Thursday, July 26, 2012

How Do I Sell My Retail Business? | Financial Solutions for Business ...

Business not growing well ? need to sell your retail store? there?s a series of steps you?ve got to follow to induce a good deal for your business. What you wish to try to to post sale of your business depends largely on how you perform pre selling method, since that?s not terribly straightforward.

Firstly, you?ve got to see the worth of your retail store. For that you simply ought to access the web to grasp the present market position of your product and services and compare them to alternative businesses. Pricing your product and services ought to be done terribly rigorously. Over and under-pricing, each keep potential consumers faraway from you. Pricing ought to be based mostly on an entire market analysis of the worth of your product. List of assets ought to be ready to judge the value of all tangible and intangible assets. A business profile has to be ready to produce data to the client regarding the retail store for sale. It should embrace details regarding the business operations, product and services, client base and past tax records. It offers the client a private bit and enhances his religion within the seller.

Financial statements ought to be presented before the client as a result of anybody would confirm to establish the profitability of the business he needs to get. Thus, Profit & Loss Account and Balance Sheet ought to be ready. you?ll be able to even take facilitate of an accountant to arrange the ultimate books your store. Not simply this, buyer or his representative might also raise for the past record of the business. So, it?s advisable to incorporate Profit and Loss account of the last 3-5 years within the Business Profile itself. It helps the client to grasp the number needed to hold out routine business operations and its maintenance.

Business Appraisal to gift a good and competitive price of the retail business for sale before the client should be done with the assistance of an accountant/broker. they?re knowledgeable in their fields and have an expertise of handling varied sellers and consumers and therefore would be able to analyze the true market position of your business and obtain you the most effective deal. All preparations would go waste while not putting up an advert regarding the sale of your business. it?s vital to well reveal sure details of your business to draw in potential consumers.

Cleaning the retail store properly before sale is imperative. Necessary replacements additionally ought to be created relating to furniture, fittings or electronics. After all preparations the ultimate paperwork has to be done. It should be tired steerage of a lawyer/broker therefore on avoid any mistake or unfair deal. If the vendor does not need to disclose abundant data to the client he ought to raise for a Non Disclosure Agreement to form positive his confidential details are safe. Deadlines should be set and met for final signatures of each the parties.

Source: http://www.voteyesc.com/2012/07/how-do-i-sell-my-retail-business/

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Wednesday, July 25, 2012

New understanding of diabetes and kidney disease: Findings may lead to effective new treatments

ScienceDaily (July 23, 2012) ? Scientists at Joslin Diabetes Center have identified biological mechanisms by which glucagon-like peptide-1 (GLP-1), a gut hormone, protects against kidney disease, and also mechanisms that inhibit its actions in diabetes. The findings, which are reported today online by Diabetes, may lead to the development of new therapeutic agents that harness the actions of GLP-1 to prevent the harmful effects of hyperglycemia on renal endothelial cells.

Renal complications, also known as diabetic nephropathy, are one of the most life-threatening complications of diabetes that often lead over time to end-stage renal disease (ESRD). About a half million people in the US -- 44 percent of whom are diabetics -- have ESRD, which requires dialysis or kidney transplantation. As a result, investigating the relationship of diabetes to renal dysfunction is a major focus of diabetes research. "We are very eager to develop new treatments for diabetic kidney disease," says George King, M.D., lead author of the study, and chief scientific officer, head of the Dianne Nunnally Hoppes Laboratory for Diabetes Complications and a professor of medicine at Harvard Medical School.

GLP-1 is an incretin hormone that is produced by the intestine in response to food. GLP-1 increases the secretion of insulin from the pancreas, slows absorption of glucose from the gut, and reduces the action of glucagon -- all of which lower glucose levels in the blood. In addition, GLP-1 reduces appetite. The drug, exendin-4 (marketed as Exenatide), which mimics the effects of GLP-1, is used to lower blood glucose in type 2 diabetes.

