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Northwood nursing home locked down
NORTHWOOD, N.D. — The nursing home at Northwood (N.D.) Deaconess Health Center went into "lockdown" for a time Wednesday afternoon when police believed a gunman was on the loose, according to Officer Matt Evenson with the town's police department.
Stan Baker, a former resident in his 30s now living in the Fargo-Moorhead area, allegedly made a reference on Facebook to "shooting up the school" in Northwood, Evenson said.
School is not yet in session.
The nursing home was locked down because three of his friends work there, but there was no evidence he threatened the home.
Police in Fargo-Moorhead eventually took him in for questioning, Evenson said.


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Fire and Ice came at a critical time in Malmsteen's career and the world of metal as a whole. As many have pointed out, grunge had just come into play and metal bands were either folding or defecting and breaking ranks in droves, and Yngwie had just done the album Eclipse, which was a stain on his career after the 4 rising force albums. So he either had to make a good album, and define the next decade of his career, or he would burn out and jump on the wagon of the has-beens.
Obviously, it worked, because the early-mid nineties were a great time for Malmsteen, and he released scorcher after scorcher. However, this album, in itself, is not that memorable. Sure, the songs are all catchy. Sure, the guitar playing is spot on. However, as I said, this album is good to a point. That point is Goran Edman, who technically doesn't fail as a singer, since he does hit the notes, fails as a successor to Joe Lynn Turner. His voice is thin and voiceless, losing power as he hits the higher notes, sounding like a teenager just getting into his new manlier voice. Thank the metal gods that Yngwie booted Edman and replaced him with Michael Vescera. The singing isn't bad, as I was led to believe, it just adds nothing to the album, and strikes the listener as extraneous and unnecessary. However, on songs like Fire and Ice, where he avoids the higher range where he loses power, and Leviathan, where he doesn't sing at all, the album works. From this, it can be deduced that Goran detracts from the overall listenability of the album.
However, the drums are good, shining in the aforementioned songs, being wonderfully technical but not stealing the spotlight from the almighty Yngwie. The bass, as always, is inaudible most of the time, but that it doesn't detract from the fun of Fire and Ice. The songwriting is a preview of what's to come, namely catchy, melodic, and aggressive power metal/shred, with blistering guitar solos and plenty of neoclassical influence, as well as influences from hard rock and blues rock. It expands slightly upon Yngwie's repertoire, as well as rectifying the mess that was Eclipse. So yes, it succeeds as an album. Get it if you like Malmsteen, chances are it won't change your opinion.

subset: commoncrawl


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Alcohol Markers - Spectrum Noir
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connie leone
Mad Swapper
Join Date: Jan 2006
Location: Central New York
Posts: 1,599
S.N. markers & copics
Originally Posted by
Thanks! Don't you love that Philosophy cart!! Can't wait for the other one to come in.
I love the little coffee caddy and it's perfect for my kitchen but if you want one for your kitchen I'm sure there is something that would work for your style with another cart you have . I would make something for you if I knew what you wanted or needed.
The cart used is a Lite cart so it is not to much and there are a lot of cute designs on there. Did you see the tea bag gift made for a friend? That was so much fun to make too !
Way to go with markers!! I have a favor- See how they blend in with the Copics. If they blend well together , it would be even more of an extension of the color palette to use!
I think I will go ahead and order a pack or 2 myself today.
Hi Paige! I have not had a chance to try the Copics & S.N. together yet. I was on you tube and they are saying that they are compatible. The person did use them both together! Did you order any S.N. yet? When I was at work last night I was looking at one of the packs I think it was a neutral pack (white,creams, etc.) and it also had a colorless blender in it. I will probably get that one next! $14.99 per pack, less 50% off coupon not bad! Just a little over a dollar per marker! I wish they had the larger packs but they don't!!!
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Wenger to rely on untested keeper Mannone
Arsenal manager Arsene Wenger will give rookie goalkeeper Vito Mannone his Champions League debut at Standard Liege on Wednesday night and admits it will be a "big challenge" for the youngster.
With regular number one Manuel Almunia sidelined with a virus and Poland international Lukasz Fabianski still recovering from knee surgery, the Italian will be thrown into the cauldron of the Stade Maurice Dufrasne as Arsenal's senior goalkeeper.
Despite just one Premier League match, against Stoke City last season, and a couple of games while on loan at Barnsley under his belt, Wenger is backing the 21-year-old to seize his opportunity.
"It is a big challenge for a young boy to come into a Champions League game with such a big pressure, especially away from home," said Wenger. "When you look at the stadium, it will be quite a difficult atmosphere."
Arsenal paid Italian side Atalanta £350,000 compensation for Mannone, then 17, four years ago.
Wenger will also be without Dutch forward Robin van Persie because of a slight knee problem. Croatia striker Eduardo is free to play following the decision by UEFA to overturn their suspension handed out after the qualifier against Celtic at Emirates Stadium last month.
Wenger said: "I am very happy we have Eduardo back because we have plenty of offensive players who are out. We have [Andrey] Arshavin, [Theo] Walcott, [Samir] Nasri and of course Van Persie.
"Eduardo on top of that would have been too many strikers to have out. That is why I am very happy to have him back. It was a good surprise I must say."
Defensive midfielder Denilson is also sidelined by a minor back complaint, so Czech winger Tomas Rosicky could be in contention having made a long-awaited comeback at Manchester City.
Wenger said: "Everybody in the squad is very happy to have Tomas back, not only because we love him but because he is a fantastic football player. He has a good chance because it is a good opportunity for him."
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Some people say that The Fabulous Sports Babe can't finish a single thought and just talks about random stuff. Guess what? That's the charm of the show! And nothing captures the essence of the Babe's show than Rollergirl's Stories We Missed, a collection of the most random stuff from the world of sports, news, and pop culture.
Tonight's edition features stories about Robert Griffin III's new house, a Seahawks lineman busted for allegedly urinating next to a parked car at a bar, a Grizzlies player using Twitter to possibly get a date with Miss Tennessee, the Tampa Theater being named one of the top venues of its kind in the world, and more!!


