+08:002008-03-11T11:18:53.895+08:00Such an interesting weekendI think the main coalition should have been played this song before the results start showing out.And now, the end is near;And so I face the final curtain.My friend, Ill say it clear,Ill state my case, of which Im certain.Ive lived a life thats full.Ive traveled each and evry highway;And more, much more than this,I did it my way.(But the continuance of this song, doesn't fit anymore.)Regrets, IveDchttp://firstname.lastname@example.com


text:
A set of super tough, insulated and padded drum bags for standard drum set shell sizes.
This Road Runner 5-Piece Standard Drum Bag Set features ballistic-quality denier exterior and interior with thick padding. The bags offer a high-quality, durable construction with reinforced double stitching; and luggage-grade zippers to protect your drum at home and on the road. Comfortable reinforced handles make it easy to tote to the gig.
Also available in individual sizes.
Order today!
Our product catalog varies by country due to manufacturer restrictions. If you change the Ship-To country, some or all of the items in your cart may not ship to the new destination.

subset: commoncrawl


text:
Explorar temas relacionados
Check out my Shopkins Collection - Get the Shopkins Checklist app on iOS and Android App Stores!
TRAJE de SHOPKINS y tiradas, chaleco, chaqueta, tutú, falda, vestido, zapatos, converse, zapatillas, zapato tenis, mezclilla, concurso, cumpleaños, niñas por DYELYFEkids
Glow in the dark Shopkins: The Mystery Edition
Shopkins display case from an old printer's tray.
Shopkins 40 piece exclusive set in box This is a box set of 40 exclusive Shopkins in the original box!! My daughter got these as a gift for Christmas and she never played with them so they are brand new without tags! Pictures should show everything but let me know if you need more details:) Shopkins Other
Gemma Stone
Resultado de imagen para imagenes shopkins
Cute Shopkins Costumes for Girls
Introducing all new Shoppies, ready to show off their style!

Colette is always chasing her dreams - the sweetest dreams! She's a softie at heart and goes out of her way to help out her friends. She keeps her place stocked with the best chocolates - a visit to her place is truly a treat!

Colette comes with a hair brush, 2 Exclusive Shopkins (her BFFs!), a purse, a doll stand, and a VIP card that unlocks bonus content in the Welcome to Shopville App.&...
Shopkins Party Favor Pack Of Rainbow Loom by JanviaBoutique
Shopkins coloring
Cumple Isabella
New Jessicake Limited Edition Golden Cupcake #shopkins
Shopkins Cupcake Queen's Sprinkle Party New 12 Exclusive Sprinkle Shopkins #Moose


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She's kind of a beauty. Er, no?
Well this isn't the first doll I've ever sewn. I made one with my mom's help back when I was a Girl Scout a few years ago. But the other night it was nice and quiet in the house and I kinda just felt like making a doll. Just to see what I could come up with since I'm such a novice with my shiny new sewing machine. I knew my little girl would love it no matter what (well, that's actually still to be determined.)
(pardon the completely open back dress . . . I just didn't want to over complicate things for myself so I just focused on the front side.)
Again, as in my fabric fish post, this is not a tutorial what so ever. Just more of a "hey, I'm gonna whip up a doll with very little sewing skills. So you could do this too."
I used materials I already had on hand:
- yarn for the hair
- buttons for eyes
- left over fabric
- a simple pattern cut out of construction paper
- stuffing
- needle and thread (and my new sewing machine)
For the backless dress number I simply cut out a piece of fabric the same shape as her body and used the sewing machine to sew it onto the front part of the doll body. I did this before I pinned and sewed the back piece to the front piece. (see, not a tutorial.)
Here are some shots of my handy work. No so handy, but I'm definitely learning from my mistakes . . .
After I sewed the front and back together on the machine, turning her right side out was the hardest part. I made her legs and arms too skinny and ended up using tweezers to turn them out. No wonder the pros usually do the limbs separately.
The hair was easier than I thought it would be. I found this great little tutorial on using yarn for hair on the blog made by bedtime tales. Again, I'm just a novice sewer, so this doll's hair is definitely not red carpet ready. Still lots of room for improvement.
I ended up stuffing her via the top of the head as well as that little slit in the leg area. I hand sewed those areas closed. I also hand sewed the button eyes. I tinkered with the machine to stitch the mouth and nose. I just wanted to see if that was even possible to do. It sorta was.
Doesn't she have kind eyes? . . .
She means well. My daughter has mixed feelings about her. But I like her. I've already created a persona for her — she's shy and only uses two to three word sentences. The next doll will be better. I promise.
Until next Monday!
linking up with Skip to my Lou


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forthcoming ROCKAOKE NIGHTS
Thu 28/09/2017:
Bunga Bunga, Battersea
Fri 29/09/2017:
The Star of Kings, Kings Cross
Sat 30/09/2017:
Orange Pip Market, Middlesbrough
Sun 01/10/2017:
Mulberry Bar, Sheffield
Thu 05/10/2017:
London Cocktail Club, Shoreditch
Fri 06/10/2017:
Radicals and Victuallers, Islington
Fri 13/10/2017:
Tram & Social, Tooting
Thu 26/10/2017:
Bunga Bunga, Battersea
SNAFU, Rotherham
1-8 Westgate Chambers
01709 836 623
Rockaoke Nights come to ROTHERHAM!!!
SNAFU is the perfect location in Rotherham for a chilled out evening listening to the best acts South Yorkshire has to offer. Come down to the SNAFU live music bar and you won't be disappointed with the music and environment.
free entry from 11pm until late.
November 2017
Fri 24/11/2017: SNAFU, Rotherham
1-8 Westgate Chambers, Rotherham, South Yorkshire, S60 1AN
(Phone: 01709 836 623 || Web: www.snafurotherham.co.uk)


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"Jesus Killed Mohammed" was written in Arabic in large red letters on the side of a U.S. Army Special Forces vehicle, armed to kill and rolling through a town in Iraq. It sounds like a bad Mad-Maxesque Hollywood adaption of the Crusades set in our contemporary context. The scene gets more chilling and horrific:
Last week my son and I spent three days in Washington, D.C., as part of the Mobilization to End Poverty. We heard challenging speakers.
"Good" Friday was real good this year. We remembered Jesus, and we remembered Jesus disguised in the "least of these" -- those who continue to be tortured, spit on, slapped, insulted, misunderstood
I've written a lot on Palestine and Gaza in recent years. Any of us who travel (or read) know that peace in the world can't be separated from peace in Israel -- peace for Jews, and peace for Muslim and Christian Palestinians.


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Guide to The New SuperMediaStore Website
After many months of hard work and dedication, the new SuperMediaStore website will be fully launching on July 31st, 2017 at 3:00pm (PDT). With a fully responsive website, you can conveniently shop on our site anytime, anywhere. There are so many other new features and additions we have added to our new site to enhance a better shopping experience. Before you start exploring our new site, please read the following important message:
We invite you to create a new account on the new site. To protect the privacy of your personal information, your credentials from our previous SuperMediaStore website will not be integrated to the new site.
3 | Step by Step Video Guide to Creating a New Account
reCAPTCHA is a Google service to protect the site from spam and abuse. It uses an advanced risk analysis engine and adaptive CAPTCHAs to keep automated software from engaging in abusive activities. Learn more >
If you are still having trouble creating an account or surfing on the new site, you may need to update your web browser to the latest versions. Click here for a quick guide on how to update your web browsers.
4 | Account Login Setting
We will be implementing a feature to edit your login information, such as email address and password, under your personal account this coming August. Please stay tuned.


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Building a new modern India through the innovative concepts and operational excellence, creating eco-friendly homes with best quality practices, reaching beyond expectations of the customers and outperforming the band wagon of other constructions has been our Vision since inception. We also strive to excel in customer satisfaction through our time bound deliveries, committed efforts and uncompromising traditional values and culture.
We pledge to serve the nation by setting benchmark in the real estate and construction industry through our Business Ethics, Professionalism and Transparency to provide luxurious affordable homes. We strive to be the pioneer in the industry by achieving on a larger scale of land acquisitions and to be a legendary success in creating millions of "Happy Customers".


