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We help you find a Denny french horn teacher. French Horn lessons are an excellent method to learn an entertaining new hobby, pick up a new talent and gain confidence in french horn. Please use our site to search for Denny french horn teachers and select which suits your needs so you can start your french horn lessons in Denny today!
This is the best place to discover Denny french horn teachers in the UK, helping you find Denny french horn lessons in your area and Denny tutors to assist with any instrument such as piano, violin or guitar. We can help you find Denny french horn tuition or a one-to-one Denny french horn tutor to prepare for french horn exams and develop your french horn skills! Our search will order Denny french horn tutors local to you by their lesson charges and proximity to you.
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Once you are certified, you must complete 30 hours of continuing education annually, including a minimum of two hours in the area of ethics. Since CPE hours reported are verified on a random basis, you should keep CPE certificates and other supporting documents for a minimum of two years.
CPE Courses And Events
IMA offers a variety of programs uniquely geared for the professional development of accountants and financial professionals in business. To make meeting your CPE requirement convenient and enjoyable, IMA offers hundreds of NASBA-approved CPE courses and events every year, with content designed with you in mind. For more information on IMA's CPE programs, visit these sites:
Maintain Your CMA Credential By Following Three Easy Steps:
*The CMA Maintenance Fee is payable at the time of a CMA member's renewal term.
Maintaining The Value Of The CMA
The CMA Maintenance Fee is used by ICMA to promote the CMA program to increase brand awareness in the marketplace and thereby enhance the value to certificants. It also covers the administrative costs of maintaining CMA records and providing confirmation of one's CMA credential to employers. CMA members receive a discount off the subscription price of IMA's NASBA-approved CPEdge learning products, as well as free access to IMA's series of CPE-earning webinars. Maintaining the CMA credential distinguishes CMAs as premium members of IMA
Promoting Your Credential
Maximize The Recognition Of Your CMA Credential:
Educate And Inform
Increase awareness of the CMA – and its value as the gold standard credential for accountants and financial professionals working in business – by sharing with your colleagues some facts about the CMA program.
Professional Member Fees
Certification Entrance Fee (nonrefundable)
Exam Fee
$350 per part
Exam Fee if a candidate registers for both parts at
the same time for the same testing window
$300 per part
Transition Exam (offered through February 28, 2013)
$225 per part
*The Certification Entrance Fee covers:
Please note:
Refund Policy
After 30 days from the date of registration, examination fees are not refundable. Within 30 days of the registration date, an examination fee may be refunded if no test appointment has been set. A $25 processing fee will be subtracted from the refund. Please note: If you purchase both parts 1 and 2 for the same testing window and received the $100 discount, you are required to take both exams in the same testing window. If you are unable to, and you request a refund of one part within 30 days of purchase, you will receive a refund of $225. After 30 days, there are no refunds. (Refund calculation: $600 paid, less $350 for the exam part you plan to take, less a$25 processing fee equals a refundable amount of $225.)
The CMA exams are computer-based and administered in hundreds of testing facilities worldwide. With three testing windows each year, you can sit for an exam part at a time and place convenient for you.
Exam Procedures
Follow These Easy Steps To Begin Your CMA Certification
Exam Locations
Exams are administered through the worldwide network of Prometric Testing Centers and are available in accordance with local customs. There are many locations throughout the U.S. and internationally. To locate a Testing Center and schedule exam appointments, visit www.prometric.com/ICMA.
Exam Sessions
Exams are offered according to the following schedule:
To schedule exam appointments, visit www.prometric.com/ICMA.
Tips On Scheduling Your Exam Appointments
To ensure your first choice of date, time, and location, it is best to schedule your appointment at least four weeks in advance. All exam appointments must be scheduled at least 72 hours in advance of the exam date. Once you are registered, you must take the exam part during your assigned testing window. If for any reason you are unable to schedule an exam appointment during the assigned testing window, you will need to pay for a new registration. If you are unable to keep a scheduled exam appointment at Prometric, you must cancel 72 hours prior to your appointment date. To cancel an exam appointment, call Prometric at (800) 479-6370, Monday through Saturday, or go to www.prometric.com/ICMA. If you do not comply with this cancellation policy, you will be considered a "no-show" and will need to re-register with ICMA and pay the registration fee.
Registration Fee Refund Policy
After 30 days from the date of registration, examination fees are not refundable. Within 30 days of the registration date, an examination fee may be refunded if no test appointment has been set. A $25 processing fee will be deducted from the refund. We do not offer extensions of exam parts; you must sit in the testing window for which you purchased a registration. If you purchase both parts 1 and 2 for the same testing window you are eligible for a $100 discount. To receive the discount, you are required to take both exams in the same testing window. If you are unable to, and you request a refund of one part within 30 days of purchase, you will receive a refund of $225. After 30 days, there are no refunds. (Refund calculation: $600 paid less $350 for the exam part you plan to take, less $25 processing fee equals a refundable amount of $225.)
Exam Retake Policy
An exam part may be taken only once in a testing window and no more than three times in a 12-month period (e.g., Part 1 may be taken only once within the January/February testing window). All exam retakes require a new registration along with payment of appropriate fees.
Expiration Of Exam Parts
All CMA candidates have three years to pass Part 1 and Part 2 of the exam. The time period will begin with the date of your entry into the CMA program. If you do not complete the two-part exam within three years, credit for the part passed will expire and you will have to retake the exam.
Instructions To Candidates
The CMA program lets you proceed at your own pace. You can earn a CMA in just six months or over a three year span. Busy professionals will find the CMA program to be time-efficient and cost-effective.
Requirements Include:

subset: commoncrawl


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About Cara
Hi there. I have a good experience with pets of quite a variety -caring for dogs, cats, rabbits, rats, fish.. even ostriches! I have even lived on a farm with livestock for a while too. I am naturally kind and caring and love nature. I love to see a happy pet in their homes, especially whilst their owners are away as naturally this may be a stressful time for a pet.
At the moment there are 3 collies in my family, and some Norfolk terriers. I have also had family experience with labradors and springer spaniels. During my childhood we also had 4 cats, fish and a rabbit. I also have a biology degree part of which involved studying animal behaviour.
Presently, I am unable to board pets at home but I can care for pets in their homes and dog walk within S10 and the surrounding areas. I work from home and my hours are flexible therefore I have good availability to look after your pets as I can plan my work around this. I really enjoy walking, especially in the parks in Sheffield with a furry friend. I also have experience taking cats out on their lead!
If you think you might like me to take care of your pet then please contact me and I will be more than happy to try and help. It would help greatly if you could give your rough address when making an enquiry. Many thanks.
- Property type: House
- Resident dogs: 0
- Outdoor space: Garden


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- Availability:
- 2
- Product Code:
- 748
- Brand:
- Compagnie de Provence
This luxurious liquid soap has been made by traditional Marseille soap makers, Compagnie de Provence. The lovely scent of fresh lavender and olive oil will gently nourish your hands.
Free from animal products, parabens, phenoxyethanol and artificial colours
Supplied in a stylish glass laquered 500ml bottle
Compagnie de Provence was founded in 1990 and combines tradition and innovation in its products. Marseille soap has been traditionally made in Marseille, France for about 600 years, with the first recorded soap maker in the area rumoured to date back to 1370.


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Monumental project, 420 m high, with Lenin atop
3 km4
A famous clock on the wall of puppet theatre
800 m7
Inside and outside of the awry monument by Zurab Tsereteli
3 km18
Zero kilometer of russian highways
1.5 km13
5 km5
A monument to knyaz who is traditionally considered to be a founder of Moscow
1 km6
See the historical heritage of Russian artillery and casting art
2 km13
1 km7
Architectural monument of ancient Russia on the Red Square
1.5 km5
An ideal and a symbol of soviet period
7 km24
Gates were constructed to honor victory in the war of 1812.
7 km20
Cute duck family walking in the green park.
6 km7


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News By Tag
* Michael C Gutierrez
* Artist
* Photographer
* Imprint New Mexico
* The Reconnect
* Albuquerque
* Photography
* More Tags...
Industry News
News By Location
Industry News
IMPRINT NEW MEXICO:A solo exhibition of IMPRINT energyscape photographs by Michael C. Gutierrez
IMPRINT NEW MEXICO The Reconnect Michael C. Gutierrez In the year of the dragon, in honor of New Mexico's centennial, IMPRINT NEW MEXICO reveals the Land of Enchantment's history via the big sky. Hydra Gallery, June 8, 2012 6-9pm
The Reconnect
A solo exhibition of IMPRINT energyscape photographs by Michael C. Gutierrez
Opening Reception with the Artist: Friday, June 8, 2012 from 6:00 - 9:00 pm
Location: Hydra Gallery, 4312 Lomas Blvd. NE, Albuquerque, NM, 87110
Show Dates: June 8 - 29, 2012
Gallery Hours: Wednesday-Sunday 11am-7pm
In the year of the dragon, in honor of New Mexico's centennial,
IMPRINT NEW MEXICO reveals the Land of Enchantment'
Albuquerque, New Mexico, June 8, 2012. In honor of New Mexico's centennial Michael C. Gutierrez will present a solo exhibition of his most prolific series to date, IMPRINT NEW MEXICO, at the Hydra Gallery on June 8th, 2012 from 6-9pm in Albuquerque, NM. The IMPRINTS, or energyscapes as referred to by Gutierrez, embody the darkness and the light that coexist within each of us; revealing vortexes, dimensional portals, dragons, and the energy imprints embodying the history of New Mexico via the big sky. Michael states, "This is my love letter to the people of New Mexico and to the only place in my life I have ever called home."
Using his systematic HE-13 style of shooting, Gutierrez' multi faceted images encompass a vision all his own. In a recent interview Gutierrez said, "In a time where most people, including myself, never look much further than our cell phones, we need reminders such as the IMPRINT series to reconnect with ourselves via the vastness of the New Mexico sky." Michael also states, "As a universal idea, I was offered this series, and feel honored to have the opportunity to share life in a new way."
Gutierrez's artistic process is intense and integrated into everything he does. Gutierrez states, "I trust what I do, in all aspects of photography. When you are your own greatest influence there are no limits. I openly receive ideas and will continue to push my medium forward."
Michael C. Gutierrez, fine art photographer, is currently residing in Las Cruces, New Mexico. Gutierrez attended the University of North Carolina Charlotte, The School of Visual Arts NY, and The International Academy of Design Technology where he learned photographic techniques and graphic design. Michael Gutierrez has shown his works in galleries throughout the United States and two of his photographs reside in the University of Texas San Antonio permanent collection.
For more information, or to schedule an interview with Michael C. Gutierrez, please contact Michael C. Guttierrez or Stephanie Sweet.
Michael C. Gutierrez:
Phone: 575.680.6912
Email: michaelgutierrezphotography@
Web: http://www.michaelgutierrezphotography.com
Stephanie Sweet:
Phone: 575.680.6912
Email: imprintnewmexico@
# # #
Michael C. Gutierrez, fine art photographer, is currently residing in Las Cruces, New Mexico. He is currently represented in Las Cruces, NM by Unsettled Gallery.
"No limits. Push your medium forward." ~ Michael C. Gutierrez
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Page Updated Last on: Mar 20, 2012