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" Genre: Fiction / Author: Kaavya Viswanathan / 320 pages / Book published 2006-03-27 by Time Warner Paperbacks "
* Prices may differ from that shown
Today I am going to review the novel
How Opal Mehta got kissed got wild and got a life
This book was written by Kaavya Viswanathan. I saw this book in a magazine but forgot about it. Luckily, while I was browsing through a charity shop, I saw it and remembered the short review I read in that magazine. It sounded so brilliant and sat on the shelf for just £1.79. I bought it, started reading and got through it within three days!
I had so much fun reading it, it deserves a review!
The plot
Opal Mehta is a dream student. She is of Indian origin and the stereotype nerd-girl.
Her parents are not very conservative but they do push her to achieve the great plan the little family has been following since Opal was born - plan HOWGIH (How Opal Will Get Into Harvard).
When Opal is about to graduate from school with brilliant grades, she goes to her interview at Harvard to enroll. While the interviewer appreciates her grades, he tells Opal that they don't simply want students with fantastic grades but real personalities. Opal is stunned when she gets told that she should get a life and then come back for the interviews that are scheduled later, when she has completely graduated. If she has enjoyed her life and become an independent, adventurous girl, she might get taken!
Opal and her family are confused and devastated - but only for a short time, until they start developing a new plan - HOWGAL - How Opal will get a life.
They parents, fanatic about planing, watch teen movies with Opal, study teen magazines, buy her new clothes and make up and also develop plans to spark Opal's popularity. Opal now has a new aim next to keeping her fantastic grades up - she needs to get wild, be popular and pretty and make new friends among the popular people at her school.
In that troublesome, chaotic year she makes new friends, looses old ones, grows up but also realizes who her real friends are and what the ballance between her old life and her new one is.
The book has 314 pages.
The author
The book gives away very little about her, but the first page says: Kaavya Viswanathan is eighten and studying at Harvard. Born in India, Kaavya lived in Aberdeen, Edinburgh, and Melrose before moving to the US. The book is devoted to her parents and there are acknowledgements on the first page.
Why is it so good?
The book is so funny because of many aspects. The characters are well formed. Opal is sweet but full of doubt. She is sensible but determined to get into Harvard.
Her parents are what gives the most comical elements to the book. Their appreciation for the new plan makes you want to die laughing. When Opal finally manages to recieve her first kiss, they spy on her and cheer because it is one if their biggest goals!
Of course, this book is less than realistic, but it still presents the problems of Opal's Indian, polite nature, the will to make it to the top and her parent's determined mindset to do whatever it takes to have their daughter succeed.
The book is full of fabulously funny moments because Opal's way to popularity is not an easy one.
It is fast-paced and never gets boring!
What does the book look like?
My edition came out in 2006 and has a mint-green cover with a girl covering the right side. She is dressed in a purple vest with a purple nice-looking shrug and carries old-looking books as well has a pair of high-heels. The title of the book is written in purple and pink letters.
The picture of the girl presents the conflict very well and fits the novel way better than the yellow cover it seems to be published with now.
The back of the book is kept in the same colour scheme and shows a bed with books next to it. You see the lower half of the girl - she has her feets up against the bed.
The text on the back of the book goes:
Opal Mehta wants to go to Harvard and her parents will do anything to get her there!
When Opal Mehta was six years old her parents carefully and thoroughly constructed HOWGIH (How Opal will get into Harvard). It is their one dream for their daughter and failure is not an option. But when the first question the Harvard admission officer asks is, "What do you like to do for fun?" Opal is stumped.
And so HOWGAL (How Opal will get a life) springs into action, and with hilarious results..
Publishing etc.
The book is published by Time Warner Books, filed under General Fiction
First published in Great Britain in March 2006
Alloy Entertainment holds the Copyright.
I defenitely recommend this book! If you are looking for an unputdownable, fun book without getting an average chic lit book, this is the thing for you!
I also recommend it as a gift. When I can't think of a present for someone, this is among the books I tend to get for them!
I have read some stuff about the book being plagiaism and that's why it isn't being sold anymore - but I sitll enjoyed it, so go pick it up in a charity shop. ;)
~The Story in the Book~
Opal Mehta is an exceptional young woman with outstanding academic prowess, virtuoso musical skills, multiple languages and lots of clubs and societies that ought to make her the perfect candidate for a place at Harvard. Her application is just about the closest thing to perfection and that's no accident. Opal didn't get all those attributes by chance alone - she's the result of the meticulous planning of her parents and their implementation of a very long plan, codenamed HOWGIH, or 'How Opal will get into Harvard'.
Opal ought to be a dead cert for a place at this prestigious university. She's got a smart suit, she's practiced all the answers to all the likely interview questions but things aren't going to plan. When the Dean of Admissions asks her to tell him what she does for fun, Opal has no answers. When he asks her to tell him about her friends, she can only think of her physics lab partner and her cat, Mr Muffty. The Dean tells her that the world is full of great candidates but he wants people with a bit more about them. In short, the message is clear - Opal needs to get a life.
~New Objective, New Plan~
Cue Project HOWGAL, short for How Opal Will Get a Life. Mr and Mrs Mehta crack into action, researching the right music, paying a fortune to buy her the right clothes, setting homework that consists of slang 'flash cards' and watching multiple episodes of The O.C., Desperate Housewives and every high school movie of the past couple of decades. Their mission is to make her the most popular girl in school and to get Opal kissed, get her wild and most of all get her into Harvard.
It's silly, unrealistic, predictable, enormously derivative, and surprisingly good fun.
As Opal goes through her transformation, drops her old geeky friends in order to hook up with the really cool and bitchy girls, chases the wrong boy and fails to spot the right one (though every reader will has seen him a mile off) we can't help but be reminded of films like Mean Girls and even Heathers (or am I just showing my age?) It's a plot that could have come from Shakespeare via Beverly Hills 90210 and The O.C. and you won't be surprised to read that I could have told you the whole plot with every twist and turn that was to come once I was about 3 chapters into the book.
Of course there will be a redemptive ending. Sucking up to the shallow nasty cool kids is never going to be allowed to be the answer. We all know that Opal will sooner or later be brought face to face with her mistakes, will have to confront her reliance on thinking that being the girl others want to be equates to being 'liked' and having friends, and that she'll eventually realise that she's unable to spot what a nerd the would-be kissee undoubtedly is.
~Young and Overly Talented or just a low-down dirty cheat?~
Kaavya Viswanathan tries to put a twist on an otherwise very obvious tale by making Opal a highly intelligent Indian-American immigrant and making the tale a sort of 'Legally Blonde in reverse' but at heart, it's just a silly and rather obvious tale that will please teenagers looking for a holiday sun-bed read. Over-privileged kids with fawning over-indulgent and over-ambitious parents will always need to be taught a lesson sooner or later. We know where this one is going and you don't need to be a hardened old cynic like me to spot how obvious this all is.
~The Story - off the Page~
From all that you've read so far, you've not got too many hints that something so seemingly light and innocuous got Kaavya Viswanathan embroiled in a major media scandal that made her one of the most googled names of her time. Google it? I can't even spell it.
Viswanathan looked to be a publisher's dream girl. She got the book deal whilst at High School preparing to get into Harvard and they must have thought she was money in the bank. Unfortunately what the publishers didn't spot but multiple readers did was that there was significantly less original material in the book than even I had spotted and Kaavya Viswanathan's greatest gift was for plagiarism. Passages in her book were identified as only slightly reworded thefts from the work of at least five other popular writers including everyone from Sophie Kinsella to Salman Rushdie - not two names you'll find in the same sentence very often. At least we can see that the young lady's reading habits were eclectic! Scandal ensued, the book was pulled and she was really put through the wringer. If you are interested to know more, Wikipedia have an excellent and very detailed article on Wiswanathan which places the disputed texts side by side. It's very hard to imagine that anyone could have accidentally recreated some of these passages.
The book did seem a bit too accomplished for a 17 year old's first attempt - turns out that large chunks weren't hers so perhaps that's why. I paid 50p in one of our local charity book shops and consider this a fair buy buy if only as a cautionary tale of just how badly copying other people's work can back fire. It's not my genre, it's very predictable but in an age when it seems that copying stuff for school is standard fare, it's reassuring to know that readers can spot a cheat and won't stand for it. I have no idea what Viswanathan did with her life post Opal Mehta - I just hope she got one!


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This Powerful Mid-Bore Round Is Suitable For All
North American Game.
The .35 Whelen was designed by Colonel Townsend Whelen in 1922 while he was commanding officer at Frankford Arsenal, the huge US Army ammunition plant near Philadelphia, Penn. James V. Howe served as chief toolmaker and gunsmith on the project, but left the next year for New York—at the recommendation of Whelen—to partner with stockmaker Seymour Griffin in forming the famous gunsmithing firm of Griffin & Howe.
It may seem odd for an Army arsenal to be involved in sporting rounds, but Frankford was also an experimental station, and almost any experiment had some potential military use. This continued after Whelen became director of research and development at Springfield Armory in 1929, and among the results was the .22 Hornet.
After Charles Newton's .35 Newton collapsed along with his company during World War I, there wasn't any powerful medium-bore cartridge for American bolt actions, which led to the design of the .35 Whelen. The .375 Holland & Holland Magnum had been around since 1912, but the .375 was considered too large for most American hunting—and also our bolt actions, despite the original .375 H&H rifles being built on opened-up 1898 Mausers. The 1903 Springfield could also have been modified, since it was essentially an American version of the 98, but the cartridge would still have been British.
Necking up the .30-06 to .35 was a simple solution, and the .35 Whelen had other advantages over the .375. Five rounds would fit in the magazine, instead of three, potentially helpful when hunting grizzlies or Alaskan brown bears, and the recoil was noticeably milder than the .375's. This not only made shooting easier, but the .375 H&H often split unreinforced stocks, and the .35 Whelen didn't. (A few years before the H&H appeared a German named Otto Bock developed the cartridge some Americans call the "metric .35 Whelen," the 9.3×62 Mauser, specifically to fit in unaltered 98 Mauser actions. But when Whelen ran Frankford there was still considerable anti-German feeling in America due to the recent war.)
In those days there weren't any truly controlled-expansion bullets, so the only way to insure adequate penetration on game larger than deer was heavier bullets of relatively modest velocity. The primary load of the .35 Whelen was a 250-grain bullet at around 2,500 fps, though some hunters preferred a 275-grain roundnose, notably a gun writer/guide/rancher named Elmer Keith, who in 1937 stopped a charging Alaskan brown bear with several 275-grain Western Tool & Cooper Works bullets from a .35 Whelen built on a Springfield action.
The Whelen became quite popular as a wildcat, but no company turned it into a commercial round until 1987. Remington had been making wildcats legitimate since 1935, when they bought out a slightly modified version of Ned Roberts' .257. World War II interrupted further introductions, but from 1955 onward they brought out their .244/6mm (.240 Page Super Pooper), .22-250, .25-06, .280 (7mm-06) and 7mm Magnum. All were based on various wildcats, and became more or less successful, but the cartridges actually designed by Remington during the same period didn't do so well, especially their 6.5 and .350 Remington Magnums. In fact the .35 Whelen probably put the last nail in the .350's coffin, since it has almost exactly the same powder capacity and works in any action suitable for the .30-06.
Remington's .35 Whelen rifles sold pretty well for the first couple of years, but after that sales slowed considerably. Apparently relatively few American hunters desire a cartridge larger than .30 caliber anymore, partly because the .338 Winchester Magnum had already filled the American medium-bore slot when it was introduced in 1958.
The .35 Whelen, however, has some advantages over the .338, just as it does over the .375 H&H. While the .338 doesn't normally split wooden stocks, it kicks hard enough to affect the aim of some hunters. Velocities are also high enough to cause occasional problems with cup-and-core bullets, but 250-grain cup-and-cores at 2,500 fps from the .35 Whelen works just as well today as it did in the 1920s—and don't cost $1 a bullet. (One of the loads listed with 250s, 59.0 grains Reloder 15, appeared in Alliant data for many years, then somehow was dropped to 54.0 grains recently, for only 2,284 fps. I don't know why, 59.0 has never shown the slightest indication of high pressure in any of my rifles with any 250-grain bullet.)
Still, some 21st century hunters prefer lighter, premium bullets, since they kick less and can be driven faster to shoot flatter, at least at "conventional" hunting ranges. Today a number of companies make premium .35-caliber bullets from 175 to 225 grains. One of the bullets tested was the new 175-grain ESP Raptor from Cutting Edge, an all-brass hollowpoint bullet designed to shed the petals on expansion, hence doing more damage. The ESP can also be turned around to use as a flatpointed solid, or a separate plastic tip snapped into the hollowpoint to increase ballistic coefficient.
Many hunters prefer 225-grain premiums, such as the Barnes TSX or the Nosler AccuBond and Partition, since they can achieve up to 2,800 fps with modern powders, turning the Whelen into a 400-plus-yard elk and moose cartridge. Nosler's most accurate listed load for the 225 AccuBond, 60.5 grains of Varget, shoots very well in most rifles, but I also decided to try Ramshot TAC. Ramshot doesn't list data for the Whelen, but the Barnes manual shows very fine results with TAC and 200- and 225-grain bullets in the .350 Remington Magnum. Since the Whelen and .350 have the same powder capacity, I worked up cautiously to close to the same charges, and got excellent results with no indication of high pressure.
The slow 1:16-inch rifling twist of most .35 Whelens won't stabilize any lead-cored spitzer above 250 grains, or monolithic spitzers heavier than the 225-grain Barnes Triple Shock. This isn't a big deal since most .35-caliber bullets above 250 grains can't be driven very fast and have relatively blunt noses, making expansion iffy except at very close ranges.
Over the years I've owned four .35 Whelens, including one .35 Whelen Ackley Improved, perhaps the most useless improved cartridge ever, since blowing out the tiny shoulder doesn't result in any meaningful extra velocity. All had traditional 1:16-inch twists, so I've haven't loaded bullets over 250 grains and never felt the need for anything heavier. Apparently not many other people do, since almost all load data maxes out at 250 grains.
True fans of the .35 Whelen often load .35-caliber handgun bullets for practice and smaller game, whether edible or varmint. A couple of those loads are included in the tables, and while neither shot close to where full-power loads did in my latest .35 Whelen, they grouped OK and sure don't kick like the heavier loads!
The real niche of the .35 Whelen in North American is game larger than deer, but some whitetail hunters chose Colonel Whelen's old round even if they never plan to hunt moose or brown bears. The big bullets put deer down solidly and don't shoot up meat, so why not?
By John Barsness
>> Click Here << To See Performance Charts
Order Your Copy Of The GUNS Magazine November 2013 Today!