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|Mr. Darren Ambrose
High School English Teacher
EMAIL: firstname.lastname@example.com
|Ms. Kiyyah Deloney
High School Business Teacher
EMAIL: firstname.lastname@example.com
|Coach Antonio Hudson
High School Physical Education Teacher
Head Basketball Coach
Assistant Athletic Director
EMAIL: firstname.lastname@example.com
|Mr. Kennedy Jones
High School Science Teacher
Assistant Football Coach
EMAIL: email@example.com
|Ms. Jennifer Kimble
High School Mathematics Teacher
EMAIL: email@example.com
|Ms. Rochelle McGuire
MS/HS Music Teacher
Choir Director
EMAIL: email@example.com
|Mr. David McLaughlin
High School ELA & Social Studies Teacher
EMAIL: email@example.com
|Mr. Jeffery Middleton
High School Mathematics Teacher
Assistant Baseball Coach
EMAIL: email@example.com
|Ms. Michelle Paudyal
High School Spanish Teacher
EMAIL: firstname.lastname@example.com
|Mr. Arthur Simpson
High School Music Teacher
LPS Band Director
EMAIL: firstname.lastname@example.com
|Mr. Johnny Thomas
High School Social Studies Teacher
Track Coach
EMAIL: email@example.com
|Ms. Candace Westbrook
High School Science Teacher
EMAIL: firstname.lastname@example.com
|Mrs. Davida Beckum
Middle School ELA Teacher
Girls Softball Coach
EMAIL: email@example.com
|Mr. Vyron Brown
Middle School History Teacher
Assistant Football Coach
EMAIL: firstname.lastname@example.com
|Ms. Vivian Davis
Middle School ELA Teacher
EMAIL: firstname.lastname@example.com
|Mr. Eumarcus Hicks
Middle School Mathematics Teacher
Head Middle School Basketball Coach
EMAIL: firstname.lastname@example.com
|Mrs. Jasmine Thompson
Middle School Science Teacher
Girls Track Coach
Cheer Coach
EMAIL: email@example.com
|Ms. Janet Davis
Kindergarten Teacher
|Ms. Cashal Taylor
Kindergarten Teacher
|Ms. Felisha Lewis
1st Grade Teacher
EMAIL: firstname.lastname@example.com
|Ms. Sherrie Emory
2nd Grade Teacher
EMAIL: email@example.com
|Ms. Hanna Richard
2nd Grade Teacher
|Ms. Kathi Mitchell
3rd Grade Teacher
|Ms. Alicia Dooley
4th/5th ELA and Social Studies Teacher
EMAIL: firstname.lastname@example.com
|Mrs. Christie Davis
4th/5th Grade Math and Science Teacher
EMAIL: firstname.lastname@example.com
|Mr. Chaunce Davison
P.E. Teacher
JV Basketball Coach
Assistant Football Coach
EMAIL: firstname.lastname@example.com
|Mr. Christian Jackson
Art Teacher
|Ms. Kelli Miley
School Librarian/ISS
|Ms. Deborah Gilliam
Computer Lab
EMAIL: firstname.lastname@example.com


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The Washington County Tourist Development Council will hold its regularly scheduled workshop and meeting on Monday, July 24, at the Washington County Chamber of Commerce. The workshop will begin at 4pm followed by the meeting. All meetings are open to the general public.
Workshop Agenda: Click Here
Meeting Agenda: Click Here


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Latest content added for Digital Library Collection: Texas Fashion Collectionhttps://digital.library.unt.edu/explore/collections/TXFC/browse/?sort=date_d&start=30&fq=str_location_country:France2015-09-02T11:34:03-05:00UNT LibrariesThis is a custom feed for browsing Digital Library Collection: Texas Fashion CollectionJacket2015-03-16T14:32:52-05:00https://digital.library.unt.edu/ark:/67531/metadc501291/

Jacket of off-white linen. Fitted, waist length jacket with wide, notched collar and long sleeves with 3" cuffs and two white, circular buttons and barred buttonholes. Two patch pockets at bust line. Unlined. Combined designer's/retailer's label: "Christian Dior / for / Lou Lattimore, Inc. / Paris New York" Care label to right of designer's label. Lot/size tag at right underarm (faded): "Lot / Size 10" With tie belt for jacket of same fabric; 1" wide.
Jacket2014-05-27T05:32:10-05:00https://digital.library.unt.edu/ark:/67531/metadc286901/

Jacket of black, green, red, pink, and yellow flannel in a large, painterly plaid pattern. The jacket is just below hip-length, and has a round neckline and no collar. Center front closure has a zipper with a gold metal rose charm pull, matching the pulls of the zippers on the two diagonal slit pockets at hips. Long-sleeved, with three non-functional buttons at wrists, formed as coiled snakes/spirals of gold metal. The jacket has inner shoulder pads and is fully lined in black satin. Designer's label: "Ungaro / Parallele / Paris"
D'Orsay Pumps2012-11-05T12:51:51-06:00https://digital.library.unt.edu/ark:/67531/metadc115005/

Pair of D'Orsay pumps of gray leather. The shoes are designed with pointed toes, and cut-away sides. Toebox has a deep "v" cut at throat of instep, edged with red as is the platform of the shoe. From the point of the cut extends back a t-strap which fastens around the ankle of wearer with a small buckle. 3 1/2" high stiletto heel covered with same gray leather. Stamped inside: "Charles Jourdan / Paris / Made in France" Accompanied by original Charles Jourdan shoebox.
Platform Pumps2012-11-05T12:51:51-06:00https://digital.library.unt.edu/ark:/67531/metadc114948/

Pair of platform pumps. Shoes are of brown patent leather, with white top stitching. Pointed toes, and a 4" block set-back heel. Stamped in each shoe: "107 N 7"; "Yves Saint Laurent / Paris". Stamped on soles: "Made / Vero / Cuoio / Italy / AA / 7"
Pumps2011-07-25T17:53:57-05:00https://digital.library.unt.edu/ark:/67531/metadc39036/

Pair of tan and black leather sling-back pumps. Uppers of tan/brown leather with black leather toe cap. Sling-back strap with gilt metal buckle. 2 3/4" continental heel covered in tan/brown leather. Shoe lined in putty colored leather. Sole of natural brown leather. Stamped in each shoe: "Made in France"; Chanel / [logo]". Stamped inside upper: "105002 37". Stamped on sole: "37 / DE / [logo] / Coupe monte fini main".
Pumps2011-07-25T17:53:57-05:00https://digital.library.unt.edu/ark:/67531/metadc39038/

Pair of speckled taupe leather pumps. Uppers of light taupe leather embellished with tiny grayish flat pebbled textural design. Toe cap of black patent leather. 3 3/4" spike heel covered in black patent leather. Lined in olive leather except inner heel, which is lined in natural light brown leather. Soles of black leather. Stamped in each shoe: "Charles Jourdan / Paris / Made in France". Stamped inside each heel: "37 X 7 2A 586855 NF". Stamped on sole: "Leather / Leder / Cuir / Made in / France"
Skirt Suit2014-05-27T05:32:10-05:00https://digital.library.unt.edu/ark:/67531/metadc286904/

Skirt suit. A) Jacket of fuchsia flat weave wool with ring collar and zip-front closure; long raglan sleeves with inner shoulder pads; circular geometrical stitched panels at front and back; two circular patch pockets at hips; crescent princess seams; fitted at waist; peplum at back with reverse box pleat and attached belt of self-wool with metal buckle above; lower hip length; partially lined in magenta synthetic. B) Skirt of black stretch wool with 2" waistband with diagonal snap closure; darts at front and back; center-back zip closure; 18 ½" length. Size 38 Designer's label: "Thierry Mugler / Paris" "Made in France"
Suit - Jacket and Skirt2015-09-02T11:34:03-05:00https://digital.library.unt.edu/ark:/67531/metadc701493/