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Science 8 - Light an optics!
- http://www.youtube.com/watch?v=5oZtx8vVnA0
THIS IS AMAZING!! My new pet. Check it out here
Are you colour blind? - Test yourself here
See some of the light labs we will be doing here
Check out Brainpop videos here
Username - fcss
Password - password
English notes are available here and some great power points and notes here


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Here is the eighth episode of MiSeason, the season I am designing myself.
iAm A Bully
After Sam befriends the meanest girl in school, Gertrude, Sam begins to turn into a big bully, even towards Carly and Freddie. Carly and Freddie can't stand it, and together they come up with a plan to get Sam back to herself.
Creddie Hints
- Carly and Freddie look at eachother with the same look of fear when Sam goes over to Gertrude.
- Sam teases Carly and Freddie by telling them they are "love freaks".
- Carly and Freddie hug eachother when Sam apologises.
Sam: You two are looove freaks.
Carly: Sam, you know that's not true.
Freddie: It'd be great if it was, though.
Sam: (walking away) Looove freaks.
Seddie Hints
- When Sam goes to Gertrude, she only says goodbye to Freddie and not Carly.
- Sam says "loooove freaks" to Carly and Freddie in a disgusted tone, implying she hates the idea of that.
- After Carly and Freddie hug, Sam tells Freddie to hug her.
Sam: (After Carly and Freddie hug) Hug me, Freddo.
Freddie: Come 'ere, Sam! (They hug eachother)
Cam Hints
- Carly is shocked when Sam befriends Gertrude, and she even says "You're MY friend, Sam".
- When Sam says "loooove freaks", she looks at Carly when she says the "looove" part, and at Freddie when she says the "freaks" part.
- Carly stands up to Gertrude for Sam's sake, which she wouldn't hae done for anyone else.
Sam: Me and Gertrude are sorta friends now.
Carly: You're MY friend, Sam!
Sam: Yeah, whatever.


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( 1960 1961 1962 1963 1964 1965 1966 )
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This period 1966 Chevrolet II Nova L79 is available in our Louisville showroom. In 1966 you could walk ... More
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With only 792 miles since the restoration, this absolutely gorgeous 1966 Chevy II Nova is for sale in ... More
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Gateway Classic Cars of Tampa is proud to offer this incredible 1977 FORD F150 4x4! This awesome truck ... More


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Prank calling is one of my hobbies. I usually call a restaurant, hit mute so they can't hear me then call again and again, saying nothing. I keep going until they leave a voicemail. One of them was saying ''You motherfucker, I'm gonna find out who you are and I'm gonna fuck you up. Motherfucker.'' in a Turkish accent. The restaurants are USA restaurants and I liv on the other side of the world. Could I get arrested?
Sometimes when I'm with my caasin Niko (LOL) we call them and make them listen to the ezan (Muslim call for prayer) just to freak them out. If we get bored by it then we play verious pop songs. We even made a Turkish restaurant listen to Kim Kardashian's PSA for the Armenian Genocide (her speaking voice is cute!). Of course they hung up the moment they heard the word genocide, but we stopped the video, called them and played it from where we left. It was amazing.
... and we may have called some ethnic hairdressers and said some certain racial slurs & they looked like some certain animals. Come on, we were just playin'
Actually we started out with strip clubs some months ago. We would call and I'd make Niko say ''Do you have black (he pronounces it like ''bleah'') women?''. Or we would sing. Man, it was fun. We also found out those private dances are very expensive.
Most Helpful Guy
They are going to kick down your door and yell "GET DOWN! GET DOWN ON THE FLOOR MOTHERFUCKER!" with their guns pointed at you.11|00|0
Most Helpful Girl
Your a horrible person and someday you will realize that what goes around comes around.00|00|1
why am i a horrible person


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.Net Developer
Oklahoma City , Oklahoma
November 24, 2016
TEKsystems is looking to hire a .Net developer for a 6 month contract role with one of our clients in Oklahoma City.
Required Qualifications:
VB.Net and/or C# experience
SQL Server experience
HTML/XML/XSLT Experience
This individual will be working with a team of developers and spending their time on new product builds, and other projects that require attention.
They will be involved in the Full lifecycle development process including design, development, testing and implementation of moderate complexity systems. Write and review portions of detailed specifications for the development of system components of simple to moderate complexity.
About TEKsystems:
Join TEKsystems®, a leading IT staffing, IT talent management and IT services firm, and get your career on the fast track. We have more than 100 offices worldwide, and we partner with over 6,000 clients and place over 80,000 consultants per year. At TEKsystems, we seek to understand our consultants' skills, goals and interests, allowing us to present targeted job opportunities on a contract, contract-to-hire or direct placement basis. TEKsystems' leadership in the market stems from our sincere and personal commitment to driving the success of our customers, consultants and each other.
The company is an equal opportunity employer and will consider all applications without regard to race, sex, age, color, religion, national origin, veteran status, disability, genetic information or any other characteristic protected by law.
If you would like to request a reasonable accommodation, such as the modification or adjustment of the job application process or interviewing process due to a disability, please call 888 472-3411 or email firstname.lastname@example.com for other accommodation options.
A little about us:
TEKsystems provides corporations with IT staffing, talent management expertise and IT services, enabling them to meet their business objective.
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What is JotForm?
JotForm is a free online form builder which helps you create online forms without writing a single line of code. No sign-up required.
At JotForm, we want to make sure that you're getting the online form builder help that you need. Our friendly customer support team is available 24/7.
We believe that if one user has a question, there could be more users who may have the same question. This is why many of our support forum threads are public and available to be searched and viewed. If you'd like help immediately, feel free to search for a similar question, or submit your question or concern.
Can't access to Unicef webformAsked by Leap Sok on January 31, 2017 at 12:27 PM
Hi Support, I am having an issue access to the Unicef Innovation Fund webform that host at jotform https://www.jotform.com/62704508221145.
Can you help to review this problem? It is quite URGENT for the submission.
JotForm Support
I am able to access the form on my end. Is there any sort of error being shown? Let us know what you can and we will be happy to have another look.
Hi, It is just returned. Thank you for looking at it.
JotForm Support
Very welcome. If the form fails to load again, let us know the error and we will have a look.


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A knee injury has forced Paul Felder out of his preliminary card fight with Jim Miller at UFC On FOX 15 on April 18th in New Jersey.
Stepping in to replace him on three weeks notice is Beneil Dariush who's coming fresh off a submission victory against Daron Cruickshank at UFC 185 just a couple of weeks ago.
Dariush is now on a three fight winning streak and is 4-1 overall since joining the UFC in January of last year.
This is a big step up in competition for Dariush though, with Miller being one of the UFC's most experienced campaigners with an 18 fight run in the promotion to date.
Miller has a 13-4 (1nc) record overall inside the Octagon, but is coming off a KO loss to Donald Cerrone back in July of last year which brought an end to a four-fight unbeaten stretch and leaves him at No.12 on the official UFC lightweight rankings.
A BJJ expert, the 25 year-old Dariush hasn't featured on the rankings himself as yet, but a win over a respected name like Miller is exactly what he needs in order to push himself into the reckoning.
UFC On FOX 15 will be headlined by a middleweight encounter between Lyoto Machida and Luke Rockhold, with a potential No.1 contender fight in the same division between Ronaldo 'Jacare' Souza and Yoel Romero occupying the co-main event spot on the televised card.
Miller Vs Dariush is expected to take the 'featured prelim' role on the card.