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A man who fled on northbound Interstate 5 Tuesday night after striking a car on the right shoulder in Encinitas was arrested when his car was disabled by spike strips in Orange County, the California Highway Patrol said.
The man, whose name and age were not yet released, was arrested on suspicion of driving under the influence and evading arrest, said CHP Officer Jesse Udovich.
The CHP had received reports of a maroon Lincoln sedan being driven erratically on I-5 near Encinitas and had been trying to locate the vehicle when a report came of the Lincoln passing other vehicles on the right shoulder. The Lincoln struck a Subaru that was stopped on the shoulder just north of Manchester Avenue about 6:53 p.m. The driver then fled.
No one in the Subaru was injured.
Two CHP officers and a Border Patrol agent attempted to stop the Lincoln at the Border Patrol checkpoint near San Onofre, but the driver continued on.
The pursuit was then taken over by CHP officers from San Juan Capistrano, who disabled the Lincoln with a spike strip on I-5 just north of the Junipero Serra Road exit in Orange County.
"The strip blew out all four tires," Udovich said.
The man was not injured and was then taken into custody, the officer said.


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Colitis (Symptoms, Types, and Treatments)
Table of Contents
- Colitis definition and facts
- What is colitis?
- Colitis and the anatomy of the colon
- What are the causes (types) of colitis?
- Infectious causes of colitis
- Ischemic causes of colitis
- Inflammatory bowel disease and colitis
- Microscopic colitis
- Allergic colitis in infants
- What are colitis symptoms and signs?
- When should someone contact a doctor about colitis?
- What kind of doctor treats colitis, and how is it diagnosed?
- How is colitis diagnosed (physical examination)?
- What blood tests and/or stool samples diagnose colitis?
- What imaging tests and procedures diagnose colitis?
- What is the treatment for colitis?
- What is the prognosis for a person with colitis?
Microscopic colitis
There are two types of microscopic colitis: 1) collagenous colitis and 2) lymphocytic colitis. Either collagen or lymphocytes (a type of white blood cell) infiltrate into the layers of the wall of the colon, presumably as a result of inflammation. This is an uncommon illness and may be an autoimmune disease. The diarrhea often is watery, and no blood is present in the stool.
Allergic colitis in infants
In infants younger than 1 year of age, colitis is often due to allergies to cow or soy milk. Allergic colitis may be seen in breastfed babies, where mothers drink cow's milk and pass that protein into their breast milk.
8/15Reviewed on 9/26/2017


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ACParadise Network: American Cosplay Paradise American Cosplay Experience American Cosplay Snapshots
About this Brand
Most Used Wigs
- Clip-in Bangs (1 Costumes)
- Name:
- Rainbow Hair Stage
- Location
- China
- Website
- Seller Status
- Open
Biggest Fans
(Based off number of wigs used)
Recent Updates
Here are some recent updates by ACParadise members using wigs from this brand. Click on the wig name at the top to view information about the wig used. Clicking on the character name at the bottom will take you directly to the costume's page.


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The HTC waiting for XDA-Devs write nice ROM for them. And XDA-Devs don't want to do that, because HTC don't paying anouth for the work...That's the true story.
Reading that made my head hurt. Please try again.
Sent from my PG86100 using Tapatalk 2
...Just in!
The ICS update (220.127.116.11) will be released for the evo 3d on december 25th, 2012. However, HTC has also claimed that due to circumstances(mayan end of days), It is not likely many users will be able to get this update.
JK nobody knows.
XDA Developers was founded by developers, for developers. It is now a valuable resource for people who want to make the most of their mobile devices, from customizing the look and feel to adding new functionality.
Are you a developer? | Terms of Service
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WASHINGTON - An unidentified guy crashed President Obama's Top Secret National Security briefing early this morning.
Sources within the Secret Service have confirmed that an unidentified male, approximately 30 years old, crashed the President's National Security Briefing early this morning, sat and listened attentively for almost 45 minutes, asked two questions about Afghan security forces, and then was arrested without incident.
Approximately 30 minutes into the 60 minute briefing, Vice-President Biden was apparently getting suspicious of the guy, whose question on the "Afghan security services' uniforms" seemed odd, especially as there is almost no uniformity among the attire of the Afghan police forces. Secretary of State Hillary Clinton apparently raised an eyebrow when the guy's second question, "So what do you want us to do about that Taliban guy we arrested before?" fell flat throughout the room.
Eventually the President, after pondering an update from the C.I.A. over closed-circuit, suddenly said, "Hey! Wait a minute, who is that guy anyway? Yeah, you! Should you even be in here?" Pushing back his chair, he allegedly pointed at the guy and said, "Ok, who let this guy in here?" at which point a sheepish Vice-President Biden reluctantly raised his hand.
"Again? That's just great," the President allegedly said, and immediately called in the Secret Service who took the guy into custody very roughly.
After being interviewed, Vice-President Biden apparently swore to his Chief of Staff that the guy "looked all right" and confessed he didn't know "what the Secret Service is making such a big deal about."


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ROBERT BELINIC (Classical)
The first guitarist to win the YCA International Auditions in NY in 2002, Mr. Belinić has established himself as a consummate guitarist of grace and stature, easy yet exciting on stage, playing with a conviction fueled by innate gift and solid study.
Mr. Belinić performs worldwide and champions new music. His program will include a diverse selection of composers including Koshkin, Lauro, Ponce and Bach. Special senior/student pricing. Young Masters Series sponsored by the Roy L. Komack Memorial Fund. www.yca.org/roster/robert-belinic
"Mr. Belinić performs with the most intense passion, energy and charisma of any guitarist I have heard. His playing has the maturity and artistry of someone twice his age." - New York Concert Review
Admission: non-member $25 member $20
Discounts (seniors, students, children) are available


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The old saying is, "Fool me once, shame on you. Fool me twice? Shame on me!"
It needs to be updated for today's political reality. That reality leads the saying to look something more like this:
"Fool me once, shame on you. Fool me twice, well, of course you did, because I'm a mindless Obamaton wh


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Sony PlayStation Vita Launches Today
Sony's latest entry into the handheld market, the PlayStation Vita, launched today in the United States and Europe.
The Vita features a 5-inch, 960x544 touch screen, a dual analog interface, 3G/Wi-Fi compatibility, and most notably, a rear touch-sensitive panel to allow players to control games with all 10 fingers while still holding the device.
Sony's new handheld also features an online store to allow gamers to download new titles rather than buying them in-store. The downloads will still require proprietary blank media cards, however, and Sony will still sell physical copies of the games for consumers who prefer them.
At $249 for the Wi-Fi model or $299 for the 3G/Wi-Fi version, plus another $39.99 for each game, the Vita's steep price has caused some industry professionals to question how successful Sony's latest offering can be in a new era of cheap, casual gaming.
With the rise of smartphones, much of the gaming industry has turned away from the "pay once for the console, pay again for the game" model of portable gaming. Instead, many companies are choosing to offer cheap or free-to-play games that are supported by either advertising or micro-transaction purchases.
The Vita first launched in Japan back in December, where it received largely positive reviews and sold 325,000 units in the first few days. However, sales had dropped 78 percent within a week, falling below 14,000 units by February and severely underperforming compared to Nintendo's 3DS.
Still, Sony Computer Entertainment America CEO and President Jack Tretton insists that the United States and U.K. launches have been "very, very positive." In an interview with IGN, Tretton said that "Memory cards have been going out the door quite aggressively… software appears to be selling quite well top to bottom."
Tretton says that the bestselling launch title in the U.S. is the adventure game Uncharted: Golden Abyss, by a very large margin. In the U.K., it's a much closer race between Uncharted and futuristic racer WipEout 2048.
Other popular launch titles include Dungeon Hunter: Alliance, Rayman Origins, Lumines: Electric Symphony, and Touch My Katamari.