Recent studies have reported that GLP-1 improves the function of renal endothelial cells (which regulate blood clotting, immune response and blood vessel activity, among other critical functions, and are impaired by insulin resistance) and can prevent some renal pathologies in diabetic rodents. GLP-1 receptors (GLP-1R), which are abundant in the intestine, are also found in the endothelium and kidney.

The Joslin study investigated the effects of GLP-1 in non-diabetic and diabetic mice with an "overexpression" of the enzyme PKC? (protein kinase C-beta) which is produced in excess when blood glucose is high. Excess PKC? can lead to diabetes complications, including kidney disease. PKC? enhances the action of angiotensin II (Ang II), a peptide hormone that affects renal filtration and blood flow and also regulates blood pressure, which increases inflammation and accelerates the progression of kidney damage.

The study looked at the interactions of GLP-1, PKC-beta and ANG II that affect GLP-1's protective action in renal endothelial cells. "We've been interested in diabetic kidney disease for a long time, particularly the role of PKC? and Ang II in promoting kidney damage," says Dr. King. "We were interested in investigating how GLP-1 could protect against the effects of hyperglycemia on renal function."

Josin researchers made two major findings: They identified the mechanisms by which GLP-1 can induce protective actions on the glomerular (renal) endothelial cells by inhibiting the signaling pathway of Ang II and its pro-inflammatory effect; and demonstrated a dual signaling mechanism by which hyperglycemia, via PKC? activation, can increase Ang II action and inhibit GLP-1's protective effects by reducing the expression of GLP-1 receptors in the glomerular endothelial cells. "We know that people with diabetes are more sensitive to Ang II; our data suggests one reason why," says Dr. King.

The results suggest that effective therapeutic agents could be developed to enhance the effects of GLP-1R on the endothelium which may prevent glomerular endothelial dysfunction and slow the progression of diabetic nephropathy. "We now know that increased PKC? decreases GLP-1R which makes the kidney less responsive to treatment with GLP-1-based drugs. Possible new treatments could combine PKC? inhibitors with higher doses of GLP-1 agonists. GLP-1 is one potential pharmaceutical that could both lower glucose and minimize the toxic effects of Ang II to lower the risk of kidney diseases," says Dr. King.

The study was funded by the National Eye Institute (NEI), a component of the National Institutes of Health.

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The above story is reprinted from materials provided by Joslin Diabetes Center, via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Akira Mima, Junko Hiraoka-Yamomoto, Qian Li, Munehiro Kitada, Chenzhong Li, Pedro Geraldes, Motonobu Matsumoto, Koji Mizutani, Kyoungmin Park, Christopher Cahill, Shin-Ichi Nishikawa, Christian Rask-Madsen, and George L. King. Protective Effects of GLP-1 on Glomerular Endothelium and Its Inhibition by PKC? Activation in Diabetes. Diabetes, July 23, 2012 DOI: 10.2337/db11-1824

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/~3/xEyYP0JA5Hk/120723105045.htm

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DVD REVIEW AND GIVEAWAY - The Wiggles Big Birthday - Mom ...

The Wiggles Big Birthday DVD

The Wiggles: Big Birthday

  • DVD Release Date: July 17, 2012
  • Run Time: 140 minutes
  • Rated: G (General Audience)
  • Number of discs: 1
  • Language: English
  • Studio: NCircle Entertainment
  • ASIN: B007J3ISK0
  • SRP $12.99

ABOUT THE WIGGLES BIG BIRTHDAY

The Wiggles Big Birthday! DVD invites children aged two-to-six to sing, dance and wiggle along with Murray, Jeff, Anthony, Sam and their friends Captain Feathersword, Wags the Dog, Henry the Octopus, and Dorothy the Dinosaur as they celebrate their Big Birthday. Filled with music, including many classic Wiggles songs performed live, the DVD also offers some terrific birthday surprises and tummy-tickling jokes for even more wiggly, giggly fun!