Suit of cream silk gaberdine(?) consisting of: A) Jacket. Hip-length; box style. Bermuda collar and yoke which covers jacket front top, makes into epaulet-like treatment at shoulder, and sailor-like collar in back; geometrically shaped with white snaps at corners. Center front of jacket fastens all the way down with white snaps. Full-length dolman sleeves. Back has center seam and two darts which start 2 1/2 inches under yoke and extend to waist. Fully lined in white synthetic fabric. Designer's label at center back neckline: "Pierre Cardin / Paris / Made in France" B. Skirt of matching fabric. Slightly gathered into 1"waistband. Street length; slightly A-lined. Center back fastens with hook, snap and zipper. Fully lined in white synthetic fabric.
Ensemble - Dress and Skirt2015-02-05T21:59:29-06:00https://digital.library.unt.edu/ark:/67531/metadc498978/

Dress ensemble of red lace with dark brown and metallic gold embroidery in floral design. A) Dress. Calf length with rolled collar. Four-snap closure down center front. Elastic waistline. Long straight sleeves with band cuffs and snap closure. Scalloped hem. Unlined. Designer's label at center back neckline: "Miss Dior / Made in France" B) Skirt of red silk. Straight with 1" waistband. Center back closure of covered hook & eye on waistband and 2 snaps. Evidence of four removed darts. C) Belt of self-covered leather; 2" wide. Gold circle buckle with two hooks and three pairs of grommets for closure.
Suit - Jacket and Skirt2015-03-16T14:32:52-05:00https://digital.library.unt.edu/ark:/67531/metadc501315/

Suit of black wool consisting of: Jacket of almost hip-length, with no collar; double breasted, with V neckline and 4 buttons center front, in rows of two. Two flap pockets front; two bust darts; Long sleeves with single button cuffs. Built-in shoulder pads, and fully lined. Designer's label at inside back neck: "Christian Dior / The Suit / Paris New York" Care label below Designer's label: "Dry Clean / Made in U.S.A." Content label at side seam: "100% / Pure Wool"; "Professionally / Dry Clean / Low Moisture / Steam Press" Skirt. Calf length, with narrow waistband. Knife pleated, with side zipper and button. Unlined.


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We got to get away to the coast this week with just us and the kids. It's the first time Mark and I have ever gone on vacation without anyone else being there to help out! I know five kids is not that many, but when you are away from home it's nice to have extra hands to help out! Well it is all hands (only our own four!) on deck this week! Mostly for greasing up babies with sunscreen before we trekked our load to the sand or for preparing snacks to take to the ocean (or just making food in general). I'm so glad we finally realized that we don't need to take any chairs to sit in on the beach as one cannot sit very long when there's a mobile baby in the mix who thinks it's super fun to crawl straight into the crashing waves! He's still new at this whole beach thing! Here are some more things I've realized while being here on this adventure…
- I need to give myself a day to get acclimated to a new surrounding. It just takes me that long!
- Have expectations and then expect them to fly out the window, or off the balcony: just roll with it.
- Less is more: less sand buckets, chairs, clothes, food options… (except in regards to sunscreen)
- Get the good sunscreen! The no tear kind and sunscreen sticks are the best. Ever. You will go through four bottles at least.
- Do not take children shopping in 90 degree heat.
- Remember to take the stroller when you do decide to take children shopping in 90 degree heat. And water.
- Enjoy the little things. Even the strange little toys they pick out at the overpriced bookstore.
- Curse all the remotes everywhere. There are four TVs in this place. That's two remotes per TV. Two remotes are missing at this moment. I can't even.
- Remember to smile! I am at the beach with my family! These are the best days! And school starts next week.
Can't believe this kid will be 3 next week!
The tie-dye shirts were so fun!