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ZachMangan admin
Appearance: Deep black leaves slightly curled.
Dry leaf aroma: This tea smells like Early Grey. The package says "A secretive tea, scented with essences of citrus and other fruits, dotted with silver needles." There is definitely bergamot and lemon peel, maybe even lime? I don't see any silver needle though…hmm.
Covered the bottom of gaiwan, water at 208F. 1st steep 3 mins. 2nd steep 2 min. 3rd steep 2 mins.
First Steep:
As I mentioned, this tea seems to be an Early Grey. The aroma is all citrus: lots of bergamot, lemon peel, a bit of orange and perhaps lime. (It honestly reminds me of the yellow Trix cereal). The tea itself has a nice balance, although maybe a bit too much bergamot for some. The liquor is a little bit sour, which I like as it blends with the citrus note in the aroma. The color of the tea is beautiful. A firey red-orange. The tea is smooth with little rough edges (the leaf is of better quality than many blends I think).
Second Steep:
The aroma is still quite strong. The tea is a bit less lemony and the taste slightly less sour. I think the 2nd steep is very similar to standard Earl Grey's (think Twining's). Color is still a deep orange.
Third Steep:
STILL a deep color. A surprisingly sophisticated flavor remains…the tea has sweetened up a bit and the balance of citrus and the body of the tea are in a nice place.
If you like early grey, you should try this. No doubt, Mariage Frères makes high quality tea. The blends are sophisticated and the tea itself is of really nice quality. While I don't often drink blends, this is a company that seems to do them right.
Listening: was feeling dramatic: put on Henryk Gorecki's Symphony No. 3 during this tasting.


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Edit Article
wikiHow to Use the RSA Encoder on Mobilefish.com
RSA (Rivest, Shamir, Adleman) Code is possibly the most uncrackable code developed in modern times, harnessing the power of prime numbers to produce some weird results. Ever wanted to encode something in a modern Enigma machine? Start with step 1!
1Go to the Mobilefish site.
2Set your key size from either 32, 56, 128, 256, 512, 1024, 2048. Remember, the higher the key size, the more secure your code is.
3Enter in a prime number, big enough to satisfy the key size. Or if you're feeling lazy, click 'Autogenerate prime numbers P and Q'.
4Click 'Generate Keys'
5Enter in your plaintext. Let's say 'wikihow'. Some hexadecimal code will appear in the box below, but ignore this.
6Click 'Encrypt with public key'. If you're using 'wikihow' it should come up as 2636271161768...6713840. (The '...' is because the real code is way, way too long to put here)
7Check the decryption. To check if it can be reversed, click 'Decrypt with private key A'.
- If it comes up as 'wikihow', success!
Community Q&A
Ask a Question
200 characters leftSubmit
- The RSA code is not intended for long messages. Keep it short and sweet.
- Don't send the message if you challenged your friend to decrypt it. He/she's going to need a quantum computer for this monster.


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TAMPA, Fla. - A Florida trooper helped with this highway delivery.
Dennis Rich with the Florida Highway Patrol was investigating a traffic crash Tuesday morning on Interstate 4 near Tampa when he was flagged down to help deliver a baby.
Authorities say the parents - Wiclef and Latoya Desamour - were on their way to St. Joseph's Hospital when their baby girl was ready to be born. The father pulled over and asked Rich for help.
The family welcomed their third daughter - and fourth child- a short time later. Fire rescue arrived and took the baby and Latoya to the hospital.
Copyright 2013 by The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.


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They're working again. Any idea who that non-naked guy is in the second pic, the one with the pink shirt sitting by the naked guy? He's a real cutie.
Ray Stevenson is sooo gorgeous too. Love his eyes.
They're working again. Any idea who that non-naked guy is in the second pic, the one with the pink shirt sitting by the naked guy? He's a real cutie.
Ray Stevenson is sooo gorgeous too. Love his eyes.
no idea sry
One of the best threads ever!
hot Spanish actor Jordi Molla from the movie "The Consul of Sodom"
more from Jordi Molla
here's Jordi again lickin some pussy
Breaking Bad men. Sorry for all the clothes!
Yes, that's the one with Javier Bardem.
Yeah, there's one really long sex scene in Segunda Piel where Jordi nails Javier up the ass and it's sooo intense. I'll never look at Javier the same way again. He was so queer and natural in this movie. You don't get gay sex scenes like this in the US.
Does anyone have shirtless pics from Patrick Duffy in the Dallas reboot? I haven't watched it because I watch too many shows already. The promo picture has a nice shot. He's always been one to keep in shape. He looks gorgeous with that full head of gray hair.
Gordon Ramsey
Richard Roxburgh
^ hot. he looks exactly like grant bowler who's also a hot aussie actor.
That's Richard from his show Rake, right? I was hoping that show was going to have him nude. He hasn't been naked since Children of the Revolution. He's one of my favorite Aussie actors.
yup from show Rake episode 6 .Actually for me is the best Aussie actor )
Richard from Episode 2. He was so hot in that underground cave movie a couple of years ago too.
yup Definetely....
Ver Los novios bulgaros Online Español Latino | Peliculas Online | Cinetube | Cine Gratis | Miracine
omg imma out of daddies ;((.Please post some <333
Albert Dupontel - Chrysalis (the frontal is from another movie, I don't know which)
Alec Baldwin - Malice
Mark Ritter - Life of a Gigolo (this guy is gorgeous - gray chest hair and sexy body)
Tom Skerritt - Poison Ivy
Last edited by hospanks123; August 20th, 2012 at 12:11 PM.
More Mark Ritter
Vincent Lindon - La Moustache
Ha I remember freezing that Poison Ivy part trying like he'll to see some Tom frontal!
Tom Skerritt was a sex god in Poison Ivy!
OMG Tom Skerrit so fucking hot.
I know, I've had a crush on him since my teens, he's like the ultimate dirty old hot daddy. So jealous of Drew there.
Arekouas, where are those Paul Doucet pics from? Nice ass...
ZOS:Zone of Seperation...But i don't remember what episode of season one is....
Anyone got shirtless or nude pictures of Robert Curtis Brown...He is so fucking hot.
OMG I LOVE Tom Skerritt in Poison Ivy. I remember locking myself in my parents room to watch that movie! Lets just say a lot of loads were shot due to him. Think im going to go watch it now and shoot another!
You'll want to see Tom in Big Bad Mama (1974). He shows his butt a few times and is a complete sex fiend throughout the whole movie.
Big Bad Mama (1974) - IMDb
Anyone got Alec Baldwin? I think he got nude in that recent romcom with Meryl Streep.
Terry O'Quinn from The Stepfather:
And My Stepson, My Lover:
Alec has never shown his penis as far as I know. He should have shown it in The Getaway with his ex-wife Kim, but those sex scenes were a total bore anyway.
Yeah, it's a Roger Corman production, so you're automatically looking at too much poontang and breasts and not enough male ass. With Tom, I'll take any shots I can get. It was interesting to see William Shatner doing it doggy-style. I wish they had shown his butt.
Michael Douglas boinking in Basic Instinct:
I think Micheal Douglas looks better now that he's older


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Mystical Pops - 12 / Box
Mystical Pops - 12 / Box
Out of stock
Mystical Pops are big 3-ounce lollipops shaped like fantastic creatures. Each pop has a scaly texture and vibrantly colored icing details. These have great flavor and will keep kids entertained for hours.
- Orange Dragon with Yellow & Purple Details
- Blue Gecko with Purple & White Details
- Green Seahorse with Yellow & Black Details
- Yellow Lizard with Green & White Details
Our Mystical Pops are packed in a 12-count display box with three of each creature.