Special Features include:

  • Everybody Clap! Everybody Sing! A documentary covering The Wiggles first 20 years
  • Birthday wishes from Terri, Bindi and Robert Irwin
  • Photo Gallery

MY THOUGHTS

I received a copy of The Wiggles Big Birthday DVD. I watched this DVD with my youngest son, who loves The Wiggles. The DVD is a great mixture of regular footage and concert footage. He got so excited when he heard some of his favorite ?oldies? like Quack Quack, Fruit Salad and Big Red Car, amongst others. Dancing and singing was involved! He had a blast watching and I had a blast watching him along with the DVD. This DVD is a must have for any Wiggles fan.

The Wiggles Big Birthday can be found at a retailer near you such as Walmart, Target, and Toys R Us, as well as online.

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1 ? Visit my Mom?s blog HereAndThere.US and leave a comment on any post there. Then return here and leave a comment on this post telling me one thing you read or learned on my Mom?s blog. (That?s two comments you need to leave for this bonus entry, one there and one here.) Unlimited entries for this method of entry. Leave an additional comment for each entry you qualify for. You must have completed the first entry according to the instructions to be eligible for any bonus entries.

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The winner will be selected using the ?And the winner is? plugin. US addresses only please, no PO Boxes. This contest will end on Monday 07/30/12 at 11:59 pm est. If you?ve entered any of my giveaways before then you know that only comments containing all of the requested information will be eligible for entry. Good luck to everyone!

The product featured was provided free of cost to me for the sole purpose of product testing and review. This post has not been monetarily compensated and is based on the views and opinions of my family and/or self. Please note that the opinions reflected in this post have not been influenced by the sponsor in any way.

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Tags: DVD, DVD Reviews, The Wiggles, The Wiggles Big Birthday

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Source: http://www.valmg.com/index.php/2012/dvd-review-and-giveaway-the-wiggles-big-birthday/

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Officials to discuss rule for using long putters

LYTHAM ST. ANNES, England (AP) ? One day after Ernie Els won the British Open to become the third major champion using a belly putter, the Royal & Ancient said long putters were "firmly back on the radar" and that a decision could come soon on whether players can keep using them.

R&A chief executive Peter Dawson said discussions with the U.S. Golf Association about longer putters anchored to the body began before Els holed a 15-foot birdie putt on the 18th hole to win the claret jug at age 42.

Keegan Bradley at the PGA Championship and Webb Simpson at the U.S. Open both used belly putters. Adam Scott, who had a four-shot lead with four holes to play in the British Open, was using a long putter that he says helped turn around his game.

"We appreciate that there is much speculation about this and that we need to clarify the position as soon as possible," Dawson said Monday. "And I think you're going to see us saying something about it one way or the other in a few months, rather than years."

But he made clear that the R&A and USGA, which set the rules for golf around the world, have not decided whether to ban them.

"This decision has not been taken," he said. "Please don't think that it has."

Tiger Woods was among those this year who recommended that the putter simply be the shortest club in the bag. Els once criticized the long putters, but when he struggled mightily with his putting, he switched to a belly putter late last year.

"As long as it's legal, I'll keep cheating like the rest of them," Els said in October.

Dawson said the discussion with the governing bodies has switched from an equipment issue to a rules issue.

"The initial determination has been that we are examining the subject from a method of stroke standpoint rather than length of putter standpoint, and that takes it into the area of the rules of play, the rules of golf, rather than the rules of equipment," he said.

The rules committees of the R&A and USGA are conducting the study, and each will make a recommendation.

Because it is being treated as a potential rule change, it would not become effective until 2016. The Rules of Golf are updated every four years.

Jim MacArthur, chairman of the championship committee for the R&A, said there were 27 long putters and 16 belly putters in the 156-man field at the Open. Dawson said the number of golfers using the long putter has dramatically increased from about 5 percent five years ago, although he did not notice an increase at the recent British Amateur.

"It hasn't yet backed its way all the way down the game, although the statistics would show ? and I've checked this with the manufacturers ? that at the club level or recreational level, they are much more used in the United States than they are anywhere else in the world," Dawson said.

Simpson and Bradley both were regarded as good putters before switching to the belly. Padraig Harrington, who always has used a conventional putter, said more players might be tempted to switch if it's clear their competitors have an advantage.