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The joke was on Hugh Eggersman when Ray Guy arrived in Hattiesburg, Miss.
The North Augustan shared punting duties at the University of Southern Mississippi the year before Guy came to town. When the tall, lanky Thomson boy stepped foot on campus in fall 1969, Eggersman's days booting the football were all but over.
At one of the first fall practices, coaches pulled their prank, telling Eggersman a new player was coming in to punt and needed a few tips. So the two went to a football field, holding a punting duel.
Guy's first punt to Eggersman sailed high, backing him up 15 yards. When Eggersman kicked the ball, Guy barely moved. The next punt by Guy? Stuff legends are made of. He launched the ball over Eggersman's head and out of the football field, staking firm claim to the punting position.
"Ray took my candy," Eggersman said. "He was phenomenal. You talk about people who have a perfect swing for baseball, a perfect swing for golf. When you watched him punt, it was almost effortless. When he followed through, it was like a mid-air split."
The legend of Ray Guy didn't stop in Thomson. It continued to grow at his new home 500 miles away from his old stomping grounds.
The trek to Southern Miss seemed an unconventional one for someone who had multiple offers to play at more prestigious programs, including the likes of Alabama and Georgia. During his recruiting visit to Alabama, Guy was told by Crimson Tide coach Bear Bryant he'd never get his uniform dirty; he would've solely played punter at Alabama. That didn't sit well with Guy, who played quarterback, safety and place-kicker, along with punter, in high school.
"I just wanted to play," Guy said. "I don't know if I could've just been a punter then."
When he visited Southern Miss one weekend, spring practice was taking place. Guy soaked it all in: the campus, the people, the football. He was hooked.
"When I stepped on the campus of Southern, there was something special about it," he said. "It was almost like home. That was the feeling I wanted.
"There was nothing against Georgia or Alabama, the great traditions, but they were huge. Southern was small at that time. When you walk around, you meet everybody, you see everybody, you know everybody. ... I made the right choice. Everywhere I went I was very happy."
Because freshmen weren't allowed to play when he started at Southern Miss, Guy saw his first football action in 1970. He made up for lost time right away, blasting a 77-yard punt in his first game at Southwestern Louisiana. He also kicked three field goals in the Golden Eagles' 16-14 win.
Later that season, Guy would help Southern Miss shock undefeated Ole Miss, a game considered one of college football's greatest upsets.
The fourth-ranked Rebels, led by Heisman Trophy contender Archie Manning, faced a Southern Miss team they defeated by 62 points the previous season. But the Golden Eagles featured three Augusta-area players who made a huge impact that day: Eggersman, Guy and North Augusta's Gerry Saggus.
Eggersman, a defensive end, posted eight tackles, with two sacks and an interception en route to being named the national lineman of the week. Saggus returned a punt 60 yards for a touchdown in the second half. And Guy showed how big a difference special teams could make.
He booted a 47-yard field goal just before halftime to stake Southern Miss to a 17-14 lead. If that wasn't enough, he kept pinning Ole Miss near its own goal line, punting 10 times for a 49-yard average.
"Every time we got the ball we had 90 yards in front of us," Manning said in a 2012 article in the Jackson Clarion-Ledger. "Ray was just amazing."
Final score: Southern Miss 30, Ole Miss 14.
Guy's punting ability continued to amaze and impress everyone. Saggus entered Southern Miss at the same time, playing punt returner throughout his collegiate career. In practice, he'd receive Guy's punts, but that was the easy part. When Saggus started downfield, he'd become a target.
"I'd get my clock rung from nowhere," Saggus said of Guy. "He would knock me into the middle of next week. I would end up running and start looking for that damn No. 44."
GUY MADE A NAME for himself at Southern Miss, not just for kicking and punting, but for playing defense as well. He was an All-America safety who intercepted 18 passes in three seasons, including eight his senior campaign. Saggus said Guy could've played another position as well.
"He probably could've been our starting quarterback if anyone could've caught his passes," he said. "He could bring the heat."
And he did. In 31 starts as a flame-throwing, right-hander for the baseball team, Guy posted 14 complete games. He also struck out 266 batters in 220 2/3 innings. In the spring of 1972, Guy tossed a no-hitter on a Saturday morning against William Carey University. Afterward, he headed to football practice and never told anyone of his accomplishment.
"He was a humble person," Eggersman said. "He never thought he was better than anyone else."
AS GOOD AS he was in baseball and football, Guy thrived in other sports as well. Eggersman said Guy would lie on his bed in his dorm room and shoot a small rubber ball through a makeshift basket the size of a Dixie cup taped to his bathroom door. The practice paid off: Guy won an intramural basketball championship all four years.
Southern Miss folks still talk about Guy winning a table tennis title while there, too. If that's not enough, he was a scratch golfer who played in a regular group of 15 players. The young men often played the school's golf course, and you had to be good.
"If you were in our group and you weren't about a scratch golfer," Saggus said, "you'd get your brains beat out."
But football was where he made his biggest mark. In his senior season in 1972, he led the nation with a 46.2-yard average, with his longest kick coming against rival Ole Miss. With the Golden Eagles backed up on their 7 and Guy standing in his own end zone, he delivered a punt that sailed past midfield, the ball bouncing all the way through the end zone. On record, it still stands as the longest Southern Miss punt, a 93-yard kick that observers say traveled about 115 yards.
"I just wanted to get the ball out of the end zone," said Guy, who posted a 44.7 career average in college, still a record at Southern Miss. "I wanted to get it as far as I could down the field, at least to the 50-yard line."
On Nov. 18, Guy gave Southern Miss fans another story to talk about for ages. In a blinding snowstorm at Utah State, he went out to midfield just before halftime.
Quarterback Buddy Palazzo started trotting off the field, thinking Guy would punt. Guy, holding a kicking tee, turned his holder around, telling him to hold the ball straight up.
"I'm going to give it a ride," Guy said.
When the ball cleared the line of scrimmage, Guy lost sight of it. He couldn't see the officials standing behind the goalposts. The kick was true, and the ball sailed over the end zone, bouncing off the fieldhouse.
"It was probably 75 yards where it landed," Saggus said of the kick, which was good from 61 yards out, which set the NCAA record at the time.
"With Ray, if we crossed the 50, we felt like he could make a field goal. He's just one of the most unbelievable athletes I've ever seen."
WITH ALL HIS accomplishments on the baseball and football fields, Guy was inducted into the Southern Miss Hall of Fame in his first year of eligibility. He also became the first Golden Eagles football player to have his number retired.
At Southern Miss, he continued what he first started at Thomson High School. But the legend of Ray Guy would expand further in the NFL with Oakland.


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We help you locate a Hawes cornet teacher. Cornet tuition are a brilliant method to learn a fun new hobby, acquire a new skill and gain confidence in cornet. Use our service to find Hawes cornet teachers and select which suits your requirements so you can enjoy your cornet tuition in Hawes straight away!
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I know this month is going fly by with Christmas shortly ahead of us. I hope to get my card making and blogging a bit ahead of schedule so that I can devote some time for the Holiday "dashing"!
So today I have a card that I made which I don't normally make, but I absolutely LOVE the monochromatic results of the way it looks every time I see someone make one.
So here's my result this Holiday Season with the "white on white" monochromatic theme:
Lawn Fawn stamp set I've owned and I really love it! It's called, of course, Let it Snow. I think I could pull this one out over and over and come up with different ways to use it every time. (I'm hoping they'll soon come out with a coordinating die set for it! So maybe if they're listening?....)
On the Lawnscaping Challenge, they're hosting a "White on White" theme and this was probably the first stamp set that came to my mind. You will also notice that I've incorporated a "dots" theme which is also part of my thought process in making this card. I wanted to play along with the Addicted to CAS challenge where the theme for that is "dots".
To get a better angle shot, I've laid the card down so you can see some more details:
You can also see that I've dry embossed some "dots" on the background front base of the card.
Here's a closer view of the main panel:
Lawn Fawn Stitched Rectangle die and cut out the main panel where I embossed the trees and snow filled sky with white embossing powder. I then mounted that onto a white glittered card stock panel. I finished off with accents of the Lawn Fawn Silver Sparkle Single Cord Lawn Trimmings. I've also added some both silver and gold sequins to the white embossed trees and then placed a small "dot" of white liquid pearls in the center of each one.
I really like the way this one turned out! Another Christmas card for my "pile"! YAY!
Thanks so much for stopping in with me today! I hope you've enjoyed my creation and I'll be seeing you right back here again on Friday!! Enjoy your day!
Here's the challenges I'd like to enter this card for:
Lawnscaping Challenge:


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Hi all,
we need advice on how to get from bellagio/varenna to florence by train. we will be travelling on the 4th june 2013. thanks to you all for your help
Hi all,
we need advice on how to get from bellagio/varenna to florence by train. we will be travelling on the 4th june 2013. thanks to you all for your help
You take a train from Varenna to Milan Central, and change there for a fast train to Florence. See www.trenitalia.com looking for trains from Varenna to Firenze SM Novella.
Book now for the best prices. The cheapest tickets will already have all been sold.Edited: 6:12 am, March 05, 2013
For cheap prices, book as soon as possible from Varenna-Esino to Firenze S. M Novella on www.trenitalia.com - click the British flag for English, and enter your desired 'hour' of departure e.g. '13' for 13.00.
Still plenty of cheap deals for your date, but they will sell out.Edited: 6:16 am, March 05, 2013
Hello, I am also trying to book a train ticket round trip from Florence to Varenna dates 6/27-7/1 and it is listing that there are no schedules available. Is it too early to book? or are tickets sold out? I put in Firenze sm novella to Varenna Esino.
Any help you can provide is much appreciated! Thank you in advance!
As is said in at least a dozen other threads, there is a timetable change on 8 June and times have not yet been published for after that date. Just keep checking the web site.
Thanks for your help. I did not see your other threads.
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Sea, air search for Norwegian boatie
The Customs Service is carrying out sea and air searches for the yacht Nilaya, amid concerns a Norwegian adventurer may be making another voyage to Antarctica, after a similar trip a year ago ended with three deaths.
Customs said it sent a boat this morning to search in the Auckland Harbour and Waiheke Island area. A plane would do an aerial sweep, working on the time and distance the Nilaya may have covered.
The Ministry of Foreign Affairs and Trade said Norwegian Jarle Andhoey was in New Zealand early this month and failed to declare, as required, that he had previously been deported from Canada.
The Norwegian government had notified Antarctic Treaty Parties it was concerned Andhoey may be planning another voyage to the Ross Sea, and had advised that no expedition had been authorised by it as required by Norwegian law.
The Southern Ocean was one of the most remote and inhospitable areas in the world and New Zealand government agencies were obviously concerned about any possibility there could be a repeat of last year's events in the Ross Sea, MFAT said.
Customs appealed for information on the Nilaya's location, noting it was an offence to leave New Zealand waters without obtaining Customs clearance, and complying with relevant New Zealand legislation.
Anyone able to help was asked to contact 0800 4 Customs (0800 428 786).
The suspected new voyage comes a week after Norway television ran a documentary made by Andhoey on last year's disaster. Family of the three killed went to court unsuccessfully to stop the broadcast.
The documentary was screened last week on TVNorge.
Families of the dead tried to block its airing.
The Oslo District Court ruled it supported TVNorge's argument that the events of significant public interest, and believed the TV series could not be temporarily halted.
TVNorge said the crew knew about and agreed that the recordings would be published.
The court said the documentary did not harm or defame the reputation of the dead men.
Nilaya - which means "paradise" or "pleasure" - has been on sale in New Zealand for $345,000 - down from the original asking price of $570,000.
The registered owner of the yacht and the man advertising it for sail is Douglas Easton of Auckland, who runs a building consultancy firm. He could not be contacted for comment this morning.
"Nilaya is a magnificent, New Zealand-built 54 foot custom steel pilothouse yacht," a website sale note says.
"Well equipped, easily handled, a comfortable and good looking luxury sailboat.
"The 22 ton 'small superyacht' is well suited to safe blue water cruising, live aboard or simply entertaining out in the Bay."
Registered to the Royal New Zealand Yacht Squadron, the yacht is described as being of rare quality.
"She has a large saloon and dining area, master stateroom with ensuite and generous guest accommodation. All is low maintenance.
"This is a vessel that needs to be seen in person and is ready and capable of taking her new owners on the cruise of a lifetime in comfort, safety and style. Her shallow draft and strong construction make her an ideal vessel for live-aboard cruising."
Last February Andhoey was skipper of 14-metre steel yacht Berserk, which sailed to Antarctica without a permit or permission from the Norwegian government.
He and crewman Samuel Massie were dropped off near Scott Base to undertake a trip to the South Pole on four-wheel-drive quad bikes.
The yacht's emergency beacon was activated soon after they were dropped off. It lasted for several hours before transmissions ceased and it was believed the yacht, and three remaining crew, had sunk in one of the worst Antarctic storms in 20 years.
Once they knew the yacht had disappeared, Andhoey and Massie went to the US base at McMurdo Sound, to catch a flight back to Christchurch.
A week-long international search and rescue operation for Berserk, coordinated by the Rescue Coordination Centre of New Zealand, covered more than 25,000sq km, in often-treacherous seas and 180kmh winds.
At the time, Antarctica New Zealand chief executive Lou Sanson said the trip at that time of year was unusual, and Andhoey broke safety protocols.
Auckland Now