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The aim of this study was to test the hypothesis that maternal undernutrition (MUN) alters offspring vascular expression of micro-RNAs (miRNAs), which, in turn, could regulate the expression of a host of genes involved with angiogenesis and extracellular matrix remodeling. The expression of miRNA and mRNA in the same aortic specimens in 1-day-old (P1) and 12-mo-old offspring aortas of dams, which had 50% food restriction from gestation day 10 to term, was determined by specific rat miRNA and DNA arrays. MUN significantly downregulated the expression of miRNAs 29c, 183, and 422b in the P1 group and 200a, 129, 215, and 200b in the 12-mo group, and upregulated the expression of miRNA 189 in the P1 group and 337 in the 12-mo group. The predicted target genes of the miRNAs altered in the two age groups fell into the categories of: 1) structural genes, such as collagen, elastin, and enzymes involved in ECM remodeling; and 2) angiogenic factors. MUN primarily altered the expression of mRNAs in the functional category of cell cycle/mitosis in the P1 group and anatomic structure and apoptosis in the 12-mo age group. Several of the predicted target genes of miRNAs altered in response to MUN were identified by the DNA array including integrin-β1 in the P1 aortas and stearoyl-CoA desaturase-1 in the 12-mo age groups. These results are consistent with the hypothesis that MUN modulation of offspring gene expression may be mediated in part by a miRNA mechanism.
- aorta
- DNA array
micro-RNAs (miRNAs) are short, noncoding RNA molecules of 20–25 nucleotides in length that regulate gene expression at the posttranscriptional level (2, 4) and play a significant role in the regulation of physiologic and pathologic processes. Several thousand miRNAs have been cloned and/or predicted and may regulate up to 90% of human protein-coding genes, primarily through translational repression, and, in some cases, mRNA degradation (9, 19, 35). The role of miRNAs in fetal development and postnatal maturation is largely unstudied, and their role in fetal programming of adult disease is unknown. It is well known that maternal undernutrition (MUN) alters fetal gene expression, and changes in transcription rates cannot explain all these effects. Therefore, we have hypothesized that MUN influences the expression of offspring miRNAs, which then would influence processing of key developmental proteins, and this might represent a novel epigenetic mechanism for regulation of gene expression in the offspring.
Previously, we reported that MUN induced significant vascular remodeling of offspring vascular extracellular matrix (17, 18) and inhibited angiogenesis (16). miRNAs have been shown to play a role in the regulation of both of these processes, and therefore we sought to determine whether MUN alters miRNA expression, which, in turn, might influence the regulation of genes important in angiogenesis and ECM remodeling. Recent accumulating evidence indicates a significant role for miRNAs in the regulation of genes involved in angiogenesis (40) and vascular differentiation (7). In multiple species ranging from fish (12) to humans (20, 39), alterations in miRNA maturation produce significant defects in expression of VEGF and its receptors (45) and correspondingly, changes in blood vessel and capillary formation, which can be embryonically lethal (6). Collectively, these reports provide strong evidence for a role of miRNAs in regulating vasculogenesis, angiogenesis, and cardiovascular remodeling, and raise the possibility that these molecules may play a role in changes in vascular structure and function associated with MUN.
Animals and tissue collection.
The protocol for this study was approved by the Animal Use and Care Committee at La BioMed at the Harbor-University of California Los Angeles Medical Center Medical Center. First-time pregnant Sprague-Dawley rats (Charles River Laboratories, Hollister, CA) were housed in a facility with constant temperature and humidity and a controlled 12:12-h light-dark cycle. At 10 days of gestation, rats were provided either an ad libitum diet of standard laboratory chow (23% protein, 4.5% fat, 3,030 kcal/kg metabolizable energy; Lab Diet 5001; PMI Nutrition, Brentwood, MO) or 50% food-restricted diet determined by quantification of normal intake in the ad libitum-fed rats. The respective diets were given from 10 days of pregnancy to term. Maternal body weights and the food intake were recorded daily. At day 1 after birth, all offspring from food-restricted and control rat dams were cross-fostered to rat dams fed ad libitum, and litter size was culled to four males and four females per dam. Offspring were weaned at 3 wk of age to ad libitum standardized laboratory chow. Animals were anesthetized under isofluroane gas. Thoracic aortas were dissected and cleaned of periaortic fat and snap frozen in liquid nitrogen and stored at −80°C. This vessel was chosen because, in our previous work, we have extensively characterized the effects of MUN on angiogenic genes and genes regulating ECM remodeling. For immunohistochemical studies, blood vessels were fixed in 4% paraformaldehyde for 24–48 h and then transferred to 70% ethanol. These conditions were previously shown to be optimum for immunohistochemical detection of proteins of interest. Arrays were used to examine three specimens from each dietary group, representing pooled RNA from four to six animals in the case of P1 offspring for each data point and two animals in the case of 12-mo-old offspring. Offspring tissues were obtained from six different dams in both age groups, and for pooling purposes, specimens were derived from different litters.
miRNA expression profiling.
Total RNA was extracted from aortas using Trizol (Invitrogen) with their quantity and quality determined using an ND-1000 Spectrophotometer (NanoDrop Technologies, Wilmington, DE) and Agilent Bio-analyzer (Agilent Technologies, Foster City, CA), respectively. The isolated miRNAs were 3′-end labeled with Cy3 using the mirVana miRNA Array Labeling Kit (Ambion, Austin, TX) and the Post-Labeling Reactive Dye Kit (Amersham Bioscience, Pittsburgh, PA). miRNA profiling was performed by Ocean Ridge Biosciences (Jupiter, FL) by using custom-developed microarrays containing 237 NCode-2 35–44-mer rat miRNA oligonucleotide probes manufactured by Invitrogen and spotted in duplicate. At the time of analysis, these miRNAs represented an entire coverage of Sanger mirBASE version 9.0 content. After hybridization, the arrays were scanned using a GenePix 4000A array scanner (Axon Instruments, Union City, CA). The intensity of each oligo probe was averaged among triplicate spots and then normalized and analyzed using GeneSpring 7.0 Software (Silicon Genetics, Redwood City, CA). Normalization was performed by expressing each miRNA abundance relative to control miRNA (Ambion) added to each sample. Threshold and 95th percentiles of negative controls (TPT95) were calculated based on the hybridization signal from negative control probes, including mismatch and shuffled control probes and nonconserved Caenorhabditis elegans probes. The two base pair mismatch probes demonstrated a signal below or at TPT95 on all arrays. The computational algorithms TargetScan (http://www.targetscan.org/), PicTar (http://pictar.mdc-berlin.de/), miRDB (http://mirdb.org), and miRanda (http://www.ebi.ac.uk/enright-srv/microcosm/htdocs/targets/v5/) were utilized for identifying predicted target genes of miRNAs.
DNA microarray.
Total RNA isolated from the same tissues was also subjected to large-scale transcript profiling using RatRef-12 Expression BeadChip representing 22,524 probes for a total of 22,228 rat genes selected primarily from the NCBI RefSeq database (Release 16; Illumina, San Diego, CA). The arrays were utilized in accordance with the manufacturer's instructions. Following amplification and cDNA synthesis, 5 μg of purified cDNA was reverse transcribed and labeled with the TotalPrep RNA Labeling Kit using biotinylated-UTP (Ambion, Austin, TX). Hybridization was carried out in Illumina Intellihyb chambers at 58°C for 18.5 h, followed by washing and staining. The signal was developed by staining with Cy3-streptavidin. The BeadChip was scanned on a high-resolution Illumina BeadArray reader.
The expression values were background subtracted and globally normalized using BeadStudio version 22.214.171.124 (Illumina), and probes with differential scores of ≥ 13 were independently removed from each cohort. The transformed expression values were subjected to unsupervised and supervised learning and statistical analysis in "R" programming as previously described (41). Gene expression values having a statistical significance of P ≤ 0.05 (ANOVA, Tukey test) were selected and subjected to a 1.5-fold cutoff change (statistically significant) either positively or negatively. These values were subjected to functional annotation and visualization using the Database for Annotation, Visualization, and Integrated Discovery (http://david.abcc.ncifcrf.gov) (DAVID) software.
RT-PCR chain reaction.
Using 2 μg of total RNA isolated from the above samples, complimentary DNA was generated using Taqman reverse transcription reagent. The newly synthesized cDNA was used for PCR performed in 96-well optical reaction plates by using cDNA equivalent to 100 ng RNA in a 50-μl reaction volume containing 1× Taqman Universal Master Mix; optimized concentrations of FAM-labeled probe and specific forward and reverse primer were selected from Assay on Demand (Applied Biosystems). Real-time PCR was carried out using Applied Biosystems 7300 Fast Real-Time PCR System at 95°C for 10 min, 95°C for 15 s, and 60°C for 1 min for 40 cycles. The miRNAs and mRNAs expression values were analyzed using the comparative method (34) following transformation and normalization to RU6B and 18S rRNA expression, respectively, according to the manufacturer's guidelines; the threshold cycle was set within the exponential phase of the PCR and converted into fold change based on a doubling of PCR product in each PCR cycle.
Histologic analysis for elastin was performed using Van Giesen staining and images analyzed as previously described in detail (17). To avoid variation in staining conditions, all specimens from each age group were stained simultaneously. The slides were analyzed by the same investigator blinded to the treatment groups under the same magnification and light intensity. The area of staining and staining intensity were quantified by image analysis by using the Image Pro 4.1 software (Media Cybernetics) coupled to an Olympus BHS microscope/spot RT digital camera. The images were calibrated for background intensity and converted to gray scale. The concentration of the immune reactive antigen was determined using integrated optical density; these values were proportional to the unweighted average optical density per area. Integrated optical density of four sections of the aorta (×20 images) were analyzed, and mean values were obtained for the analysis.
Western blot analysis.
Western blot analysis for AT1-receptor protein, which was identified on the 12-mo age group DNA array and was determined to be significantly altered, was performed using a monoclonal antibody (Santa Cruz Labs, Santa Cruz, CA). We used 7.5% polyacrylamide gel and 5% milk buffer as a blocking agent. GAPDH was used as an internal control. Details of the procedure have been previously published (16).
Statistical analysis.
The results are expressed as means ± SE and were statistically analyzed using Student's t-test for comparison of two groups and ANOVA followed by Tukey's test for multiple comparisons after verification of normal distribution. For nonnormally distributed data, the Mann-Whitney U-test or Kruskal-Wallis multiple-comparison test was used. P < 0.05 was considered significant.
The expression profile of the significantly altered miRNAs and some of their predicted target genes in P1 and 12-mo-old offspring aortas are shown in Tables 1 and 2, respectively. Out of the 248 miRNAs on the array, 173 rat miRNAs profiled were detectable in the aorta. Statistical analysis showed one miRNA (miRNA 189) was significantly expressed more in the P1 MUN aortas, and three that were significantly expressed less (miR-29c, miR-183, miR-422b) compared with age-matched controls (Table 1); in the 12-mo aortas, four miRNAs (miR-200a, miR-200b, miR-129, and miR-215) were significantly downregulated in the 12-mo MUN aortas and one miRNA (miR-337) was upregulated (Table 2). The predicted target genes of miRNAs altered by MUN in the two age groups included 1) structural genes, such as collagen, procollagen, protocadherins, and elastin; 2) enzymes involved in ECM remodeling and synthesis (ADAM, matrix metalloproteinases, hyaluronidase synthase-3); 3) angiogenic genes such as ephrin, neuropilin, thrombospondin, VEGF, FGF and its receptor, TGF-related genes; and 4) genes regulating cell proliferation, such as BCL2, and signaling factors (MAP kinase, STAT, NCOA3).
There was a striking difference in the expression profile of miRNAs in the two age groups studied, which was independent of the in utero nutritional history of the offspring (Table 3). The level of expression of miRNAs influenced by postnatal maturation is listed in Table 3 in descending order of magnitude of change in expression levels. Comparison of the two age groups shows that the level of expression of many miRNAs were significantly higher in the P1 group compared with the 12-mo group. The predicted target genes for miRNAs that showed the greatest change in expression during development are shown in Table 4.
The results of transcript profiling, as determined by a rat-specific DNA array and organized into functional categories using DAVID bioinformatic analysis, are shown in Tables 5 and 6 for the P1 and 12-mo groups, respectively. The complete list of mRNAs showing significant change in expression is shown in the Supplemental Tables S1–S4 (Supplemental data for this article is available online at the American Journal of Physiology–Regulatory, Integrative and Comparative Physiology website.). In P1 aortas, 221 mRNAs were statistically significantly upregulated (127 were > 1.5-fold) and 125 were downregulated (91 > 1.5-fold) in controls compared with MUN aortas. In contrast to the P1 aortas, in the 12-mo aortas 338 mRNAs were expressed significantly more (240 > 1.5-fold) in control aortas compared with MUN aortas, and only 30 mRNAs (29 > 1.5-fold) were expressed more in MUN aortas compared with controls. There was little overlap between the mRNAs that commonly showed a change in expression in the two age groups in response to maternal undernutrition. Only three mRNAs were upregulated significantly in the MUN groups in both the P1 and 12-mo age groups (C11orf8h, LOC313778, LOC498945), and three mRNAs were downregulated (Prpsap1, LOC500216, LOC501549). Two mRNAs were upregulated in the P1 group but downregulated in the 12-mo age group (LOC498682, Rn.46489). In the P1 group, out of the 319 DAVID IDs, 175 genes could not be clustered into any functional category; in the 12-mo groups, out of 344 DAVID IDs, 149 genes could not be clustered into any functional group. As demonstrated in Table 5, in the P1 group genes regulating cell cycle/mitosis and DNA replication had the highest enrichment score (greatest representation), whereas in the 12-mo group genes regulating anatomic structure/development and apoptosis had the highest enrichment scores. There was a significant overlap of genes that fell in multiple functional categories in both age groups. In the angiogenic functional category, VEGFD, fibroblast growth factor binding protein (FGFBP), p-selectin, MMP14, and thrombospondin 2 were significantly altered in the P1 group, whereas in the 12-mo group CTGF, FGF2, AT-receptor 1b, integrin-αV, and TNF receptor 12 were altered (Tables 5 and 6). Each age group had functional categories that were unique to it. In the case of the P1 group, these categories included DNA modification with constituent genes, such as DNA methyl transferase-1, and steroid metabolism with such members as HSD1 and HSD7. In the 12-mo group, a number of genes fell into the category of sulfotransferases with constituents, such as heparan sulfate 3-0 sulfotransferase-1. Notable genes showing a decrease in expression in the P1 MUN aortas were FGFBP-1, HSD1, and Arginase-1. Genes showing an increase in expression in P1 MUN aortas were thrombospondin-1 and -2, collagen 5A1, ADAM, p-selectin and Notch3. In the 12-mo aortas, specific genes of interest with decreased expression in MUN aortas were integrin-αD and integrin-α5, serpine1, angiotensin II receptor type 1, hyaluronidase, ADAM, FGF2, annexin A1. Only a few genes were upregulated in the 12-mo MUN aortas including IL-17β and stearoyl-CoA desaturase 1 (SCD1).