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Class II histone deacetylases (HDACs) 4, 5, 7, and 9 repress muscle differentiation through associations with the myocyte enhancer factor 2 (MEF2) transcription factor. MEF2-interacting transcription repressor (MITR) is an amino-terminal splice variant of HDAC9 that also potently inhibits MEF2 transcriptional activity despite lacking a catalytic domain. Here we report that MITR, HDAC4, and HDAC5 associate with heterochromatin protein 1 (HP1), an adaptor protein that recognizes methylated lysines within histone tails and mediates transcriptional repression by recruiting histone methyltransferase. Promyogenic signals provided by calcium/calmodulin-dependent kinase (CaMK) disrupt the interaction of MITR and HDACs with HP1. Since the histone methyl-lysine residues recognized by HP1 also serve as substrates for deacetylation by HDACs, the interaction of MITR and HDACs with HP1 provides an efficient mechanism for silencing MEF2 target genes by coupling histone deacetylation and methylation. Indeed, nucleosomal histones surrounding a MEF2-binding site in the myogenin gene promoter are highly methylated in undifferentiated myoblasts, when the gene is silent, and become acetylated during muscle differentiation, when the myogenin gene is expressed at high levels. The ability of MEF2 to recruit a histone methyltransferase to target gene promoters via HP1-MITR and HP1-HDAC interactions and of CaMK signaling to disrupt these interactions provides an efficient mechanism for signal-dependent regulation of the epigenetic events controlling muscle differentiation.
The assembly of chromatin into higher-order structures plays a critical role in the control of gene transcription. The structure of chromatin is profoundly influenced by posttranslational modifications of the conserved amino-terminal tails of histones. Acetylation, methylation, and phosphorylation of histones have been shown to control the on-off states of genes by creating a code that is interpreted by transcriptional activators and repressors that recognize these specific histone modifications (reviewed in reference 14). Emerging data suggest that extracellular cues alter signal-responsive genes in part by changing the activities, subcellular localization, and protein-protein interactions of histone-modifying enzymes.
Acetylation of histone tails by histone acetyltransferases (HATs) results in chromatin relaxation due to disruption of histone-DNA and histone-histone interactions. Acetylated histones also serve as binding sites for bromo-domain proteins, which possess HAT activity and act as transcriptional activators (6, 13, 34, 45). Conversely, histone deacetylation by histone deacetylases (HDACs) results in chromatin condensation and transcriptional repression (reviewed in references 15 and 31). Recent studies have also revealed an important role for histone methylation as an epigenetic mechanism for the regulation of heterochromatin assembly and gene silencing (27, 30, 35, 36, 39). Methylation of lysine 9 in the tail of histone H3 by the SUV39H1 histone methyltransferases (HMTases) results in repression of transcription by creating binding sites for chromodomain (CD) proteins such as heterochromatin protein 1 (HP1), which represents a family of adaptor proteins involved in transcriptional silencing (4, 17, 37). HP1 associates with a variety of transcriptional repressors and thereby provides a mechanism for widespread silencing of gene expression in response to histone methylation (18, 32, 38).
Since the lysines in histone tails that are methylated by HMTases are also the substrates for HATs (reviewed in reference 14), HDACs play an intermediary role in these modifications by removing the acetate group and thereby creating a substrate site for either HATs or HMTases. Vertebrate HDACs are categorized into three classes based on homology with three distinct yeast HDACs (reviewed in reference 10). The class I HDACs HDAC1, -2, -3, and -8 are expressed ubiquitously, while the class II HDACs HDAC4, -5, -7, and -9 are expressed in a tissue-restricted manner, with highest expression in heart, brain, and skeletal muscle. These class II HDACs are also distinguished by an amino-terminal extension that mediates association with myocyte enhancer factor 2 (MEF2), which regulates muscle differentiation (7, 19-22, 28, 42, 48; reviewed in reference 24), and C-terminal binding protein (CtBP), a widely expressed transcriptional corepressor (47). Class I and II HDACs are also capable of homo- and heterodimerization, which allow for the formation of multicomponent HDAC complexes (11, 41, 44), and recent evidence suggests that repression by class II HDACs requires the recruitment of class I HDACs (8, 9).
Another unique characteristic of class II HDACs is their signal responsiveness. The amino-terminal extensions of HDAC4, -5, -7, and -9 contain two conserved serine residues that are targets for phosphorylation by calcium/calmodulin-dependent protein kinase (CaMK) (22). When phosphorylated by CaMK, these phosphoserines in class II HDACs are bound by 14-3-3 chaperone proteins, resulting in the dissociation of MEF2-HDAC complexes. HDAC4, -5, -7, and -9 are also exported from the nucleus to the cytoplasm as a result of their association with 14-3-3 proteins, which mask the HDAC nuclear localization sequence while exposing the HDAC nuclear export sequence (12, 16, 23, 25, 43). MEF2-interacting transcriptional repressor (MITR) is a naturally occurring splice variant of HDAC9 that shares high homology with the amino-terminal extensions of class II HDACs but lacks a catalytic domain (41, 48, 49). Like class II HDACs, MITR acts as a transcriptional repressor and is subject to CaMK-mediated release from MEF2. However, MITR cannot be exported from the nucleus due to the absence of a nuclear export sequence (25, 48). Since MITR lacks intrinsic HDAC catalytic activity, it is thought to repress transcription by recruiting other corepressors, such as CtBP and HDACs (41, 47, 50).
To further understand the mechanisms that regulate the activities of MITR and class II HDACs, we screened for MITR-interacting proteins by using the yeast two-hybrid system. Here we show that MITR, as well as HDAC4 and -5, associate with HP1 and that CaMK signaling disrupts these interactions through a mechanism independent of the phosphoacceptors in MITR and HDACs that mediate binding to 14-3-3 proteins. Furthermore, the acetylation and methylation states of histone H3 lysine 9 at a MEF2 element in the myogenin gene promoter, which becomes activated during muscle differentiation, showed reciprocal changes during skeletal myogenesis, with the histone H3 lysine 9 being methylated in undifferentiated myoblasts and acetylated in differentiated myotubes. The association of MITR and HDACs with HP1 provides a mechanism for efficiently coupling histone deacetylation and methylation and for regulating these modifications in response to signaling events that promote cellular differentiation.
A cDNA encoding a mutant of MITR containing alanines in place of serines 218 and 448 was fused in frame to the yeast GAL4 DNA-binding domain (GAL4-MITR S218/448A) and used as bait to screen a mouse embryonic day 17 cDNA library (Clontech), as described previously (47). Positive clones were isolated via growth on selection medium and on the basis of β-galactosidase expression. Putative positive clones were further tested for specificity using the GAL4 DNA binding domain alone as the bait. Those clones specific for interaction with GAL4-MITR S218/448A were subjected to sequencing. Filter lift and liquid β-galactosidase assays were performed according to the recommendations of the manufacturer (Clontech).
All yeast two-hybrid baits were constructed in the pGBKT7 vector (Clontech). Mammalian expression vectors for epitope-tagged derivatives of human HDAC4, HDAC5, HDAC1, and HDAC3 and mouse CtBP1 and MITR have been described previously (47). Complementary DNAs encoding amino-terminally Myc- or FLAG-tagged MITR mutants and mouse HP1α, -β, and -γ were cloned into the pcDNA3.1 mammalian expression vector (Invitrogen). T. Kouzarides kindly provided the mammalian expression plasmid for hemagglutinin (HA)-SUV39H1. Expression of glutathione S-transferase (GST)-HP1 derivatives or GST-MITR (389 to 506) was achieved by using the pGEX-KG bacterial expression vector (Amersham Pharmacia Biotech). The cDNA for constitutively activated CaMKI, which contains a stop codon in place of isoleucine 294, was provided by A. Means. A derivative of this cDNA encoding an HA-tagged version of activated CaMKI was constructed in pcDNA3.1. The integrity of all plasmids was confirmed by sequencing.
COS, 293T, and C2 cells were maintained in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal bovine serum, 2 mM l-glutamine, and penicillin-streptomycin. For differentiation of C2 cells, confluent myoblasts in growth medium (DMEM containing 10% fetal bovine serum) were shifted to differentiation medium (DMEM containing 2% horse serum) for 2 days.
Transfections were performed with the lipid-based reagent Fugene 6 (Roche Molecular Biochemicals) and cells growing at a density of 5 × 105 to 10 × 105 cells/35-mm-diameter dish. For MEF2-dependent transcription assays, COS cells in 35-mm-diameter dishes were transfected with a luciferase reporter plasmid under control of three copies of consensus MEF2-binding site and the E1b minimal promoter, 3XMEF2-luciferase, and pcDNA3.1-based expression plasmids for MEF2C, MITR, and HP1α. A plasmid encoding β-galactosidase under the control of the cytomegalovirus (CMV) promoter, CMV-lacZ, was included for transfection normalization. Cells were harvested 36 h after transfection, and luciferase and β-galactosidase values were measured under conditions of linearity with respect to time and cell extract concentration.
GST fusions of wild-type HP1α, -β, and -γ, HP1α deletion mutants, and residues 389 to 506 of mouse MITR were expressed in the BL21(DE3) strain of Escherichia coli and purified by using glutathione-conjugated agarose beads (Sigma). 35S-labeled HDACs, HP1α, SUV39H1, or CtBP1 was generated by using the TNT kit (Promega). Ten microliters (~10,000 cpm) of labeled protein was mixed with 0.5 to 1 μg of GST fusion protein-bound agarose beads in GST binding buffer composed of phosphate-buffered saline containing 0.5% Triton X-100, 1 mM EDTA, 1 mM phenylmethylsulfonyl fluoride, and protease inhibitors (Complete; Roche Molecular Biochemicals) for 1 h at 4°C. Beads were collected by brief centrifugation and washed five times in GST binding buffer. Bound proteins were resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed by autoradiography.
COS or 293T cells were transiently transfected with plasmids encoding the indicated proteins and were harvested at 48 h posttransfection in lysis buffer composed of PBS containing 0.5% Triton X-100, 1 mM EDTA, 1 mM PMSF and protease inhibitors (Complete; Roche Molecular Biochemicals). Following brief sonication and removal of cellular debris by centrifugation, FLAG-tagged proteins were immunoprecipitated from cell lysates by using anti-FLAG resin (M2; Sigma). Alternatively, Myc-tagged proteins were precipitated with rabbit polyclonal anti-Myc antibody (A-14; Santa Cruz) and protein A/G Plus beads (Santa Cruz). The bound proteins were washed five times with lysis buffer, resolved by SDS-PAGE, and transferred to polyvinylidene difluoride membranes. Membranes were immunoblotted with either anti-Myc antibody (9E10; Santa Cruz), anti-HA antibody (Y-11; Santa Cruz), or anti-FLAG antibody (M2; Sigma), and proteins were visualized with a chemiluminescence detection system (Santa Cruz).
HDAC activity was assayed as described previously (20). Briefly, immunoprecipitates were washed twice in HD buffer (20 mM Tris-HCl [pH 8.0], 150 mM NaCl, 10% glycerol) and incubated with ~20,000 cpm of 3H-acetylated histones derived from MEL-TK cells in HD buffer at 37°C for 1.5 h. Reactions were terminated by addition of acetic acid and HCl to final concentrations of 0.12 and 0.72 M, respectively, and extracted with 600 μl of ethyl acetate. The released [3H]acetate was measured by scintillation counting of the organic phase.
Chromatin immunoprecipitation (ChIP) assays with C2C12 myoblasts or multinucleated myotubes were performed as described previously (21). Briefly, equal amounts of soluble chromatin were immunoprecipitated from each sample with either an anti-acetyl histone H3 lysine 9-lysine 14 or an anti-dimethyl histone H3 lysine 9 antibody (Upstate Biotechnology). Ten percent of the immunoprecipitated DNA was subjected to PCR for 28 cycles with primers specific for either the myogenin gene promoter or the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene promoter. Primer sequences that flank the MEF2 site in the myogenin gene promoter have been described previously (21). Primers were also designed to flank the transcription start site in the GAPDH gene: plus, 5′-GCTCTCTGCTCCTCCCTGTT-3′; minus, 5′-CAATCTCCACTTTGCCACTGC-3′. As a control for DNA input, PCR was also performed with chromatin prior to immunoprecipitation. [α-32P]dCTP was included in the PCRs to facilitate visualization and quantitation of DNA. Twenty percent of each PCR mixture was resolved through a 5% native acrylamide gel, visualized, and quantified using a phosphorimager (Molecular Dynamics).
To investigate the mechanisms involved in transcriptional repression by MITR, we performed yeast two-hybrid screens with a cDNA encoding MITR fused in frame to the GAL4 DNA-binding domain as bait (Fig. (Fig.1A).1A). We initially used a mutant of MITR containing alanines in place of serines 218 and 448 (MITR S218/448A) to abolish the binding of MITR to 14-3-3 proteins, a family of ubiquitously expressed proteins that associate with MITR when these serines are phosphorylated (48). One of the most strongly interacting clones in this screen encoded full-length HP1α. The HP1α-GAL4 activation domain prey identified in the screen did not interact with a variety of nonspecific GAL4 baits (data not shown), indicating that its association with the GAL4-MITR S218/448A bait was specific. The association of HP1α with wild-type MITR in yeast two-hybrid assays was as efficient as that with the MITR S218/448A mutant, suggesting that the alanine substitutions did not affect the binding (Fig. (Fig.1A).1A). By using two MITR deletions fused to the GAL4 DNA-binding domain as baits, the HP1α-interacting region of MITR was localized to residues 351 to 586 (Fig. (Fig.1A1A).
To further test the specificity of the interaction between MITR and HP1α, we performed binding assays with a bacterially expressed GST-HP1α fusion protein and in vitro-translated MITR and HDAC proteins (Fig. (Fig.1B).1B). GST-HP1α interacted efficiently with 35S-methionine-labeled MITR, as well as with HDAC4 and HDAC5 (Fig. (Fig.1C).1C). No interaction was detected between GST-HP1α and HDAC1, HDAC3, or the CtBP corepressor, which also associates with class II HDACs and MITR (47).
The association of HP1α with MITR and class II HDACs was further tested by coimmunoprecipitation assays using protein lysates from transfected cells. Consistent with the GST binding experiments, Myc-tagged HP1α associated with FLAG-tagged MITR, HDAC4, and HDAC5, and in this assay, these three proteins bound HP1α with comparable efficiencies (Fig. (Fig.1D).1D). HP1α did not interact with HDAC3 in the coimmunoprecipitation assay, but in contrast to the GST binding experiments, HDAC1 could be coimmunoprecipitated with HP1α (Fig. (Fig.1D).1D). Although the basis for this difference between the two assays remains unknown, it could reflect a role for additional cellular proteins that are present in the cell extracts but absent from GST pull-down assays. For example, class II HDACs can interact with HDAC1 (11, 41). Thus, endogenous class II HDACs in COS cells could potentially interact with Myc-tagged HP1α and recruit FLAG-tagged HDAC1 to the complex. Notwithstanding this uncertainty, our results reveal that HP1α is capable of associating with MITR and class II HDACs in three independent assays: yeast two-hybrid interaction, GST pull-down, and coimmunoprecipitation.
As a final test for the interaction between HP1α and HDACs, we expressed Myc-tagged HP1α in 293T cells, which express both class I and class II HDACs, and performed HDAC assays on anti-Myc epitope immunoprecipitates (Fig. (Fig.1E).1E). Deacetylase activity was readily detectable in the immune complex, indicating that HP1α associated with endogenous HDACs.
In order to map the region of MITR that mediates the association with HP1α, we initially generated a series of MITR deletion mutants and assessed their capacities to associate with GST-HP1α (Fig. (Fig.2A,2A, B, and C). Deletion of residues from amino acid 400 to the carboxyl terminus of MITR had no effect on HP1α binding, whereas a deletion mutant containing amino acids 1 to 300 (mutant 1-300) failed to bind HP1α. Deletions from the amino terminus showed that mutants lacking up to the first 370 amino acids had no effect on MITR-HP1α interaction (see mutant 371-586). Based on these assays, the HP1α-interacting region was localized to residues 371 to 400 of MITR. Surprisingly, however, an internal deletion mutant of MITR lacking residues 371 to 400 (mutant Δ371-400) also bound HP1α (Fig. (Fig.2C),2C), indicating that more than one domain in MITR can mediate HP1α binding.
The HP1α-interacting region of MITR was further delineated by coimmunoprecipitation assays using Myc-tagged MITR mutants and FLAG-tagged HP1α expressed in transfected cells (Fig. (Fig.2C).2C). Progressive extension of mutant 1-300 toward the carboxyl terminus showed that residues through amino acid 390 were insufficient to mediate HP1α binding, whereas mutant 1-400 bound HP1α as efficiently as wild-type MITR. These results are consistent with the GST pull-down results (Fig. (Fig.2A)2A) and further suggest that amino acids 391 to 400 of MITR are important for association with HP1α.
Sequence analysis of MITR failed to reveal amino acids that were conserved between residues 391 to 400 and elsewhere in the protein that could account for the association of the Δ391-400 mutant of MITR with HP1α; however, through sequence analysis by the program NPS@ (http://pbil.ibcp.fr/cgi-bin/secpred_consensus.pl), the predicted secondary structure of MITR suggests that amino acids 391 to 400 form an α-helix and that another α-helical stretch is formed by the amino acids immediately carboxy terminal to this region (Fig. (Fig.2D).2D). Consistent with a role for both putative α-helices in governing the interaction between MITR and HP1α, the Δ391-490 mutant of MITR, lacking these two helices in the context of the full-length protein, completely failed to bind HP1α in the GST pull-down assay (Fig. (Fig.2B2B).
Together, these results indicate that there are at least two independent HP1α-binding domains in MITR (Fig. (Fig.2D),2D), each of which is sufficient to mediate the HP1α interaction. One HP1-interacting domain is located between amino acids 390 and 400, and the other is located between amino acids 400 and 490.