Phil Mickelson experimented with the belly putter last year in the FedEx Cup playoffs.

"Obviously, if the standard of putting goes up, which it clearly does ... guys wouldn't be using them if they didn't putt better with them, yeah?" he said. "If the standard of putting goes up, it puts more pressure on the guys that aren't using one just to compete. So all of a sudden, it's hard for a normal putter. Is he doing the right thing? Should he be using the long putter?

"So it actually has a negative effect on others as much as a positive effect on some."

Scott made the biggest turnaround. He felt such despair over his putting that he switched at the Match Play Championship in February 2011. His good friend, Geoff Ogilvy, said that his fellow Australian still was capable of making putts and winning even with a short putter.,

"It just makes his bad days better," Ogilvy said. "It doesn't make his good days better."

The objection Dawson has heard the most is that if players can't putt with a conventional club, why should they have a crutch to compete with those who can.

"That's the general argument one hears," Dawson said. "But we're also seeing now people who can putt perfectly well in the conventional way thinking that an anchored stroke gives them an advantage. I think that's the fundamental change that we've witnessed in the last couple of years."

Source: http://news.yahoo.com/officials-discuss-rule-using-long-putters-104003632--golf.html

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Monday, July 16, 2012

A Brief History of Air Conditioning

1758 All liquid evaporation has a cooling effect. Benjamin "I invented everything" Franklin and Cambridge University professor John Hadley discover that evaporation of alcohol and other volatile liquids, which evaporate faster than water, can cool down an object enough to freeze water.

1820 Inventor Michael Faraday makes the same discovery in England when he compresses and liquifies ammonia.

1830s At the Florida hospital where he works, Dr. John Gorrie builds an ice-making machine that uses compression to make buckets of ice and then blows air over them. He patents the idea in 1851, imagining his invention cooling buildings all over the world. But without any financial backing, his dream melts away.

1881 After an assassin shoots President James Garfield on July 2, naval engineers build a boxy makeshift cooling unit to keep him cool and comfortable. The device is filled with water-soaked cloth and a fan blows hot air overhead and keeps cool air closer to the ground. The good news: This device can lower room temperature by up to 20 F. The bad news: It uses a half-million pounds of ice in two months? and President Garfield still dies.

1902 Willis Carrier invents the Apparatus for Treating Air for the Sackett-Wilhelms Lithographing and Publishing Co. in Brooklyn, N.Y. The machine blows air over cold coils to control room temperature and humidity, keeping paper from wrinkling and ink aligned. Finding that other factories want to get in on the cooling action, Carrier establishes the Carrier Air Conditioning Company of America.

1906 Stuart Cramer, a textile mill engineer in North Carolina, creates a ventilating device that adds water vapor to the air of textile plants. The humidity makes yarn easier to spin and less likely to break. He's the first to call this process "air conditioning."

1914 Air conditioning comes home for the first time. The unit in the Minneapolis mansion of Charles Gates is approximately 7 feet high, 6 feet wide, 20 feet long and possibly never used because no one ever lived in the house.

1931 H.H. Schultz and J.Q. Sherman invent an individual room air conditioner that sits on a window ledge?a design that's been ubiquitous in apartment buildings ever since. The units are available for purchase a year later and are only enjoyed by the people least likely to work up a sweat?the wealthy. (The large cooling systems cost between $10,000 and $50,000. That's equivalent to $120,000 to $600,000 today.)

1939 Packard invents the coolest ride in town: the first air-conditioned car. Dashboard controls for the a/c, however, come later. Should the Packard's passengers get chilly, the driver must stop the engine, pop open the hood, and disconnect a compressor belt.

1942 The United States builds its first "summer peaking" power plant made to handle the growing electrical load of air conditioning.

1947 British scholar S.F. Markham writes, "The greatest contribution to civilization in this century may well be air-conditioning?and America leads the way." Yet somehow people still say a brilliant new idea is "the best thing since sliced bread."

1950s In the post-World War II economic boom, residential air conditioning becomes just another way to keep up with the Joneses. More than 1 million units are sold in 1953 alone.