An analysis was performed to determine which predicted target genes of miRNAs that changed in response to MUN could also be identified by the DNA array to show the expected up- or downregulation, and these genes are listed in Table 7. The miRDB and PICTAR were mainly used for sources of the predicted miRNAs. In the P1 offspring, miRNAs 29c and 183 were upregulated in expression in MUN, and therefore their predicted target genes would be expected to be downregulated. The integrin-β1 gene met this criterion showing decreased expression by the DNA array. In the 12-mo group SCD1 mRNA, a target of miRNA 200b upregulated in the MUN group, showed a decreased expression by the DNA array. Although few of the predicted targets of the significantly altered miRNAs were identified by the DNA array, many of the genes detected by the DNA array to change in expression had significant functional similarity to the predicted target genes of the miRNAs, an example of which is miRNA29c, which has several collagen subtypes as predicted targets.
Confirmation studies were performed for both miRNA and mRNA data. Real-time RT-PCR showed a significant decline in the expression of miRNA 29c in MUN aortas in two age groups, namely 3-wk-old and 12-mo-old offspring, and a trend toward a decrease in the P1 offspring (Fig. 1A). One of the genes regulated by miRNA 29c is elastin. We examined the expression of elastin by histological analysis and image analysis in aortas obtained from P1 and 12-mo-old offspring (Fig. 1B). Based on the decline in expression of miRNA 29c, the expectation would be to detect increased elastin mRNA and protein expression. As expected, the expression of elastin in MUN aortas from both groups was elevated. We also confirmed the changes in the DNA array for thrombospondin 1 involved in inhibition of angiogenesis and the AT1-receptor involved in the regulation of vascular tone (Fig. 1C). As demonstrated in Fig. 1D, there was confirmation of the array data by real-time RT-PCR with an increase in expression of thrombospondin-1 mRNA in P1 MUN aortas and decreased AT1-receptor protein expression as determined by Western blot analysis in 12-mo MUN aortas.
This study profiled the expression of all known rat miRNAs and their associated mRNAs in vascular specimens from the offspring of dams undernourished during gestation. The results revealed an altered expression of only a few miRNAs but a large number of mRNAs in both age groups. The target genes of miRNAs whose expression was altered as a result of MUN included genes regulating extracellular matrix remodeling, angiogenesis, cell proliferation, apoptosis, and cell signaling in both age groups. Most prominently, MUN inhibited the expression of miRNA29c in both P1 and 12-mo-old offspring. This miRNA predominantly regulates the components of ECM, such as collagen and elastin, which we have shown be influenced significantly by MUN (17).
Our data provide new support for the hypothesis that the expression profiles of certain miRNAs and mRNAs change significantly during development independently of in utero nutritional environment. The target genes of miRNAs downregulated by development related primarily to cell structure and cytoskeletal organization (Dmn, Ina, Mtap16), regulation of cell division and apoptosis (Anxa1, Pdcl3, Sema 3d, cyclin 2), regulation of transcription and translation (eif4e, Arid), and mediators of vascular growth (FGF, FGF receptor, VEGF). In contrast, miRNAs upregulated during development were associated mainly with target genes functionally associated with ECM components, including collagens and elastin, but they also influenced genes involved in cell growth and division (Rai2, cyclin) and vascular growth factors (VEGFA, FGF9, PDGFR, IGF1). Of particular importance was the finding that two of the developmentally regulated miRNAs (29c and 189) were also influenced by MUN in the P1 offspring, which supports the hypothesis that these miRNAs are involved in the patterns of fetal vascular programming associated with undernutrition.
Our findings that MUN altered the expression of only a small number of miRNAs, but influenced expression of many mRNAs could be due to several factors. First, miRNA and mRNA expression and turnover are regulated very differently, particularly during vascular programming. Second, miRNAs regulate target gene expression at the posttranscriptional level, which implies that changes in protein abundance, function, and location can modulate the regulatory effects of miRNAs during vascular programming. Third, the currently postulated targets for each known miRNA involve considerable uncertainty and may not predict all actual target genes affected (37). Fourth, several different miRNAs may target the same gene through either additive or competitive influences. Fifth, not all genes are regulated by miRNAs, and thus miRNA-independent mechanisms may mediate some effects of MUN. Sixth, a single miRNA may target a different combination of genes in different cell types, or in the same cell type at different stages of the cell cycle. Correspondingly, inhibition of mRNA would be expected only in the cell type in which the miRNA is expressed (10). Such effects might be obscured in whole tissue homogenates that reveal only averaged relations between the miRNA and mRNA across all cell types in any given homogenate. Given these considerations, a global analysis of the miRNAs and mRNAs regulating particular pathways or physiologic processes is a more useful initial approach than a focus on a specific gene. In support of this approach, other studies that have simultaneously analyzed miRNA and mRNA in pathologies, such as acute myeloid leukemia, have also found only weak associations between miRNAs and changes in their target mRNAs at the transcriptional level (15).
Among the miRNAs influenced by MUN, miR-29C may be the most significant functionally, as this miRNA targets the expression of genes involved in two fundamental processes involved in vascular programming: angiogenesis (16) and ECM remodeling (17). Among the predicted target genes for miR-29C are components of the ECM, including collagens and elastin along with the enzymes involved in their synthesis and remodeling. Targets for miR-29C also include angiogenic genes, such as VEGF and integrin α5-β1, a suppressor of angiogenesis and known to be upregulated by hypoxia (26). Other angiogenic targets include ADAM, a disintegrin and metalloproteinase with a thrombospondin motif that binds and sequesters VEGFA, thereby inhibiting endothelial cell proliferation (25). ADAM enzymes are also involved in ECM remodeling, endothelial cell invasion, and vascular sprout formation (38), as well as vascular smooth muscle migration (43). We have also previously reported that MUN stimulates vascular collagen deposition in a pattern consistent with development of vascular fibrosis (17). Consistent with this finding, miRNA29 can also contribute to cardiac fibrosis (42), and to ECM remodeling in cancer (36). Given these findings, gene-based loss and gain of functions studies offer a promising direction for future studies of this important miRNA.
MUN upregulated only one miRNA in the P1 age group, miRNA-189. The predicted target of miRNA-189 includes at least four main genes: 1) serine/threonine kinase 3 (STK3); 2) HIF3α, a basic helix-loop-helix PAS protein that activates hypoxia-responsive genes (23); 3) regucalcin gene promoter region-related protein (RGPR), a transcription factor that binds to the regucalcin gene and controls apoptosis (44); and 4) nuclear receptor coactivator 3 (NCOA3), a transcriptional coactivator protein that has intrinsic histone acetyltransferase activity and acylates histones making downstream DNA more accessible to transcription (3). The array of functions affected by miRNA-189 suggests diverse effects on numerous genes through actions on DNA-binding proteins with secondary influences with the promoter regions of multiple different genes.
In the aortas from 12 mo olds, four miRNAs were significantly downregulated in the MUN offspring. As observed in the P1 offspring, many of the target genes of the affected miRNAs were related to regulation of the extracellular matrix and angiogenesis. Importantly, changes in the expression of some of these predicted genes were confirmed by the DNA array. Two of the miRNAs suppressed by MUN belonged to the "200" family that regulates a large number of genes in several important categories: 1) genes involved with proteoglycan synthesis such as β-1,3-glucuronyltransferase, (B3GAT) and hyaluronon synthase (HAS 2); 2) thomobomodulin (Thbd), which is an integral endothelial cell membrane protein and acts as a cofactor in the thrombin-induced activation of protein C (24); 3) several different protocadherins; and 4) angiogenic genes, such as ephrin A1 (eph A1), and semaphorin 3f (Sema 3f) (21). One of the predicted targets of miRNA 200b is SCD1, which was also identified by the DNA array as one of the few genes that were upregulated by MUN in the 12-mo-old aortas. SCD1 catalyzes the biosynthesis of monounsaturated fatty acids, thereby affecting lipid composition and fluidity of the cell membrane. Mice deficient in SCD1 exhibit cell membranes that are very rigid (27), and shear stress induces the expression of this enzyme in endothelial cells, possibly providing a protective response to atherosclerosis (31). Other angiogneic target genes of miRNA 200a include Zeb1, a two-handed zinc finger homeobox transcription factor that negatively regulates angiogenesis (13, 14), and epiregulin (32). Some of the predicted targets of miRNA-200, such as lysyl oxidase-like 3, are important in synthesis of ECM components. This enzyme encodes an extracellular copper-dependent amine oxidase that catalyses the first step in the formation of cross links in collagens and elastin (22), and vesrcisan, an extracellular secreted matrix protein and member of the large chondroitin sulfate proteoglycan family (29). Collectively, the broad range of effects of the miRNA-200 family clearly suggests great potential to modulate both vascular structure and function in the 12-mo-old animals, where changes in miRNA-200 were still prominent 1 yr after birth.
Although MUN influenced the expression of only a small number of different miRNAs, the expression profiles of many different mRNAs were altered by MUN. One potential reason for this finding is that the MUN may have influences on mRNAs independently of effects on miRNAs. The general profile of genes affected by MUN in the P1 aorta suggested activation of ECM remodeling via increased expression of ADAM, NOTCH, and MMPs, whereas in the aortas from 12-mo-olds, MUN suppressed many of these same mRNAs including ADAM, hyaluronidase, and serpine genes, which are ECM proteases. In the P1 offspring, MUN-induced changes in the expression of multiple mRNAs of genes involved in angiogenesis are consistent with our previous findings (16) and those from others (30) that indicated reduced angiogenesis in these offspring. Among the angiogenic genes identified by our array in the MUN-treated P1 aortas, FGFBP-1 was inhibited > 300-fold. The product of FGFBP-1 gene promotes angiogenesis through the activation and mobilization of stored FGF, which is bound by heparin sulfate glycans (1, 5). In addition, simultaneous inhibition of expression of neuregulin, another proangiogenic factor (33), together with increased expression of thrombospondin 1, a major inhibitor of angiogenesis (8), suggests that MUN influences angiogenesis in the newborn MUN offspring by altering the balance between proangiogenic and angiostatic influences (16).
In the 12-mo-old offspring, MUN primarily influenced the expression of gene families related to structural development with additional effects on genes governing apoptosis. Important genes that were downregulated included AT1-receptor mRNA, which was confirmed by Western blot analysis. This was an unexpected finding because the MUN animals were hypertensive, which would suggest a possible upregulation of the AT1-receptor expression in the 12-mo-old MUN vessels. Telomere dysfunction has been associated with hypertension in other studies (11), and our results were consistent with the possibility that MUN downregulated telomerase, the enzyme necessary with telomere capping. This could potentially represent a mechanism for the development of hypertension in the older MUN offspring. This intriguing possibility is an excellent candidate for further investigation.
Judging from the published literature, our study is the first to comprehensively profile the effects of MUN on the vascular expression of miRNAs and mRNAs in neonatal and mature offspring. The changes observed in miRNA and mRNA expression in the aorta may not be applicable to resistance vessels and may vary among different vascular compartments. A recent study by Yates et al. (46) examined the hepatic mRNA profile of a select battery of genes involved in atherosclerosis in the adult offspring of ApoE3 Leiden mice exposed to protein undernutrition in utero. This group showed suppression of SRBP-1 and altered expression of the LDL receptor superfamily. Nijland et al. (28) have also reported on the effect of maternal nutrient restriction on the offspring renal mRNA profile with decreased expression of genes involved in DNA/RNA and protein biosynthesis. Without a doubt, the effects of MUN are highly tissue specific and depend heavily on the model used. Nonetheless, the data presented here strongly indicate that MUN influences multiple species of miRNA with consequences for many more types of mRNA in rat aortas, and that these effects change during postnatal development but can still be detected for at least a year after birth.
Perspectives and Significance
This study demonstrates that miRNAs are subject to regulation by maternal nutritional cues and thereby may represent a novel epigenetic mechanism. MUN altered the expression of only a select few species of miRNA, but many of these influenced proteins governing transcriptional regulation and apoptosis, which may help explain why MUN affected the mRNA for many different genes, as revealed by our novel global survey approach. More directly, the miRNAs most potently affected by MUN had multiple targets among the genes that regulate angiogenesis and ECM remodeling. Together, these effects of MUN on miRNA suggest an important mechanism whereby maternal nutritional status can lead to vascular programming of the fetus. Future studies of these mechanisms offer great promise for improved understanding of both the genes governing vascular development and the roles played by miRNAs in these processes.
O. Khorram was supported by National Institute of Child Health and Human Development Grant RO3-HD-054920-01.
No conflicts of interest are declared by the authors.
We thank Jeannie Park and Diane Park for invaluable assistance with preparation of this manuscript.
- Copyright © 2010 the American Physiological Society