HP1 proteins contain three distinct domains. The amino-terminal CD, which binds methyl-lysine 9 of histone H3, is separated from the carboxy-terminal chromoshadow domain (CSD), which mediates a variety of protein-protein interactions, by a central variable hinge region (Fig. (Fig.3B).3B). Specific functions have not been ascribed to the hinge region, although it has been shown to interact with histone H1 and INCENP (2, 33). There are three mammalian HP1 proteins, HP1α, -β, and -γ, which are highly homologous in the CSD and CD domains but are divergent in the hinge regions.
The region of HP1α that bound MITR was mapped by in vitro binding assays using 35S-labeled MITR and a series of GST-HP1α deletion mutants. As shown in Fig. Fig.3A,3A, neither the CD nor the CSD was able to interact with MITR, whereas the hinge region alone and deletion mutants lacking the CSD or the CD but containing the hinge region (ΔCSD and ΔCD) bound to MITR. Mutations that bisected the hinge region abolished interaction with MITR, suggesting that the interaction motif extends across this region. These results indicate that the hinge region of HP1α is necessary and sufficient for association with MITR.
We also examined whether HP1β and HP1γ interacted with MITR. For this purpose, the β and γ isoforms of HP1 were fused to GST, expressed in E. coli, and tested for the ability to associate with in vitro-translated MITR, HDACs or the CtBP corepressor. As shown in Fig. Fig.3C,3C, the interactions of HP1β and HP1γ with MITR and class II HDAC4 and HDAC5 were comparable to those of HP1α, although GST-HP1β and -HP1γ also modestly associated with HDAC1. In contrast, in coimmunoprecipitation assays using lysates from transfected cells, neither HP1β nor HP1γ interacted with MITR (Fig. (Fig.3D).3D). We have not further investigated the divergent results between these assays, although we hypothesize that they reflect roles for cellular proteins in modulating the interactions.
HP1 associates with the HMTase SUV39H1 (1), which provides a potential mechanism for coupling methylation of lysine 9 on histone H3 with the protection of this methyl group by the binding of HP1. To determine whether HP1 could associate simultaneously with SUV39H1 and class II HDACs to form a multiprotein histone modification and protection complex, we performed coimmunoprecipitation assays with HA-tagged SUV39H1 and FLAG-tagged versions of HP1α, HDACs, and MITR (Fig. (Fig.4A).4A). HP1α was readily immunoprecipitated with SUV39H1, consistent with previous studies (1). In addition, HDAC4, HDAC5, and MITR were detected in SUV39H1 immune complexes, although the efficiency of their association with SUV39H1 was substantially lower than that of HP1α. The CtBP corepressor did not associate with SUV39H1, demonstrating the specificity of the assay. These results were consistent with those from GST pull-down assays (Fig. (Fig.4B),4B), where a GST fusion protein containing amino acids 389 to 506 of MITR efficiently associated with 35S-labeled HP1α or SUV39H1 individually or in combination. These results suggest that HP1α and SUV39H1 can form a complex with MITR. However, since the experiments were performed with rabbit reticulocyte lysates, whether or not MITR associates directly with SUV39H1 or through an intermediary such as HP1 remains unclear.
Given the ability of HP1 to associate with MITR and class II HDACs, we performed experiments to determine whether or not HP1 contributes to the mechanism by which these factors repress MEF2-dependent transcription. As shown in Fig. Fig.4C,4C, HP1α was capable of repressing a MEF2-dependent reporter gene in a dose-dependent manner, and the inhibitory action of HP1 was enhanced by a small amount of exogenous MITR. These results suggest that HP1 is recruited to MEF2 via MITR and class II HDACs to form a more potent transcriptional repression complex.
Since MITR, HDAC4, and HDAC5 are capable of associating with HP1α and SUV39H1, and since MITR and HDACs are released from MEF2 during muscle differentiation, we hypothesized that the relative states of histone methylation and acetylation at a MEF2-binding site in muscle-specific genes would be altered during myogenesis. To test this hypothesis, we performed ChIP assays. Soluble chromatin was prepared from proliferating myoblasts or differentiated myotubes and was subjected to immunoprecipitation with antibodies specific for methylated lysine 9 of histone H3 or acetylated K9 and K14 of histone H3. The amount of precipitated DNA was determined by PCR using primers that flank a functional MEF2 site in the myogenin gene promoter, which is dramatically upregulated during muscle differentiation. As shown in Fig. Fig.5A,5A, histone H3 acetylation on the myogenin promoter was significantly increased in differentiated myotubes relative to undifferentiated myoblasts. In contrast, the degree of histone H3 lysine 9 methylation was significantly higher in proliferating myoblasts than in myotubes. These dynamic changes in the modification state of nucleosomal histones correlated precisely with the expression level of the myogenin gene (data not shown) and were not due to nonspecific consequences of differentiation, since there was no change in the state of histone acetylation or methylation in the GAPDH promoter, which is expressed at comparable levels in myoblasts and myotubes. These data support a model in which MEF2 recruits an HMTase to target genes via HP1 and HDAC or MITR, resulting in transcriptional repression. In response to myogenic cues, HDACs and MITR are released from MEF2, allowing the transcription factor to associate with HATs, which acetylate nucleosomal histones and promote gene expression (see Fig. Fig.6C6C).
We have shown previously that CaMK mimics myogenic signals that release MEF2 from the repressive effects of class II HDACs and MITR. CaMK phosphorylates HDAC4, HDAC5, and MITR at two conserved serine residues, creating docking sites for the intracellular chaperone protein 14-3-3. When bound to 14-3-3, HDACs and MITR are released from MEF2. The association of 14-3-3 with HDAC4 and -5 also exposes a carboxy-terminal nuclear export sequence in the repressors, which results in their relocalization to the cytoplasm, thereby allowing MEF2 to stimulate muscle-specific gene expression. However, since MITR lacks the carboxy-terminal nuclear export sequence, it is not exported to the cytoplasm in response to CaMK but is relocalized within the nucleus.
Given the ability of CaMK to promote myogenesis by impinging on MEF2-HDAC or MEFZ-MITR complexes and the observed decrease in histone methylation at a MEF2 site in the myogenin gene promoter during muscle differentiation, we hypothesized that CaMK may influence the interaction of HDAC5 and MITR with HP1α. To test this hypothesis, cells were transfected with expression vectors encoding HDAC5 or MITR in the absence or presence of a construct for constitutively active CaMKI, and the integrity of HP1-HDAC or HPI-MITR complexes was assessed by coimmunoprecipitation analysis. As described above, the association of HDAC5 and MITR with HP1α was readily detectable in the absence of activated CaMK (Fig. (Fig.5B).5B). In contrast, in the presence of activated CaMKI, there was no detectable interaction between HP1α and HDAC5 or MITR (Fig. (Fig.5B5B).
The CaMK phosphorylation sites in HDAC5 and MITR that are bound by 14-3-3 proteins and mediate MEF2 association and subcellular redistribution are serines 259 and 498 in HDAC5 and −218 and −448 in MITR (22, 48). To determine whether dissociation of HP1α from HDAC5 and MITR in response to CaMK signaling was mediated by phosphorylation of these sites or by a different mechanism, we examined the association of HP1α with a mutant of MITR in which these CaMK phosphorylation sites were replaced with alanine residues. As shown in Fig. Fig.5B,5B, the serine-to-alanine mutant of MITR (MITR S218/448A) associated with HP1α in the absence of CaMK signaling and, like wild-type MITR, dissociated from HP1α in response to CaMK. These findings demonstrate that dissociation of HP1α from HDAC5 and MITR in response to CaMK signaling is mediated by a mechanism independent of the CaMK phosphorylation sites that are bound by 14-3-3, which controls the subcellular localization of MITR as well as its association with the MEF2 transcription factor (48).
The results of this study reveal previously unrecognized interactions of HP1 with the MITR corepressor and class II HDACs. The HMTase SUV39H1 is also contained in these complexes. The association of HDACs, HMTases, and HP1 provides an efficient mechanism for modifying nucleosomal histone tails and stabilizing the methylated state of histone H3 lysine 9 via the docking of HP1. The integrity of these chromatin-remodeling complexes is subject to CaMK-dependent control, providing a means to regulate histone methylation in response to extracellular cues that alter intracellular calcium concentration and promote muscle differentiation.
Lysine 9 of histone H3 is targeted by both acetylation and methylation. Thus, HDAC activity serves as an intermediary between the actions of HATs and HMTases by creating the substrate site for methylation upon removal of the acetate group from lysine 9 of histone H3 (Fig. (Fig.6A).6A). The competition between acetylation and methylation of lysine 9, or other lysines in histone tails, has the potential to create a switch to determine the on-off states of genes to which the histones are associated.
The association of HDACs with HP1 may result in the propagation of the repressive state of chromatin through two distinct but related mechanisms. (i) HP1 binding to methylated histone tails may recruit class II HDACs, which could deacetylate adjacent nucleosomal histone tails, thus creating substrates for HMTase activity of SUV39H1. Methylation of these deacetylated histone tails by SUV39H1 would then create new HP1-binding sites, allowing for the subsequent recruitment of HDACs, with resulting propagation of the repressive state of chromatin. (ii) HP1 could be initially recruited to specific genes via its association with class II HDACs that are bound to these genes through interactions with sequence-specific DNA-binding proteins such as MEF2. Once localized to a specific genomic region through interaction with HDACs, the HP1-HDAC complex could also recruit the HMTase, which could methylate deacetylated histone tails that have been created by HDACs. In either case, the interactions among class II HDACs, HP1, and SUV39H1 provide a means of stabilizing the repressive state of chromatin.
In addition to interacting with SUV39H1 and HDACs, HP1 has been shown to associate with the transcriptional repressor TIF1b (32), the nuclear body component SP100 (40), the lamin B receptor (46), and the chromatin assembly factor 1 subunit p150 (29) through the CSD domain. HP1 also binds histone H3 through its CD region and histone H1 and INCENP through its hinge region (2, 33).
Class II HDACs are being found to associate with a growing number of proteins involved in transcriptional repression (Fig. (Fig.6B).6B). Class I HDACs interact with an as-yet poorly defined region within the amino-terminal extensions of class II HDACs, as well as with the catalytic region of class II HDACs (9, 11, 41, 47). The interactions between class I and II HDACs allow for the formation of multiprotein HDAC complexes and allow for cross talk between class II HDACs, which are signal responsive and cell type restricted, and class I HDACs, which are ubiquitous. The class I HDAC HDAC1 has also been shown to interact with SU(VAR)3-9 in Drosophila, which leads to permanent transcriptional silencing of specific genomic regions (5).
The CtBP corepressor interacts with a motif near the extreme amino terminus of MITR and class II HDACs (Fig. (Fig.6B).6B). CtBP also associates with class I HDACs and with other corepressors, such as N-CoR and SMRT, which have previously been shown to interact with class I and II HDACs. Thus, the bridging between multiple types of repressor proteins and HDACs allows for the formation of large multiprotein repressor complexes. The region of MITR and class II HDACs that recruits HP1 is distinct from the binding sites for other proteins identified thus far, which further suggests that these repressors can serve as a bridge between multiple transcriptional regulators.
Previous studies demonstrated that CaMK signaling leads to the phosphorylation of two conserved serine residues in the amino-terminal extensions of class II HDACs (22, 48). Phosphorylation of these sites creates docking sites for 14-3-3 chaperone proteins, which mask the nuclear localization signal and result in the unmasking of a nuclear export sequence at the carboxy termini, with resulting export of HDAC-14-3-3 complexes to the cytoplasm. CaMK-mediated phosphorylation of class II HDACs and MITR also results in dissociation from MEF2. Serine-to-alanine substitutions of these sites prevent CaMK-dependent association with 14-3-3 proteins, disruption of MEF2-HDAC complexes, and HDAC nuclear export. MITR also dissociates from MEF2 in response to CaMK signaling. However, since MITR lacks a nuclear export sequence, it is redistributed within the nucleus but is not exported to the cytoplasm in response to CaMK (48).
Like MEF2, HP1 dissociated from HDAC5 and MITR in response to CaMK signaling. However, a mutant of MITR lacking the CaMK phosphorylation sites also dissociated from HP1. These findings indicate the existence of another mechanism that confers CaMK sensitivity to the HDAC-HP1 complex. At present, we do not know the target for CaMK that mediates this response. We have identified a single CaMK phosphorylation site in HP1α. However, mutation of this site to alanine does not prevent dissociation from MITR in response to CaMK signaling (data not shown). There are numerous CaMK phosphorylation sites in HDAC5 and MITR, only two of which are required for binding of 14-3-3 proteins and dissociation from MEF2 (22, 48). Whether one or more of the other sites are responsible for signal-dependent dissociation from HP1 remains to be determined. It is also possible that other proteins mediate the effects of CaMK on the complex.
Previous studies have shown that class II HDACs play important roles in muscle cell differentiation and myocyte hypertrophy as a consequence of their association with MEF2 (20, 21). The region of class II HDACs that mediates interaction with HP1 is distinct from the MEF2-binding region. Thus, HDACs have the potential to serve as a bridge between MEF2 and HP1-HMTase (Fig. (Fig.6C).6C). In this way, MEF2 could target the repressive complex to specific genes that are critical for muscle differentiation. Consistent with this notion, nucleosomal histones surrounding a MEF2 target site in the myogenin gene promoter, which is transcriptionally active only in differentiating muscle, are differentially modified by methylation and acetylation during myogenesis. Specifically, high levels of histone methylation are observed at this site in undifferentiated myoblasts. Upon differentiation, the level of histone methylation is decreased at this MEF2 element, with a concomitant increase in histone acetylation. Since histone methylation is thought to be irreversible, the reduction in histone methylation observed during myogenesis may be due to exchange of methylated histones with unmodified or acetylated histones through DNA synthesis. In this regard, myoblasts are still capable of synthesizing DNA immediately following serum withdrawal and prior to differentiation (3). It also remains possible that an as-yet-unidentified histone demethylase catalyzes the demethylation reaction, thus providing the substrates for subsequent acetylation by a HAT.
It is also interesting that MEF2 regulates genes involved in proliferation and differentiation, which are expressed in opposing manners (26). Whether the targeting of repressive complexes to some genes and activating complexes to others accounts for the opposing expression patterns of these MEF2 target genes is an intriguing issue to consider.
We thank T. Kouzarides, S. L. Schreiber, A. Means, and C. D. Allis for reagents and S. Huang and S. Brandt (Vanderbilt University) for advice regarding HDAC activity assays. We are grateful to A. Tizenor for graphics and to J. Page for editorial assistance.
This work was supported by grants from the National Institutes of Health, the D. W. Reynolds Clinical Cardiovascular Research Center, the Texas Advanced Technology Program, and the Robert A. Welch Foundation to E.N.O. T.A.M. is a Pfizer Fellow of the Life Sciences Research Foundation.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Find pain medications for dogs are important and find those medicines which can relief pain quickly and safely with least amount of side effects. But dogs are not human, it is very important to take those medicines which are suitable for pets. For this reason, always ask your vet to advise you the right med for dog and try to use prescribed medicine by a vet. Many people ask "which is the best pain medicine for dog to their vet and friends" etc. So, the right answer is mentioned in this article, read this article carefully and you know the right medication for dogs
Pain Medicine for Dog- Over the Counter Medicines
Basically over the counter medicines are non-prescribed medicines for humans as well as dogs. These medicines are easily available in general medical stores. These medicines are used to cure minor level and a mild level of pain and other health problems. Some over the counter medicine are with PM formula like Tylenol PM which contains the main ingredient of Diphenylamine HCL which has a mild effect. Some Pain medications which are with PM formula are not good for dogs and some are prescribed by vets.
Aspirin for Pets or Dogs
Aspirin is safe and reasonable medicine for humans as well as dogs and aspirin are used to reduce fever and inflammation. The best medicine for stomach irritation is buffered aspirin. It is usually used for minor health problems if your dog suffers from serious health issues then immediately consult with a vet. Aspirin is commonly used for short-term treatment for minor pains and aches and also it is very important to be careful about the dose of aspirin because every medicine has possible side effects.
Tylenol Medicines for Dogs
Most vets and expert are not advice to give Tylenol to dogs. The reasons are:
- It is not considered as effective and safe pain relief medicine for dogs.
- It can be toxins in high doses to dogs.
- Most of the times, small doses may cause serious health issues in dogs.
Always check first with a vet before give your dog a Tylenol. If your vet gives you the permission, be very careful about the dosage. Side effects of Tylenol are usually kidney damage and liver damage. Our advice is it is best to avoid Tylenol for dogs.
Flex Pet for dogs
Flex pet has same ingredients which are found in Flexcin for humans and it is more than a pain relief medicine. It is decrease inflammation and reduces pain and lubricates the joints of the dogs. This medicine allows the dog to move easily in the case of arthritis main and it also reduces the arthritis pain. This medicine is a chewable tablet for your dog and your dog can take daily of one tablet.
Ibuprofen for Dogs Health issues
Ibuprofen is a common medicine for pain relief and that should not be given to the dogs that mean simple ibuprofen, Advil, and Motrin should not use for your dog. Naproxen is another pain relief hidden medicine for dogs and it is also not good and safe pain medicine for dog. If you give your dog any of above medicines, it is important to immediately visit a vet.