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Friday, May 29, 2009
Nick Miroff's May 28 front-page article, "As if It Needed to, Virginia Bans Smiles at the DMV," was an unacceptable, opinion-laden cheap shot at the Department of Motor Vehicles. Your readers deserve unbiased reporting. The facts:
In conjunction with Virginia's new secure driver's licenses and central issuance process, the DMV is taking steps for possible future security enhancements. The DMV may use technology to compare customer photos taken today to photos taken in the future. The technology compares facial features to ensure a match. This technology works best when the photos are similar -- for example, when a customer has a neutral expression in both photos vs. a neutral expression in one photo and a smile in another.
Using technology to ensure matching photos, the DMV can further reduce the risks of fraud and identity theft.
The DMV does not use the technology today. However, by capturing neutral-expression photos today, the agency will be in a position to implement photo comparison sooner rather than later, if funding and authorization are granted for the technology.
Regarding the smiley-face stickers at the camera station: The mouths are closed with no teeth displayed. Smiley hasn't lost his identity in his 40-plus years. The DMV is working to help keep your identity secure, too.
Director of Communications
Virginia Department of Motor Vehicles
View all comments that have been posted about this article.


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RIP1 is a central mediator of cell death in cell stress, but can also mediate cell survival by activating NF-κB. Here, we show that RIP1 is a switch in EGFR signaling. EGFRvIII is an oncogenic mutant that does not bind ligand and is co-expressed with EGFRwt in glioblastoma (GBM). EGFRvIII recruits ubiquitin ligases to RIP1 resulting in K63-linked ubiquitination of RIP1. RIP1 binds to TAK1 and NEMO forming a EGFRvIII-RIP1 signalosome that activates NF-κB. RIP1 is essential for EGFRvIII-mediated oncogenicity and correlates with NF-κB activation in GBM. Surprisingly, activation of EGFRwt with EGF results in a novel negative regulation of EGFRvIII with dissociation of the EGFRvIII-RIP1 signalosome, loss of RIP1 ubiquitination, NF-κB activation, and association of RIP1 with FADD and Caspase-8. If EGFRwt is overexpressed with EGFRvIII, adding EGF leads to a RIP1 kinase dependent cell death. The EGFRwt-EGFRvIII-RIP1 interplay may regulate oncogenicity and vulnerability to targeted treatment in GBM.
The receptor interacting protein (RIP, RIP1, RIPK1) is widely expressed and is a member of a kinase family that mediates cellular responses to inflammation and stress (Festjens et al., 2007; Meylan and Tschopp, 2005). RIP1 is also an important mediator of cell death (Weinlich et al., 2011). RIP1 plays a key role in apoptotic cell death induced by stimuli such as TNFα, DNA damage, or cIAP inhibitors (Bertrand et al., 2008; Petersen et al., 2007; Varfolomeev et al., 2007; Vince et al., 2007). In addition, RIP1 plays a key role in necrotic forms of cell death triggered when Caspase activation is blocked (Feoktistova et al., 2011; Hitomi et al., 2008; Tenev et al., 2011). Necrotic cell death under these conditions requires the kinase activity of RIP1 and is inhibited by a specific inhibitor of RIP1 kinase, termed Necrostatin-1 (Degterev et al., 2008).
RIP1 is an essential component of signaling platforms involved in either NF-κB activation or cell death signaling (Bertrand and Vandenabeele, 2011). For example, RIP1 forms complexes with IKKγ (NEMO), TRADD and TAK1 to activate NF-κB in response to stressful stimuli. The core signaling complex involved in cell death signaling by RIP1 includes RIP1, FADD and Caspase-8 (Feoktistova et al., 2011; Tenev et al., 2011). K63-linked ubiquitination, may play a key role in determining the partners RIP1 associates with, and in determining whether RIP1 acts as a prosurvival adaptor protein or participates in cell death (Bertrand et al., 2008; Declercq et al., 2009; Ea et al., 2006; O'Donnell et al., 2012; O'Donnell et al., 2007; O'Donnell and Ting, 2012; Wang et al., 2008). The cIAPs and TRAF2 play an important role as ubiquitin ligases that mediate K63-linked ubiquitination of RIP1 (Bertrand et al., 2008). cIAP inhibitors/SMAC mimetics target cIAPs leading to a RIP1 dependent cell death. Thus, substantial evidence suggests that RIP1 plays a pivotal role in determining cell survival or death depending on the cellular context.
Aberrant activation of NF-κB is widespread in human cancer (Karin et al., 2002; Pacifico and Leonardi, 2006) including GBM (glioblastoma), and generally promotes survival of tumor cells. It has been suggested that two major pathways activate NF-κB in GBM (Bredel et al., 2011). Firstly, EGFR gene amplification and aberrant EGFR signaling are detected in 40-50% of GBMs. EGFR signaling is known to activate NF-κB (Habib et al., 2001; Sun and Carpenter, 1998; Yang et al., 2012). Secondly, NF-κB inhibitor-α (NFKBIA, which encodes lκBα) is commonly deleted in non-EGFR amplified GBMs, resulting in NF-κB activation (Bredel et al., 2011). A specific and oncogenic EGFR mutant (EGFR Type III, EGFRvIII, de2-7, ΔEGFR) can be detected in about one third of GBMs (Hatanpaa, 2010; Huang et al., 2009). EGFRvIII is generated from a deletion of exons 2-7 of the EGFR gene, which results in an in frame deletion of 267 amino acids from the receptor. EGFRvIII is unable to bind ligand and thought to signal constitutively.
EGFRvIII is usually co-expressed with EGFR wild type (wt) in GBM (Biernat et al., 2004; Ekstrand et al., 1991). The deletion of exons 2-7 in EGFRvIII occurs in EGFR gene amplified tumors (Biernat et al., 2004; Frederick et al., 2000), suggesting that the genetic abnormalities that lead to overexpression of EGFRwt and to expression of EGFRvIII co-exist in individual tumor cells. Immunohistochemical studies also suggest that the two receptors are expressed in the same tumor cells, although in some GBMs, EGFRvIII may be expressed in a more focal distribution compared to EGFRwt. However, even focally distributed EGFRvIII is expressed in cells with EGFRwt expression (Biernat et al., 2004; Nishikawa et al., 2004). A recent study has suggested that EGFRvIII activates NF-κB via mTORC2 (Tanaka et al., 2011). NF-κB plays an important role in EGFRvIII-mediated oncogenicity (Bonavia et al., 2012; Tanaka et al., 2011).
We previously showed that RIP1 is commonly expressed at high levels in GBM and confers a worse prognosis (Park et al., 2009). In this study, we propose an essential role for RIP1 in EGFRvIII mediated NF-κB activation. Silencing RIP1 inhibits EGFRvIII mediated NF-κB activation and oncogenicity in an orthotopic mouse model. Expression of EGFRvIII leads to recruitment of the ubiqitin ligases, TRAF2 and cIAP2, to RIP1 and to EGFRvIII resulting in K63-linked ubiquitination of RIP1 and NF-κB activation. EGFRvIII forms a signaling platform that incorporates RIP1, NEMO and TAK1. Both EGFRvIII and RIP1 are required for assembly of this signalosome. Importantly, we show that EGFRvIII mediated activation of NF-κB is negatively regulated by co-expressed EGFRwt. Thus, addition of EGF to cells which activates EGFRwt, results in a rapid loss of RIP1 ubiquitination and loss of its association with EGFRvIII, NEMO and TAK1 and a loss of EGFRvIII-mediated NF-κB activation. RIP1 now becomes associated with the death adaptor FADD in an EGF-dependent manner. When EGFRwt is overexpressed, as is common in GBM and other human cancers, EGF becomes a death signal and this cell death requires the kinase activity of RIP1. Thus, RIP1, previously implicated in cell stress and inflammatory signaling, is also a key life/death switch in a major RTK signaling system and turns a normally trophic signal into a death signal. These findings reveal a novel antagonistic interaction between EGFRwt and EGFRvIII and add a layer of complexity to our understanding of EGFRvIII and NF-κB activation in GBM.
EGFRvIII is a tumor specific EGFR mutant not expressed in normal tissues or in established GBM cell lines. Stable expression of EGFRvIII in U87MG cells results in activation of NF-κB. (Bonavia et al., 2012; Tanaka et al., 2011). Since EGFRvIII does not bind ligand, we generated U87MG cell lines conditionally expressing EGFRvIII in response to tetracycline (Figure 1A) as a tool to examine regulated EGFRvIII signaling. Two tetracycline inducible clones were identified and named U1 and U26. EGFRvIII can be distinguished from EGFRwt on Western blots as a faster migrating band (Figure 1A). Consistent with previous studies, conditional expression of EGFRvIII in U1 and U26 cells leads to activation of NF-κB as determined by phosphorylation of the p65 subunit of NF-κB (Figure 1A and SFigure 1A). We also confirmed phosphorylation of p65 in U251-vIII cells (Figure 1A). U251vIII cells conditionally express EGFRvIII in response to tetracycline (Ramnarain et al., 2006). Additionally, constitutive EGFRvIII expression in LN229 cells also results in phosphorylation of phospho-p65 (Figure 1A) demonstrating that EGFRvIII activates NF-κB in multiple GBM cell lines. Additionally, we confirmed that EGFRvIII activated the transcriptional activity of NF-κB by reporter assays in the various cell lines using an NF-κB luciferase reporter as shown in Figure 1B. All the GBM cell lines used express endogenous EGFRwt.
In addition, we examined a panel of primary GBM stem like cultures grown as neurospheres for the presence of EGFRvIII (Figure 1C). We selected GBM9 neurosphere cultures (GBM9-NS) that retain substantial expression of EGFRvIII with a low level of EGFRwt and demonstrate phosphorylation of the p65 subunit of NF-κB. Importantly, inhibition of EGFR kinase activity by Erlotinib addition abolished phosphorylation of p65 in GBM9-NS, indicating that EGFRvIII is driving NF-κB activation in these cells (Fig 1D). Erlotinib also blocks NF-κB transcriptional activity in GBM9-NS (SFigure 1B). A dose response for the concentration of Erlotinib required to inhibit EGFR in U1 cells is shown in SFigure 1C-D. A second EGFR kinase inhibitor, AG1478, also blocked EGFR phosphorylation in U1 cells (SFigure 1E).
Next, we examined the effect of combined EGFRwt and EGFRvIII activation by exposing these cells to EGF. Unexpectedly, we found that exposure of cells to EGF leads to a complete loss of EGFRvIII-mediated NF-κB transcriptional activation in multiple cell lines (Figure 1E-F). Adding EGF to U251vIII cells not exposed to tetracycline (not expressing EGFRvIII) results in activation of NF-κB (Figure 1E). However, when EGFRvIII is expressed, ligand-mediated EGFRwt activation not only fails to activate NF-κB, but also abolishes EGFRvIII-mediated NF-κB activation. Similarly, Figure 1F and SFigure 1F-G show that addition of EGF abolishes EGFRvIII-mediated activation of NF-κB in U1 cells, U26 cells, and LN229-vIII cells. Electrophoretic mobility shift assays also demonstrate a loss of EGFRvIII-mediated NF-κB DNA binding in U1 cells in response to EGF (SFigure 2A). Thus, EGF-mediated activation of EGFRwt results in a complete reversal of EGFRvIII-mediated NF-κB activation in multiple cell lines. We examined the ability of EGF to abolish EGFRvIII-mediated NF-κB activation in U251vIII cells with silenced EGFRwt. We find that EGF did not abrogate EGFRvIII-mediated NF-κB activation in EGFRwt silenced cells (SFigure 2B-C). The levels of EGFRvIII expressed in our experimental system are similar to GBM tumors (Figure 1G).
Next, we examined whether co-expression of both EGFRwt and EGFRvIII can be detected in the same cells in primary GBM cultures. Primary neurosphere cultures from both GBM9-NS and 748-NS show co-expression of both EGFRwt and EGFRvIII (Figure 1C). We generated single cell suspensions from these tumors by limiting dilution and expanded single cell clonal populations. Multiple colonies derived from single cells were examined for expression of EGFRwt and EGFRvIII by Western blot. In all clonal populations from both tumors both EGFRvIII and EGFRwt are co-expressed (SFigure 3). Our data thus supports the evidence from previous studies that EGFRvIII is usually co-expressed with EGFRwt in the same tumor cells.