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GiggleSugar Reader Spotlight: Junebrug
Junebrug, like many writers, wants to be known for her words and not for her image. So it's fitting that this week she shares her ideas, but not her picture. Her comments on Giggle are observant and sharp, and we're glad she joins in on the fun!
GS: What is your motto?
Junebrug: There are too many of them to list, but I'll go with: Fortune Favors the Bold.
GS: Where are you from?
Junebrug: Ohio originally, now a resident of Los Angeles.
GS: What do you do?
Junebrug: I'm a writer.
GS: How would you describe your sense of humor?
Junebrug: Mostly sarcastic, sometimes so dry people don't if I'm kidding or not. And occasionally just plain goofy.
Junebrug: What's your favorite GiggleSugar Post?
GS: Anything with puppies is always good with me. I like the Eligible Bachelor Du Jour posts too, they remind me why I'm single.
GS: Who is the cutest funny man and funny woman?
Junebrug: Amy Poehler is pretty hot these days….men? Eh, does he have to be funny? Can't I be funny enough for both myself and George Clooney?
GS: Who are your favorite male and female comedians?
Junebrug: I love John Pinette, and Janeane Garafalo has been cracking me up for a decade.
GS: What's your favorite comedy of all time?
Junebrug: The movie Some Like It Hot.
GS: If your life were a comedy, what would it be?
Junebrug: A dramedy definitively. I think most people can relate to "Curb Your Enthusiasm." Everything that can go wrong, generally does. The only comedy I can completely relate to is one that I wrote. No you haven't seen the film yet. You will (fingers crossed, cross your fingers for me, dear reader).
GS: Do you look like someone famous?
Junebrug: Oh my. There was a time people were so convinced I was Anna Nicole Smith, they asked for autographs. Grr. I get Kirstie Alley a lot too. Grr. It doesn't occur to anyone that being compared to women who are older (and one who had questionable sanity) than I am would be annoying. Grr.
Junebrug Free-for-all: I am a writer and I have a pet lovebird named Madeleine who restores my sense of humor when I've lost it. And if I don't get it back fast, she just bites me, and the biting continues until morale improves.
Thanks, Junebrug!
(Curb Your Enthusiasm, Amy Poehler, John Pinette, George Clooney, Janeane Garafalo)