1970s Window units lose cool points as central air comes along. The units consist of a condenser, coils, and a fan. Air gets drawn, passed over coils, and blasted through a home's ventilation system. R-12, commonly known as Freon-12, is used as the refrigerant.

1994 Freon is linked to ozone depletion and banned in several countries. Auto manufacturers are required to switch to the less harmful refrigerant R134a by 1996. Brands like Honeywell and Carrier develop coolants that are more environmentally friendly.

2003 In "Hey Ya," Andre 3000 raps, "What's cooler than being cool? Ice cold!" They aren't talking about air conditioning.

Source: http://www.popularmechanics.com/home/improvement/electrical-plumbing/a-brief-history-of-air-conditioning-10720229?src=rss

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Wednesday, July 4, 2012

AP Source: Hawks agree to deal Joe Johnson to Nets

FILE - In this April 4, 2012, file photo, Atlanta Hawks' Joe Johnson, right, drives against Charlotte Bobcats' Gerald Henderson,in an NBA basketball game in Atlanta. Multiple media outlets, starting with ESPN and all citing anonymous sources, are reporting the Hawks and New Jersey Nets have agreed to a trade that would send Johnson from Atlanta to Brooklyn, Monday, July 2. (AP Photo/David Goldman, File)

FILE - In this April 4, 2012, file photo, Atlanta Hawks' Joe Johnson, right, drives against Charlotte Bobcats' Gerald Henderson,in an NBA basketball game in Atlanta. Multiple media outlets, starting with ESPN and all citing anonymous sources, are reporting the Hawks and New Jersey Nets have agreed to a trade that would send Johnson from Atlanta to Brooklyn, Monday, July 2. (AP Photo/David Goldman, File)

The Hawks have agreed to deal All-Star guard Joe Johnson to the Brooklyn Nets for five players and a draft pick, and Atlanta will send forward Marvin Williams to the Utah Jazz for guard Devin Harris.

A person familiar with the Hawks-Nets deal told The Associated Press on Monday night that Atlanta will receive guards Anthony Morrow, Jordan Farmar and DeShawn Stevenson and forwards Jordan Williams and Johan Petro, along with a draft pick Brooklyn received from Houston in a prior deal. The selection only belongs to the Nets if it is not a lottery pick.

The person confirmed the trade on condition of anonymity because it cannot become official until Stevenson signs as a free agent with Brooklyn. Free agents cannot be signed until July 11.

Johnson has four years and $90 million left on his contract and new general manager Danny Ferry decided it was time to shed payroll and rebuild.

The 31-year-old Johnson averaged 18.8 points per game last season, his 11th in the NBA and seventh with Atlanta.

The Nets are hoping to team Johnson with free agent point guard Deron Williams, whom they are working to re-sign, in the franchise's first season in New York City after decades in New Jersey.

Utah CEO Greg Miller acknowledged the deal for former first-round pick Marvin Williams while picking up guard Mo Williams at Salt Lake City International Airport in preparation for Tuesday's introductory news conference.

The Jazz acquired Mo Williams in a multi-team deal last week that also sent Lamar Odom to the Clippers.

Miller said it was difficult to part with Harris but he was excited by what Mo Williams brings to the team.

Mo Williams said it felt good to be back where he started his career in 2003 and he had always hoped to start for his first team.

The Harris-Marvin Williams deal now clears the way for that to happen.

"It's always unfortunate when we have to let a player go because all of our players work so hard and they're so invested in helping us win." Miller said. "And it's got to be a tough thing for them. I know it is for us. I wish Devin the best in his career."

Mo Williams, dressed in a red T-shirt, black shorts and a New Orleans Saints cap, arrived in Salt Lake City about 8:30 p.m. MDT.

He only has one year left on his current deal but expressed hope that he could be in Utah long term.

"I'm very excited about a new start for me and a second homecoming," Williams said Monday night.

Jazz general manager Kevin O'Connor has called letting Mo Williams leave after just one season "the worst: mistake of his career.