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Is my gynecomastia operable? (Photos)
Doctor Answers 9
Candidate for gynecomastia removal surgery
You should meet with a board certified plastic surgeon to be able to get a formal diagnosis and to be able to decide on a course of treatment if necessary.
Is my Gynecomastia Operable?
Learn more: http://www.horowitzmd.com/male-plastic-surgery-newport-beach/gynecomastia/
Operable Gynecomastia
Yes, it is operable, and you do have enough tissue to make a decided improvement. You do not have much body hair, and in our practice we would offer you our preferred technique with no scar on the chest and no drainage tubes. I hope this has been helpful. Robert D. Wilcox, MD
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Is my gynecomastia operable?
You have to make sure to pick the right surgeon
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Gynecomastia Surgery
Evaluation and Treatment of Gynecomastia
Are you taking or using anything associated with man breasts? Using anabolic steroids, smoking pot, using certain antacids or antidepressants? The list is long but it's well worth going over.
Finally, the vast majority of Gynecomastia cases can be treated nicely with liposuction and some excision of the breast gland. I would see a qualified Plastic surgeon for it.
Dr. Peter A. Aldea
Memphis, TN
These answers are for educational purposes and should not be relied upon as a substitute for medical advice you may receive from your physician. If you have a medical emergency, please call 911. These answers do not constitute or initiate a patient/doctor relationship.