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AndyMalroes wrote:And How! Where the fuck's |Y|?
AndyMalroes wrote:I think it's more plausible in an anarchist society than capitalism, seriously most of our scientists are working on hair regrowth and prolonging erections because that's where the money is.
AndyMalroes wrote:Now if someone could figure out how to expand and contract space, we'd be set!
|Y| wrote:Mmm, the starburst image has a nice spacey feel to it. Anarchy in Space baby!
The Japanese have devised a way to extract uranium from sea water (without large energy intensive industrial suction stations). You lower canisters of uranium attracting compounds and after a few months you have yellowcake. It's rather novel. So there's your fuel.
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Originally published June 2, 2012 at 9:00 PM | Page modified December 28, 2012 at 12:57 PM
Victims of violence: The homicide victims in Seattle this year
This year, Seattle has had 26 homicides — six more than in 2011.
So far this year, Seattle has had 26 homicides, all but three due to firearms.
Two victims were killed with knives and one person, 51-year-old Greggette Guy, of Kent, whose body was found in Puget Sound off West Seattle, died of a neck wound and asphyxia due to drowning.
All of the victims were adults and none of the deaths were the result of domestic violence. According to police, eight of 2012's homicides remain unsolved, including Guy's slaying
Beyond the numbers are the lives cut short. A young woman who moved to Seattle with dreams of becoming a chef and a Navy petty officer in town celebrating a promotion. Two close friends and musicians who were well-known performers in the local vaudeville scene.
Here are the stories of their deaths:
Ashton Reyes
January 3, 2012: Ashton Reyes, 22, is shot at a Subway shop on Rainier Avenue South during a marijuana buy; her boyfriend is wounded. Jacob Mommer, 24, was arrested in February and charged with first murder in connection with Reyes' death. He is being held in the King County Jail on $1 million. Reyes had recently graduated from Everest College in Seattle to become a dental assistant.
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Tirone Jermaine Finkley
January 9, 2012: Tirone Jermaine Finkley, 30, is shot in the chest while in a car in the 5900 block of 37th Avenue South. Omar Tweedy, 39, claims he shot Finkley in self-defense during a drug sale. Tweedy, a felon, is charged in U.S. District Court with unlawful possession of a firearm. On a memorial website, friends and family say Finkley loved basketball, football and baseball.
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Darek Darewski
January 17, 2012: Darek Darewski, 49, is shot in the chest in the 1700 block of Harvard Avenue, behind Seattle Central Community College. He had served a day in jail two weeks earlier for a 2010 harassment incident that happened at a Seattle sobering center. Police said he was a part-time Alaska fisherman.
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Michael Travis Hood
January 21, 2012: Michael Travis Hood, 36, is shot four times outside Feedback Lounge in West Seattle and dies the next day. Lovett James Chambers, a 67-year-old felon, is charged with first-degree murder. Hood had just moved to Seattle for a fresh start and gotten a job at Charlie's Produce after his two brothers and his best friend had been slain in Florida.
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Gregory Wayne Anderson Jr.
February 5, 2012: Navy Petty Officer 3rd Class Gregory Wayne Anderson Jr., 25, is fatally shot during a scuffle outside Republiq nightclub on First Avenue South in Sodo. The father of two came to Seattle to celebrate his recent promotion and a friend's birthday.
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Desmond Jackson
February 12, 2012: Desmond Jackson, 22, is fatally shot outside Club X, a Sodo nightclub on First Avenue South. His great-aunt said he was a masterful cook and lover of vintage styles who valued quality more than quantity.
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Precious Reed Jr.
February 20, 2012: Precious Reed Jr., a 31-year-old father of four and evangelist, is shot in Woodland Park during an apparent drug deal. Michael Bienhoff, 33, is charged with second-degree murder, his third strike if convicted. Bienhoff is associated with the Rolling 90s street gang, according to police.
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George Hendricks Jr.
February 21, 2012: George Hendricks Jr., 41, is shot in the parking lot of Maya's Mexican Kitchen on Rainier Avenue South. Hendricks and Lucky Dozier, 33, both felons and gang members, possibly shot and killed each other in an argument over a woman.
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Lucky Dozier
February 21, 2012: Lucky Dozier, 33, is shot in a possible altercation with George Hendricks Jr. in the parking lot of Maya's Mexican Kitchen on Rainier Avenue South.
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Alpha Lake Rajai
March 8, 2012: Alpha Lake Rajai, a 59-year-old homeless man, is fatally shot in Ravenna Park. Timothy James Murray, 26, is charged with second-degree murder. Known to many as "The Sentinel," Rajai lived much of the time in Ravenna Park, where he could often be seen reading. He got to know members of UW Psi Upsilon fraternity and sometimes was a bouncer for their parties. Police said a man has been charged with Rajai's slaying.
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Greggette Guy
March 12, 2012: The body of Greggette Guy, 51, of Kent, is found floating off Beach Drive Southwest in West Seattle. She died from a knife wound to the neck and asphyxia due to drowning. Guy, who led her daughter's Girl Scout troop for years, loved hiking through national parks across the country.
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Zerabruk Habtemariam
April 2, 2012: Zerabruk Habtemariam, 59, is fatally stabbed outside a doughnut shop on Aurora Avenue North. Karen Latham, 23, is charged with second-degree murder. Friends say he gave her a ride when she flagged him down. Prosecutors say she then stabbed him when he wouldn't give her more than $5.
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Nicole Westbrook
April 22, 2012: Culinary student Nicole Westbrook, 21, is hit by a stray bullet from a drive-by shooting in Pioneer Square as she walks home with her boyfriend in the early morning. They had just moved to Seattle from Albuquerque, N.M.
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Courtney Taylor
May 16, 2012: Courtney Taylor, 31, is shot during a scuffle at Jack in the Box in Rainier Beach. Troy D. Sanders is charged with second-degree murder. Taylor was a father of five and certified electrician.
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Justin Ferrari
May 24, 2012: Justin Ferrari, 42, is hit by a stray bullet at East Cherry Street and Martin Luther King Jr. Way. Ferrari, a software-development engineer and water-polo coach, was driving with his children and parents when he was struck. Andrew Jermain Patterson was charged with second-degree murder for allegedly firing the shot that killed Ferrari in July.
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Son Hai Le
May 27, 2012: Son Hai Le, 28, dies after being shot in the chest by an intruder at a house in North Seattle's Pinehurst neighborhood where there was a marijuana operation.
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May 30, 2012: Four people are fatally shot, and one man is seriously injured, at Cafe Racer in the University District. About a half-hour after the Cafe Racer shootings, a woman is fatally shot in a carjacking downtown. The gunman in both attacks, Ian Stawicki, escapes to West Seattle, where he kills himself several hours later.
Drew Keriakedes
Drew Keriakedes, 45, was a husband, musician, songwriter and colorful performer steeped in the local vaudeville/circus scene.
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Joseph Vito Albanese
Joseph Vito Albanese, 52, a bass player, was Keriakedes' best friend, bandmate and roommate.
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Donald Largen
Donald Largen, 57, was an urban planner who played the saxophone and earned a master's degree from the UW.
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Kimberly Layfield
Kimberly Layfield, 36, was a sunny actress in independent films and had an Internet sitcom. All were regulars at the cafe.
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Gloria Koch Leonidas
May 30, 2012: About a half-hour after the U-District shootings, Gloria Koch Leonidas, 52, a Bellevue married mother of two who was a lighting expert, is fatally shot in a carjacking at Eighth Avenue and Seneca Street downtown.
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Sherry Soth
July 1, 2012: Sherry Soth, 21, was slain by an unknown gunman July 1 as she and some friends were leaving a house party in South Seattle. Soth had planned to move to Hawaii in the fall. She was good friends with Desmond Jackson, 22, who was gunned down Feb. 12 outside a Sodo nightclub.
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Yancy Noll
Aug. 31, 2012: Yancy Noll, 43, a wine steward at a QFC store on Capitol Hill, was fatally shot Aug. 31 while he was in his car at 15th Avenue Northeast and Northeast 75th Street, in the Roosevelt neighborhood. Police say the gunman, who was driving a silver BMW Z4 convertible, may have opened fire after some sort of road-rage incident. Dinh Bowman, 29, of Seattle, was arrested in September and charged with first-degree murder in Noll's death.
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Henry Frankie Lee Sr.
Sept. 23, 2012: According to Seattle police, Henry Frankie Lee Sr., 77, was fatally shot by Seattle police officers on Sept. 23 at his home in the 6300 block of South Bangor Street after he called 911 through a medical alert company with concerns about a possible prowler. Police said Lee told the operator he had a gun and would use it. When police responded to his house, Lee came to the door with a gun in his hand and would not drop it despite repeated warnings, police said. An inquest into the shooting has been called.
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Jamie J. Turner
Oct. 4, 2012: Jamie J. Turner, 26, was found shot to death in the driver's seat of a blue Buick Le Sabre which was on the side of the road at 54th Avenue South and South Grattan Place South on Oct. 4. Residents of the neighborhood called police around 4 a.m. after hearing gunshots, police said. Turner's case remains unsolved.
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Faustino Cervantes
Oct. 26, 2012:Faustino Cervantes, 21, was stabbed to death on Oct. 26 shortly before 2 a.m. outside of the Belltown nightclub, Tia Lou's after he had been in an argument with his attacker, police said. Hever Zuniga-Guzman, 22, who was identified by a witness through his Facebook account, has been charged with second-degree murder.
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Related: Gun-related 911 calls map | 2012 Seattle homicides map
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