While it is well known that EGFRvIII activates NF-κB, the underlying mechanisms are not well understood. On the other hand, NF-κB activation by cytokines such as TNFα has been extensively characterized and involves RIP1. Furthermore, we previously reported that RIP1 forms a complex with EGFRwt when both are expressed at high levels although the significance or mechanism of this interaction was not investigated (Habib et al., 2001). We examined whether EGFRvIII uses a mechanism similar to TNFα to activate NF-κB. To examine a possible role for RIP1 in EGFRvIII signaling, we silenced RIP1 in U1 cells and U251-vIII cells. Silencing RIP1 inhibits EGFRvIII-induced NF-κB reporter activity (Figure 2A-B and SFigure 4A-B). EGFRvIII-mediated NF-κB activation is abolished by Necrostatin-1, a specific inhibitor of RIP1 kinase (Figure 2C, ,1D1D and SFigure 4C). Thus, both Necrostatin-1 and Erlotinib inhibit EGFRvIII-mediated NF-κB activation. These findings suggest that RIP1 is required for EGFRvIII-mediated NF-κB activation. A necrostatin-1 dose response for the concentration of necrostatin-1 required to inhibit the RIP1 activity in U1 cells was determined by EGFRvIII-driven phosphorylation of phospho-p65 (SFigure 4D-E). RIP1 knockdown by siRNA also inhibits phosphorylation of p65 (SFigure 4F).
Next, we examined the biological consequences of silencing RIP1 in EGFRvIII expressing cells. We used shRNA to stably silence RIP1 in U1 cells using lentiviral shRNA directed against RIP1 or control shRNA followed by puromcyin selection. Stable clones with silenced RIP1 were identified (Figure 2D). We found that silencing RIP1 resulted in significantly decreased numbers of cells in culture compared to controls (SFigure 5A-C). Next, we tested U1 RIP silenced cells for growth in an orthotopic xenograft model of GBM in athymic nude mice. We first confirmed that EGFRvIII was conditionally expressed in U1 (control shRNA) cells in intracranial tumors in animals exposed to doxycycline in drinking water and feed (Figure 2E). Next, we injected cells with silenced RIP1 or control shRNA intracranially into groups of nude mice. Animals were sacrificed at the onset of neurological symptoms or after eight months. Kaplan-Meier survival analyses were computed to compare the two groups on time until the appearance of neurological symptoms (the event), where time was defined as number of days elapsed from injection to symptom appearance. The median number of days until the event for the shRIP1-L11 group was 240 days (100% censored data), as opposed to 57 days for control shRNA group (Figure 2H). The log rank test was significant (χ²(1) =15.47, p <.0001), indicating that shRIP-1-L11 mice remained symptom-free for a significantly longer period of time than the control mice, Surprisingly, no animals injected with the shRIP1 silenced cells formed tumors, while all of the animals with shControl cells formed tumors as shown in Figure 2F-H. Both RIP1 and EGFRvIII can be detected in tumors from U1control shRNA mice (Figure 2G). This experiment suggests that RIP1 is required for EGFRvIII mediated oncogenicity.
The ubiquitin ligases involved in K63 linked ubiquitination of RIP1 have been identified as c-IAP1, c-IAP2 and TRAF2. Thus, we tested whether conditional EGFRvIII expression leads to increased recruitment of ubiquitin ligases to RIP1. Figure 3A-C shows that expression of EGFRvIII in U1 cells results in increased associated of cIAP2 and TRAF2 with RIP1. cIAP1 is associated with RIP1 in these cells, but the cIAP1-RIP1 association does not increase with EGFRvIII expression. We also detected an increased recruitment of c-IAP1, cIAP2 and TRAF2 to EGFRvIII. As is discussed below, RIP1 is also recruited to EGFRvIII suggesting that RIP1 ubiquitination may occur in EGFRvIII associated complexes. A similar result is detected in U251vIII cells (Figure 3D-F). Expression of EGFRvIII results in increased K63-linked ubiquitination of RIP1 in U1 cells (Figure 3G). Importantly, the K63-linked ubiquitination of RIP1 is lost when EGF is added to cells, consistent with the loss of EGFRvIII-mediated NF-κB activaton. Similar results were found in U26 cells and U251vIII cells (Fig. 3H and SFigure 5D). In U251 cells, RIP1 appears to be constitutively K63-linked ubiquitinated as has also been reported for other cancer cell types (Feoktistova et al., 2011). Addition of EGF results in a loss of K63 linked RIP1 ubiquitination although this is delayed compared to U1 cells (SFigure 5D).
RIP1 associates with EGFRvIII in U1 and U251vIII cells. Thus, when we immunoprecipite with EGFR antibodies and perform Western blot analysis with RIP1, the RIP1 -EGFRvIII association is detectable only in cells exposed to tetracycline. Interestingly, the RIP1-EGFRvIII association is rapidly lost when EGF is added (Figure 4A). No significant association of RIP1 with EGFRwt is detected with or without ligand. IKKy (NEMO) is an important partner for RIP1 in NF-κB activation. We find that NEMO forms a complex with RIP1 that is dependent on EGFRvIII, as demonstrated by immunoprecipitation with NEMO antibodies followed by Western blotting with RIP1. These data suggest that EGFRvIII induces formation of an NF-κB signaling complex. Remarkably, the RIP1-NEMO complex dissociates when EGF is added (Figure 4B). Furthermore, NEMO also binds to the EGFRvIII, suggesting the formation of a RIP1-NEMO containing signaling complex associated with EGFRvIII. TAK1 is another important component of the NF-κB activation network and phosphorylates the IKK complex, an event that culminates in NF-κB activation. TAK1 also forms a complex with RIP1 when EGFRvIII is expressed and dissociates from RIP1 and EGFRvIII when EGF is added to cells (Figure 4C). Exposure of GBM9-NS cells to an EGFR kinase inhibitor, Erlotinib, blocks the EGFRvIII-RIP1 association, as does necrostatin-1, albeit to a lesser extent (Figure 4D). In these cells, the NEMO-RIP1 association is not inhibited by Erlotinib while it is inhibited by Necrostatin-1 suggesting that RIP1 kinase activity is required (Figure 4E). Association of NEMO with the EGFRvIII, however, is decreased by both Erlotinib and Necrostatin-1 (Figure 4E). Importantly, RIP1 siRNA knockdown abolishes recruitment of NEMO but not TAK1 to EGFRvIII in U1 and U251-vIII cells (Figure 4F-G). RIP1 does not influence EGFR levels in these cells. These experiments suggest that expression of EGFRvIII leads to recruitment of RIP1, NEMO and TAK1 to EGFRvIII and that EGFRvIII promotes association of RIP1 with NEMO and TAK1 in this complex.
While EGFRvIII expression leads to increased association of NEMO and TAK1 with RIP1, it does not induce the association of FADD with RIP1. Interestingly, when EGF is added to EGFRvIII expressing cells, RIP1 loses its association with NEMO and TAK1 and forms a second complex with FADD. The FADD-RIP1 association is EGF-dependent and can be detected in U1 as well as U251vIII cells (Fig. 5 A-B). Caspase 8 appears to be complexed with RIP1 in U1 cells (Figure 5C). Thus, a death complex with RIP, FADD and Caspase 8 forms in the presence of EGF. However, we do not detect cell death when EGF is added to U1 cells expressing EGFRvIII (Figure 5D).
EGFRvIII becomes constitutively tyrosine phosphorylated and activated upon expression in cells. Next, we examined whether EGF influenced EGFRvIII tyrosine phosphorylation in U1 cells. If EGF is added to EGFRvIII expressing cells, tyrosine phosphorylation of EGFRvIII in unaltered (Figure 5E). As has been reported previously (Luwor et al., 2004), we find that EGFR coimmunoprecipitates with EGFRvIII, but the association does not appear to be altered by EGF (Figure 5F).
In the experiments described above, we observed that RIP1 becomes associated with FADD in response to EGF, but this does not result in cell death. These experiments were conducted in cells with a relatively low level of endogenous EGFRwt. We examined whether overexpression of EGFRwt would result in a RIP1 dependent cell death. It should be noted that the EGFR gene amplification is detected in 40-50% of GBMs and results in overexpression of both EGFRwt as well as mutant forms of EGFR. Thus, EGFRwt is usually expressed at high levels in tumors cells expressing EGFRvIII. We stably overexpressed EGFRwt in U1 that conditionally express EGFRvIII in response to tetracycline (U1wt cells). The level of EGFRwt in U1wt cells is similar to levels in actual GBM tumors (SFigure 5E).
Next, we examined whether exposure of U1wt cells to EGF results in cell death. Expression of EGFRvIII by exposure of cells to tetracycline induces no cell death. However, if cells are exposed to EGF for 24h, there is a robust cell death that has elements of both apoptosis and necrosis (Figure 6A and SFigure 6A). Importantly, this cell death is blocked by the use of necrostatin-1, indicating a requirement for RIP1 kinase activity (Figure 6B). A FACS plot of original data for Figure 6A-B is shown in SFigure 7A. If EGF exposure is continued for 72h, the cell death detected is primarily necrotic and again blocked by Necrostatin-1 (SFigure 6A). siRNA knockdown of RIP1 also blocks EGF-induced cell death in U1wt cells, confirming the essential requirement for RIP1 in EGF-mediated cell death (Figure 6C-E and SFigure 6B). EGF induced and RIP1 dependent cell death is also detected in a second cell line expressing both high levels of EGFRwt and EGFRvIII (U251vIIIwt cells, SFigure 6C-D).
We also confirmed a loss of EGFRvIII-induced NF-κB activation in U1wt cells in response to EGF (SFigure 6E). This loss of NF-κB activation is consistent with the EGF-induced switch to cell death, since NF-κB activation generally promotes cell survival. Furthermore, treatment of U1wt cells with EGF results in a rapid formation of a death signaling complex with increased EGF-dependent association of FADD with RIP1 and Caspase-8 (Figure 6F). Moreover, the complex persists for up to 24 hours (SFigure 6F-G).
Next, we examined expression of EGFR, RIP1 and phospho-p65 in tumor lysates made directlyfrom GBM tissue (Figure 7A). EGFRvIII mRNA levels were also detected by quantitative realtime PCR (SFigure 7B). In this series of 23 GBMs, 30% of tumors express EGFRvIII. In 6/7GBMs, EGFRvIII is expressed in the presence of EGFRwt, while EGFRvIII appears to be expressed without EGFRwt in one tumor. While phosphorylation of p65 can be detected inevery tumor that expresses EGFRvIII, p65 is also phosphorylated in tumors that are not EGFR amplified, consistent with an additional mechanism(s) of NF-κB activation in GBM. Aspreviously noted, a major mechanism of NF-κB activation in GBMs is deletion of NFKBIA, detected usually in GBMs that do not have amplified EGFR. Importantly, RIP1 is expressed widely in GBMs and the presence of RIP1 correlates with phosphorylation of p65 in GBM asshown in Figure 7A-B (p<0.05, Pearson correlation). Thus, the major components of the EGFRvIII-RIP1-pp65 network are detectable in GBM.
RIP1 has emerged as a key mediator of survival and cell death in the context of cellular stress and inflammatory signaling. RIP1 has been reported to play an essential role in activation of NF-κB in response to TNF-alpha, TLR3 and DNA damage. Recent studies have elucidated a key role for RIP1 in both apoptotic and necrotic forms of cell death. In general, the prosurvival actions of RIP1 are likely to be mediated largely by activation of NF-κB. Post-translational modifications of RIP1, such as K63-linked polyubiquitination, may determine the nature of RIP1 signaling partners and the biological outcome. Receptor tyrosine kinase (RTK) signaling pathways are of central importance in cancer. Our study suggests that RIP1 play a role as a cell life/death switch in a classical oncogenic RTK signaling pathway in an interaction between EGFRwt and the oncogenic EGFR mutant EGFRvIII.