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This qr code contains the url of current webpage.
Gaseulgap-sa was a temple located on Mt. Unmunsan, and currently only its site remains. The temple is said to have been established by the great Buddhist monk, Won-gwang who had just returned from the Sui Kingdom of China after being disciplined in the period of King Jinpyeong of the Silla Kingdom. When the great Buddhist monk stayed in the temple, Guisan and Chuhang, who belonged to a disciplinary group of Hwarangdo, visited him and asked for words by which to live in their lives. In response, the monk gave them five disciplinary rules, which are called 'Sesok Ogye' (Five Rules for Living in the World).
These rules were followed as ethical instruction and practical ideology, and then contributed greatly to the development of Hwarangdo and the preparation of the basis on which to unify the Three Kingdoms.
The Statue in Memory of the Hwarang Spirit Birthplace represents Guisan abd Chuhang being given 'the Five Rules for Living in the World' by Won-gwang


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Welcome to Chestnut!
Your teacher will very soon be filling this page with exciting class news, pictures of things we've done and more.
Do you have any ideas for this page? Why not let your Teacher know!
Have you seen the Kids' Zone? Play games and visit some cool websites. You can vote for your favourites.
Revision Time
For something different this year, we had fun, yes fun, revising! We covered the tables in white paper and then wrote 'graffiti style' all the information we had learnt, then pinned them up on the walls.