We propose a model for EGFRvIII-mediated activation of NF-κB that involves recruitment of components of the network that mediates TNFα induced NF-κB activation. Firstly, EGFRvIII recruits the ubiquitin ligases c-IAP1, c-IAP2 and TRAF2 to RIP1 and to EGFRvIII resulting in K63-linked ubiquitination of RIP1. EGFRvIII forms a signaling complex by recruiting RIP1, NEMO and TAK1 to EGFRvIII and also increases the association of RIP1 with NEMO and TAK1. Importantly, RIP1 is required for the recruitment of NEMO to EGFRvIII. An unusual feature of EGFRvIII mediated NF-κB activation is the requirement for the kinase activity of RIP1. Previous studies suggested that RIP1 kinase activity is dispensable for NF-κB activation. However, in a recent study it was shown that Etoposide-induced NF-κB activation occurs in two phases and that RIP1 kinase activity is required for the second phase (Biton and Ashkenazi, 2011).
Our study demonstrates that RIP1 is required for EGFRvIII-mediated oncogenicity. Stable silencing of RIP1 in U87MG cells expressing EGFRvIII results in slowed proliferation of cells in culture and importantly, abrogates EGFRvIII mediated tumorigenicity in an in vivo orthotopic model. In our experiment, none of the eight animals with inoculated with RIP1-silenced EGFRvIII cells formed intracranial tumors over an observation period of eight months while all of the animals with control shRNA formed intracranial tumors in about 57 days. Presumably, the lack of EGFRvIII-mediated tumorigenicity results from a loss of the ability of EGFRvIII to activate NF-κB.
An intriguing observation is the unexpected finding that ligand mediated activation of EGFRwt abolishes EGFRvIII-mediated NF-κB activation using RIP1 as a switch. This is unexpected since both EGFRwt and EGFRvIII are known to activate NF-κB, and one would predict a synergistic effect. Synergistic interactions reported previously include EGFRvIII mediated induction of the EGFRwt ligand HB-EGF in an autocrine loop and paracrine effects of EGFRvIII on EGFRwt via an IL-6 mediated pathway (Inda et al., 2010; Ramnarain et al., 2006). The antagonistic effect of EGFRwt on EGFRvIII is highly novel and to our knowledge, antagonistic interactions between RTKs in the EGFR family have not been reported previously. EGFRvIII is expressed almost exclusively in tumors with EGFR gene amplification and EGFRwt overexpression. As discussed, immunohistochemical studies examining expression of EGFRwt and EGFRvIII and our data support the co-expression of EGFRwt and EGFRvIII in individual tumor cells. Our current studies show that ligand mediated activation of EGFRwt results in a dissociation of the EGFRvIII associated signaling complex composed of RIP1, NEMO and TAK1 as well as a separation of RIP1 from NEMO and TAK1. This is associated with loss of K63-linked RIP1 ubiquitination and a complete loss of NF-κB activation. We propose that activation of EGFRwt induces conformational changes in EGFRvIII leading to a loss of EGFRvIII signalosome, a hypothesis that will be examined in future studies.
Our study provides evidence that a RIP1 switch operates in EGFR signaling. Firstly, EGFRvIII forms a physical complex with RIP1 and associated signaling proteins, recruits ubiquitin ligases to RIP1 resulting in K63-linked ubiquitination of RIP1 leading to NF-κB activation via a RIP1 dependent pathway. Ligand-mediated activation of EGFRwt results in a dissolution of the EGFRvIII signalosome, leading to a loss of RIP1 association with key signaling proteins, such as NEMO, TAK1, EGFRvIII, deubiquitination of RIP1, and a complete loss of NF-κB activation. Addition of EGF now results in an association of RIP1 with FADD and Caspase-8. Thus, addition of EGF in the presence of EGFRvIII shifts RIP1 towards a cell death role. While exposure to EGF does not result in cell death when cells express a low level of EGFRwt, when EGFRwt is overexpressed to levels similar to those detected in actual GBM tumors, EGF becomes a death signal. This is remarkable since EGF is normally a trophic factor. This cell death has features of both apoptosis and necrosis and it requires the kinase activity of RIP1. Thus, the addition of EGF results in unleashing the RIP1 switch all the way from an EGFRvIII-RIP1-NF-κB oncogenic signal to a RIP1-FADD-Caspase 8 cell death signal. Although it is somewhat counter-intuitive that a growth factor receptor would induce cell death, there are precedents for life/death signaling switches. For example, Caspase-8, traditionally viewed as an apoptotic protein also has a role in survival (Dillon et al., 2012). Similarly, increased expression of EGFRwt has previously been implicated in growth suppression and apoptosis (Armstrong et al., 1994; Gill and Lazar, 1981).
RIP1 is expressed in most GBMs and is co-expressed with EGFRvIII in tumors showing evidence of NF-κB activation, suggesting that the mechanisms detected in our experimental system may be operational in GBM. Thus, EGFRvIII mediated activation of NF-κB may be a major target for treatment. Since RIP1 mediates EGFRvIII mediated activation of NF-κB, inhibition of RIP1 using either chemical inhibition of silencing approaches could be a potentially important treatment in GBM. In addition, our data suggest that EGFRwt activation could be a mechanism for activating the cell death function of RIP1 in GBM. This is a very novel approach since so far all effort has been focused on inhibiting the EGFR in GBM with limited success (Karpel-Massler et al., 2009). Furthermore, the availability of endogenous EGFRwt ligand(s) in the vicinity of EGFRvIII expressing GBM cells may influence the oncogenic effects of EGFRvIII by abrogating EGFRvIII mediated NF-κB activation and by diverting RIP1 into a cell death pathway that renders tumor cell populations vulnerable to targeted or conventional therapy.
The glioblastoma cell lines U251MG and U87MG were used to generate cell lines conditionally expressing EGFRvIII using the T-Rex Tet-on system from Invitrogen as we have described previously (Ramnarain et al., 2006). EGFRwt with an HA tag and EGFRvIII with an HA tag was cloned into PcDNA3.1 (Neo) vector using standard molecular techniques. Lipofectamine 2000 (Invitrogen) was used for all transfections. To generate cell lines that express high levels of EGFRwt constitutively along with conditional expression of EGFRvIII, we stably transfected EGFRwt into U1 and U251vIII cells followed by selection in G418. Primary GBM cultures were generated directly from human GBMs. A papain dissociation system was used to dissociate tumors and cells were then cultured in Neurobasal medium supplemented with B27 without Vitamin A, and with EGF (10ng/ml) and bFGF (10ng/ml). LN229-EGFRvIII cells have been described previously (Li et al., 2004). At least 3 independent experiments were done unless otherwise indicated.
Cells were plated in 48 well dishes followed by transfection with either along with NF-κB-LUC plasmid using lipofectamine. A dual-luciferase reporter assay system was used according to the instructions of the manufacturer (Promega, Madison WI). Firefly luciferase activity was measured in a luminometer and normalized on the basis of Renilla luciferase activity.
For transient silencing of EGFR, we used a pool of siRNA sequences directed against human RIP1 or control (scrambled) siRNA obtained from Dharmacon or Qiagen. siRNA was performed according to the manufacterer's protocol using Lipofectamine 2000 reagent (Invitrogen). For stable silencing of RIP1, ready to use RIP1 lentiviral particles or control shRNA particles were obtained from Santa Cruz Biotechnology followed by puromycin selection according to the manufacterer's protocol. For stable silencing of EGFRwt we used two shRNA sequences directed against exon 3 of EGFRwt (Smith et al., 2005) or control vector followed by selection in G418.
Western blot and immunoprecipitation was performed according to standard protocols. For analysis of RIP1 ubiquitination we followed a protocol described previously (Biton and Ashkenazi, 2011) and as described in supplemental methods. Details of antibodies used in this study are outlined in supplemental methods. Necrostatin-1 was obtained from Tocris Bioscience and used at a concentration of 300nM (overnight exposure). Erlotinib and AG-1478 were obtained from Selleck Chemicals and used at a concentration of 10uM (overnight). EGF was purchased from Peprotech and used at a concentration of 50ng/ml.
Frozen tissue specimens of human GBMs were received from the Research tumor bank at UT Southwestern Medical Center according to IRB approved protocols. Resected tumors were initially frozen at −80°C.
Annexin assay was done by using Annexin −V-FLUOS Staining kit (Roche applied Science). Cells were cultured in DMEM (10% FBS and Pen/Strep). Cells (1×106) were plated in 6 well plates and treated with EGF for 24h or 72h if indicated. The cells were trypsinized and washed 2 times with 1X PBS. The cells were incubated for 25 minutes at Room temperature with Propidium Iodide and Annexin −V-FLUOS labeling solution in incubation buffer (supplied by the manufacturer). Annexin and or PI positive cells were detected by Flow Cytometry.
For intracerebral stereotactic inoculation, 2 × 105 cells were suspended in PBS and matrigel (5 μL) and injected into the right corpus striatum of the brains of 6-8 week old nude mice using a stereotactic frame (BALB/c nu/nu).Animals were monitored for neurological signs and sacrificed when neurological signs appeared or after 240 days. All animal studies were done under IACUC approved protocols.
Error bars represent the means ± standard deviations of three independent experiments. All data were analyzed for significance using GraphPad Prism 5.0 software, where P < 0.05 was considered statistically significant. One-way ANOVA and two-tail t-test were used to compare groups. Survival analysis for mice is described in the results.
Additional information about experimental procedures is provided in Supplemental methods.
EGFRvIII expression activates NF-κB by promoting ubiquitination of RIP1
RIP1 complexes with EGFRvIII, NEMO and TAK1 to activate NF-κB and promotes oncogenicity
EGFRwt activation abolishes the EGFRvIII-RIP1 signalosome and NF-κB activation
EGFRwt activation results in formation of a RIP1-FADD-Caspase-8 complex and cell death
We thank Dr. Mien-Chie Hung (MD Anderson Cancer Center) for the EGFRwt-Myc plasmid and Dr. James Van Brocklyn (Ohio State University) for GBM9-NS cells. This work was supported in part by NIH grants RO1 NS062080 to AH, by RO1 grants CA139217 and CA102792 to DAB, and RO1 CA149461 to SB and by grants from National Aeronautics and Space Administration (NNX13AI13G) and the Cancer Prevention and Research Institute of Texas (RP100644) to SB.
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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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Amana #22004475 Washer Tub Cover Assemblely W`Heater
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Engage, Educate, and Qualify Show Attendees
Quiz 'n Qualify™ is an interactive quiz activity that engages and educates show attendees on an exhibitor's offerings. For use with our SVCapture™ and No Badge, No Worries™ systems, Quiz 'n Qualify walks attendees through a brief quiz that asks questions that work to educate with subtly providing information as answers to the questions are revealed. Attendees get information without being "hit over the head" with it which makes the experience feel more organic and pleasant.
Call us today at (877) 474-6982, email, or fill out the quick form below to find out more about using Quiz 'n Qualify™ along with a SVCapture™ or No Badge, No Worries™ system for your next trade show or event.


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- Description
This stylish and functional backer's rack updates your dining room immediately, Traditional all metal style, Cradles for wine bottles, A rack for stemmed glasses, Three spacious glass shelves for storage or display
1 Baker Rack
Baker Rack : 39.8" x 18.6" x 75.1"
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Additional Information
SKU 20900564 MPN LILY-BR GTIN UPC 845046019636 Brand Chintaly Imports Collection No Assemble Length 42.3 Assemble Width 76.8 Assemble Height 4.5 Assembly Required Yes Material Other Finish Brown Styles Modern Shipping Time 1-2 Weeks Free Shipping Yes
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Disclaimer: Pictures displayed may include optional products not included in the price. Computer monitors often display color variations. Color swatches are shown if alternative colors are available. Please call us or email us if you have any questions!


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15 Baby Shower Girl Themes Planning a baby shower is such a fun experience. Everyone is anxiously … [Read more...]
15 Baby Shower Girl Themes
Twin Bunnies Baby Shower
Celebrating one bundle of joy is fun, but celebrating TWINS - now that's Double the Fun! This sweet … [Read more...]
Baby Girl Sparkles and Sprinkles Baby Shower
Everybody was over the moon with excitement for this Baby Girl Sparkles and Sprinkles Baby Shower … [Read more...]
Tutu Cute Baby Shower
The delight truly is in the details and this sweet Tutu Cute Baby Shower had an extraordinary amount … [Read more...]
10 Creative Baby Keepsake Ideas
As a mom, I know how quickly times passes and children grow. Before my son was born, I knew I wanted … [Read more...]
Modern Garden Baby Shower
Nothing welcomes a new baby more than a beautiful baby shower! This Modern Garden Baby Shower was a … [Read more...]
Dream Catcher Themed Baby Shower
This Dream Catcher Baby Shower was planned to welcome an adorable baby girl into a family that … [Read more...]
Floral Inspired Baby Shower
Spring is in the air! Throw a baby shower that is full of bright, vibrant colors, a nice and … [Read more...]
Girly Vintage Garden Baby Shower
This Girly Vintage Garden Baby Shower, planned by the mom-to-be herself, featured some of her … [Read more...]
Mary Had A Little Lamb Baby Shower
This Mary Had A Little Lamb Baby Shower was truly the sweetest celebration for mom-to-be Mary. … [Read more...]
Boho Themed Baby Shower
This earthy and natural Boho Themed Baby Shower was the perfect celebration for this mama-to-be, who … [Read more...]
15 Free Baby Shower Printables
Baby Showers are such a fun event! It's great to be able to get together with your friends and … [Read more...]
Chic Animal Inspired Baby Shower
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Little Lady Baby Shower
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Vintage Baby Girl Shower
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This episode's featured guest is Social Media Historian Allison Graham. Allison is a graduate of Southern Methodist University and has worked all over the country and globe bringing the written word to life on the big screen.
She has worked for Artisan Entertainment, Universal Studios, Paramount Pictures, Warner Brothers, New Line Cinema, 20th Century Fox, Miramax and Dreamworks SKG as Assistant Director, Production Manager, and Producer working with such titans as Jerry Bruckheimer, Michael Bay, Timur Bekmamvetov and Tim Burton. She was one of the key business strategists behind The Blair Witch Franchise marketing campaigns, leading the team responsible for revolutionizing the way the Internet and film marketing were viewed.
Allison also gave a landmark TED talk entitled, "How Social Media Makes Us Unsocial."
Learn more about author and host, Sarah Raymond Cunningham, at sarahcunningham.org.