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Welcome to the Official Website of Pedro P. Cruz Elementary School
Classes as USUAL today.
Note that after the last subject, pupils are dismissed on official/regular time.
Message from Sec. Luistro
Welcome, dear Department of Education Employee!
This is the first step in acquiring your very own official DepEd Email account. Email helps make work and communication in the department easier with a more efficient process of transmittal and exchange of information and correspondence. Powered by Google, the account not only includes the email service but also many applications and tools that are useful in office management, classroom management, and file storage. We hope that you will utilize the applications and the email service to facilitate a better work process.
Br. Armin A. Luistro, FSC
News / Announcements
To Concerned Stakeholders:
NAT Review for both Grade III and VI
March 3-8, 2014
Grade VI NAT Review
(Rooms 1-7) Morning Sessions 7:00-12:00
(Rooms 8-14) Afternoon Session 12:00-5:00
Grade III Regular Time


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FamilySearch Wiki:WikiProject Social Media
From FamilySearch Wiki
Revision as of 20:24, 2 April 2012 by Mccormickmw (talk | contribs) (added tasks discussed today, and added my name to contributors)
This is the Social Media WikiProject page. A focused community effort to create or revise content relating to a single topic.
To develop information in the wiki about how to use social media as a resource for research.
Userbox for WikiProject Social Media
|Project members: you can also add {{User WikiProject Social Media}} to your user page to identify yourself as a member of the project and add your name to the Category:WikiProject Social Media participants.
Genealogy Research Communities (GRC) Content
- Evaluate content from GRC Admins Google Site
- Move relevant data to the wiki in a way that applies to both GRC admins and the broader audience
How to use Social Media as a resource for Research and Sharing
- Most of the current Social Media pages focus on use of social media by genealogy administrators
- Add a separate section on existing wiki pages (Facebook, Twitter etc) that will explain the benefits of research help and sharing within social media for the average population
WikiProject Templates
| {{WikiProject Social Media}}
Template showing an article, image, category, or template is part of this WikiProject. Placed at the top of talk pages, not articles.
| {{Social Media-stub}}
Stub notice for Social Media articles; placed at the bottom of article pages


text:
Category: precision medicine
Dec 2, 2016
Emily S
How 'digitizing you and me' could revolutionize medicine. At least in theoryThere's a whole lot of hype around precision medicine. Proponents — up to and including President Barack Obama — predict a revolution that will bring us medical treatments as precisely tailored as a bespoke suit: Drug doses adjusted to your genome. Chemotherapy customized to your tumor's DNA....
Sep 13, 2016
Emily S
Sharing personal health information can never be risk-free, but it can be low-riskThe growing use of electronic medical records, electronic insurance claims, and other medical software systems is generating massive volumes of personal health information. While the primary purpose of capturing this information is to provide patient care, researchers have a voracious appetite for...
Mar 18, 2016
Emily S
The NIH, in pursuit of precision medicine, tries to avoid ghosts of its pastThe National Institutes of Health is preparing to recruit 1 million volunteers for one of its most significant research projects in years, one meant to develop personalized medical treatments. As it does so, officials are trying to dodge the ghosts of a similarly ambitious research initiative, one...
Jan 11, 2016
30-Year-Old Woman Races Time to Find Cure for Rare Form of Cystic FibrosisFor most, turning 17 proves an awakening of sorts. The occasion marks the final year of the carefree trappings of adolescence, placing one squarely on the precipice of adulthood and a world of exhilarating changes.
Apr 16, 2015
IBM Creates Watson Health to Analyze Medical DataIBM is taking its Watson artificial-intelligence technology into health care in a big way with industry partners, a pair of acquisitions and an ambitious agenda.
Mar 9, 2015
On the Case at Mount Sinai, It's Dr. DataJeffrey Hammerbacher is a number cruncher — a Harvard math major who went from a job as a Wall Street quant to a key role at Facebook to a founder of a successful data start-up.
The Penn Medicine Center for Health Care Innovation engages interdisciplinary teams to reimagine health care delivery for dramatically better value and patient outcomes.
The Leonard Davis Institute of Health Economics (LDI) is Penn's center for research, policy analysis, and education in health systems. Its 200 Senior Fellows analyze the medical, economic, and social issues that influence how health care is organized, financed, managed, and delivered across the U.S.
We are passionate about pursuing impactful research and eager to explore opportunities that will enable a culture of social media and health innovation at Penn, Penn Medicine, and beyond. Have an idea for a project? Interested in collaboration? Click here to learn more about how to contact us.


text:
Skip to comments.NBC Minimizes Obama's Iraq Pullout As Contributing Factor to Islamist Advance
Posted on 06/16/2014 8:20:54 AM PDT by Cheerio
National Baraq Channel
On Friday's NBC Nightly News, Brian Williams strongly hinted that the recent Islamist blitzkrieg in Iraq was completely former President Bush's fault: "Make no mistake: what's happening in Iraq right now is a direct outgrowth of the U.S. decision to invade the country over a decade ago." However, he glossed over the Obama administration's failure to negotiate a continued U.S. presence and pulling out all American forces in late 2011 as a factor in the crisis.
Williams repeated his point to David Gregory: "How does the President sell any action at all to the component of the American people who feel...it's not our dance...even though...we broke it?" Gregory seconded his contention: "Right, that Pottery Barn rule: you broke it; you own it; you got to somehow fix it." Later, Stephanie Gosk did reference the troop pullout, but didn't mention President Obama by name: [MP3 audio available here; video below]
(Excerpt) Read more at mrc.org ...
Raise your hand if this surprises you.
NBC works for the DNC.
The main reason why ?
All they have are failures.
Shame on NBC...
Campaigner in chief, Obama, promised a 16 month pull out. It was all political to him.
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