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I'm a sophomore in college and I've never gotten a girlfriend through means of meeting in "real life" every girlfriend I've had i met online, and it usually turned out fairly well, but women i meet throughout my days are cold, shut off and basically saying "don't bother because I'm not interested" so how in the hell am I supposed to befriend one of these women then get her to go on a date with me if I have to completely hold up any conversation and inniate contact (which is usually ignored). I'm a really shy guy with depression and a anxiety disorder so I'm not the most confident person. And I don't want to be. Confidence IS NOT the most important factor here. So I'll ask you, where could I find someone (I don't have time for clubs so that's out)? What is the best way to approach?
Most Helpful Girl
online or singles group at church10|10|0
Singles group at church? That's a thing?
- Show AllShow Less
maybe even try an anxiety or depression support group, I'm not even kidding I've been to many of those. though they might have a policy against dating until it's over but it could be worth a try Lool
I don't think there are any of those support groups around here.
Most Helpful Guy
You go to college. There are girls in your classes. You talk to them. If you think it's difficult being a college student when you get out it's even more difficult. You meet girls in your classes and you talk to them. And you talk to them about the school work and that starts the conversation.
And if you really have depression and anxiety you need a therapist and someone who can prescribe medication for you. You don't accept your diagnosis and do nothing about it. If you shoot back at me saying you see a therapist and that discounts everything I said, sorry that's why you stay where you are. You are not really looking for a place you are looking for a place in your mind11|00|0
Actually I'm already on medication so that's not a problem. But with the classes, I haven't really had any luck speaking to women there. They just act very uninterested and have no desire to have a conversation. This may make me sound shallow, but I only talk to specific women in my class that look like someone i am attracted to, and that has been very few and far between since so many of the women at my college are not physically fit and honestly very over weight.
Congratulations – you have effectively discounted everything that I said. You have what I call, "the yes but..." syndrome. I'm old so I can only use the Beatles as an example. Do you know why they were fabulous? They went to Hamburg Germany and played together for 10,000 hours. Practice practice. One of the greatest baseball pictures ever was Sandy Koufax. He was terrible when he first entered the majors – practice practice. I don't care if you have to speak with one eye green Martians for the next year – practice practice. By discounting all women at your college except the ones that look like hot stuff you are limiting your practice practice. You get my drift? You are looking for reasons not to practice.


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|Page (1) of 1 - 03/28/12
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Lawyers say Utah activist punished in prisonLawyers say prison punishing Utah environmental activist convicted of thwarting oil auction
Page: 1
Related Keywords:National Parks-Drilling, Environmental activism, Environment and nature, Outdoor recreation, Recreation and leisure, Lifestyle, Leisure travel, Travel, Environment, National parks
Source:Copyright 2012 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.. All Rights Reserved


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Coffee is one of the most preferable beverages for peoples of all ages and they use to consume coffee to refresh the moods and mind. The coffee is basically the brewed drink which is prepared from the roasted beans or coffee beans and these are mainly the seeds of coffea and berries plant. Coffees are presented and prepared in many varieties such as cappuccino, espresso, café latte and others and served as iced as well as hot coffee.
The one of the most important technique to get coffee on beverage form is coffee brewing which is also termed as coffee making method and it is very important to turn the raw beans into the powdered coffee. The brewing technique basically follows the 4 common and important method which is :
- The roasting of the raw coffee beans.
- Then the roasted beans should be grounded
- After sometime, the grounded coffee beans amalgamated with hot water for some time and this method mainly called as brewing method or coffee brewing
- Then the liquid form of coffee is going to be separated with the grounded one
The above steps are 4 basic things which should be followed while coffee making methods but there are plenty of ways to make coffee and you can also try some other brewing method which is different from the traditional brewing method of coffee. Let we discuss some of them:
- Boiling method: It is one of the most simple and economical method of coffee brewing which is not actually brewing but coffee boiling method. Due to its easiness, anybody can do this method. In this method, the coffee grounds are placed inside any cup or vessel and then boiling water is to be poured over them. After sometime on the bottom of the vessel, grounds start sinking and this is the indication that the coffee is now ready to drink. This is the method by using which tea is also brewed and had been performed by most of the peoples
- Cowboy coffee: Because of this coffee came from the campfire, it is called cowboy coffee and it is prepared by mixing few coffee grounds with hot water. It is also one of the most simple and common method which required no equipments and gives clear cup production of coffee.
Apart from these, there are certain other brewing methods and one of the most prominent among them is Pressure brewing methods which also have number of techniques such as:
- Vacuum Coffee Brewing: This technique need the device called vacuum brewer for brewing coffee and it is spectacular device also called Vac pot or vacuum pot. This device consists of two bowls one upper and one on lower and on the upper bowl, coffee grounds had been placed and on lower on, water is to be placed. Then the pot is set on the burner and after sometime, the coffee had been brewed.
There are certain other methods are also there such as steeping method, gravity brewing method and others.


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Luxembourg casinos and gambling guide
Casinos and Gambling Facts
Luxembourg is a country in Western Europe with legal gambling.
There are 1 cities with gambling facilities in Luxembourg which have 1 legal gambling facilities available in total.
The types of gambling available in Luxembourg are: casinos.
The largest gambling city in Luxembourg is Mondorf-les-Bains with 1 gambling facilities, 6 tables games, 280 gaming, slot, and video poker machines.
The largest casino in the entire country of Luxembourg is Casino 2000 Luxemburg which is located in Mondorf-les-Bains. Casino 2000 Luxemburg has 6 table games, 280 gaming and video poker machines.
Luxembourg Casino List
- Casino
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Luxembourg Casino Statistics
Table games: 6
Slot machines: 280
Coming Soon
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How Jennifer Hann Shed 100 Pounds In 12 Months Eating Wild
Jennifer shed over a 100 pounds by cooking up gorgeous Wild recipes, practicing intermittent fasting, and cutting processed food out of her diet. Here's her story.Learn More
Full Podcast Page | All PodcastsSubscribe on iTunes
Jennifer shed over a 100 pounds by cooking up gorgeous Wild recipes, practicing intermittent fasting, and cutting processed food out of her diet. Here's her story.Learn More
The Wild Diet is now officially a New York Times Bestseller! Thank you so much for the support, reviews, and spreading the word about real food.Learn More
When you join the Fat-Burning Tribe and get in on The Wild Diet 30-Day Challenge, you'll not only get access to my video library, quick-start guide, step-by-step 30-day meal plan, shopping lists, and community support, you'll also get to ask my wife Alyson and me your most pressing questions.Learn More
Learn how readers lost 42+ pounds, reduced inflammation, and reclaimed their health with The Wild Diet.Learn More
On this week's show with Dr. Andrew Saul, The MegaVitamin Man, you'll learn how to take your health into your own hands with inexpensive, readily available, and easy-to-use vitamins.Learn More
This week we're here with my friend Dr. Tom O'Bryan, and among other things, you're going to learn about hidden sources of gluten in your diet, autoimmune disease, and how to properly order at a restaurant without sacrificing your health.Learn More
Today's success story is from a now svelte sales manager from Manchester, England, Jason Delvard. Those of you who have followed the traditional "healthy" low-fat, grain-filled diet and experienced fat gain, inflammation, and health problems, this one is for you. When Jason followed the conventional-wisdom-fueled weight loss advice of magazines, media, and even his […]Learn More
I love getting your e-mails. I especially love e-mails like this one from Nicole. Quite honestly, this one in particular left a lump in my throat and a smile on my face. Nicole listened to my "Wheat Belly" podcast, downloaded the book, and decided to take her lovely family (pictured above) gluten, wheat, and grain-free. Then […]Learn More


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A vain venue for solipsistic sophists, verbal voyeurs, lubricious logorrheics, and serial-comma lovers.
Tuesday, October 04, 2016
dream lover
At the stoplight, he glanced into the rearview mirror. It framed a vision. She was looking down, obviously at her phone, at a text or a message, who knows perhaps a YouTube video. She was young, with dark hair, dark eyes, dark eyebrows, long, dark hair. Time stopped before the light changed. What a dream, he thought, relieved the light was turning green, relieved she never locked eyes, as can happen in those mirrored exchanges. "Merrily, merrily, merrily, life is but a dream" floated into his head as he put his left foot on the clutch, pressed the gas, and turned left.
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I am looking for a return of 5-10k monthly. I live in Ecuador southamerica
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You can buy the stock of our website ( b-c-e.us ) and get 10% profits of your money monthly. Make contact with me by Skype : auref_handsome
I represent lots of businesses looking for silent equity partners. What type of Investment were you looking to make and do you prefer an industry? I have 2 great businesses looking for around 100k and offering very nice returns. I also have companies in the oil and gas industry, as well as the LEGAL marijuana industry. All of these business have been prescreened for legitimacy, bank records, and taxes. Let's talk soon. Would love to help you grow your investment, and help a small business.
Hello Julian. I currently own a mortgage field inspection company where we work with banks to inspect properties that are in the process of foreclosure or are already foreclosed and vacant, we also work on fixing up and maintaining these vacant properties to keep them up to code and in marketable condition . This is a volume based industry, the more work orders we can do per month the more we can make. As a company we already perform close to 5,000 inspections per month. The opportunity to make $5K-10K+ per month is already available as this is a pretty big industry with hundreds of thousands of potential work orders we can potentially perform . It does take our clients up to 60 days to pay us for work performed and we pay our contractors bi-weekly. I am looking for an investment to take on much more work volume and bridge the payroll gap. Since we already have existing contracts with some major clients, it's very easy to expand our work load. If interested in getting more details please contact me at firstname.lastname@example.com
Hello,I´m selling my private Forex trading strategy. Strategy offers 3.5% - 10.00% annual profit. If you would be interested in more information, you can to contact me on email email@example.com you
Hi Julian. email me for details vladamirlenski999 at gmail. com
Hi Julian, My partner and I have set the ground work to start a freight company. We already have a contract set up that will give us approximately $3500 a week, but we need the truck to get going. We have other options for revenue once we get going and we have our federal requirements in place. My partner has been in the trucking business for over 10yrs and I have been in project management for over 16yrs. Please feel free to contact me at taylorfreightsolutions at gmail. Thank you