"I know he says that a lot, but at the same time I was a young basketball player at the time," Mo Williams said. "Obviously he made a decision he thought was best for the organization. I never had a bad taste in my mouth about the organization. I always respected them because they gave me a shot.

"I watched 30 teams pass me in the first round. I always had a part of my heart for the Jazz and I'm glad I'm able to come back and prove my worth to them."

Harris arrived in Utah in 2011 as part of a blockbuster deal that sent Deron Williams to New Jersey.

But Harris struggled to find his niche with the Jazz, and while he stepped up his game late last season, he still has a career 31.5 percent shooting percentage from beyond the arc.

Harris, 29, is scheduled to make $8.5 million in 2012-13, the final year of his current contract.

Marvin Williams, 29, has averaged 11.5 points for Atlanta in his seven-year career, including 10.2 and 5.2 rebounds last season.

Mo Williams was an All-Star as recently as 2009, and was part of a Cleveland team that won 66 games with LeBron James and advanced to the Eastern Conference Finals in 2009. He joined the Los Angeles Clippers in 2011.

"I think it's going to be great for us to have Mo here," Miller said. "Obviously he competed at the highest level. He knows what it takes to win. . I think he's going to help us win games."

Asked if there were more moves to come for the small-market Jazz, Miller said, "I hope so."

___

DeBruin reported from Salt Lake City.

Associated Press

Source: http://hosted2.ap.org/APDEFAULT/347875155d53465d95cec892aeb06419/Article_2012-07-03-BKN-Hawks-Nets-Trade/id-8b22dce1656b482498032052e492f000

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Year 2200

Year 2200

The world no longer is owned by humans, but by a force powerful enough to destroy everything.

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Tuesday, July 3, 2012

Obama T-Shirt Showdown Escalates From 'BFD' to 'BFTax'

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[ [ [['did not go as far his colleague', 8]], '29438204', '0' ], [ [[' the 28-year-old neighborhood watchman who shot and killed', 4]], '28924649', '0' ], [ [['because I know God protects me', 14], ['Brian Snow was at a nearby credit union', 5]], '28811216', '0' ], [ [['The state news agency RIA-Novosti quoted Rosaviatsiya', 6]], '28805461', '0' ], [ [['measure all but certain to fail in the face of bipartisan', 4]], '28771014', '0' ], [ [['matter what you do in this case', 5]], '28759848', '0' ], [ [['presume laws are constitutional', 7]], '28747556', '0' ], [ [['has destroyed 15 to 25 houses', 7]], '28744868', '0' ], [ [['short answer is yes', 7]], '28746030', '0' ], [ [['opportunity to tell the real story', 7]], '28731764', '0' ], [ [['entirely respectable way to put off the searing constitutional controversy', 7]], '28723797', '0' ], [ [['point of my campaign is that big ideas matter', 9]], '28712293', '0' ], [ [['As the standoff dragged into a second day', 7]], '28687424', '0' ], [ [['French police stepped up the search', 17]], '28667224', '0' ], [ [['Seeking to elevate his candidacy back to a general', 8]], '28660934', '0' ], [ [['The tragic story of Trayvon Martin', 4]], '28647343', '0' ], [ [['Karzai will get a chance soon to express', 8]], '28630306', '0' ], [ [['powerful storms stretching', 8]], '28493546', '0' ], [ [['basic norm that death is private', 6]], '28413590', '0' ], [ [['songwriter also saw a surge in sales for her debut album', 6]], '28413590', '1', 'Watch music videos from Whitney Houston ', 'on Yahoo! Music', 'http://music.yahoo.com' ], [ [['keyword', 99999999999999999999999]], 'videoID', '1', 'overwrite-pre-description', 'overwrite-link-string', 'overwrite-link-url' ] ]

Source: http://news.yahoo.com/obama-t-shirt-showdown-escalates-bfd-bftax-153549559--abc-news-politics.html

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Lobster glut drives price per pound lower than bologna

This year soft-shell?lobsters?began showing up in abundance in fishermen's traps weeks earlier than normal.

By Clarke Canfield,?Associated Press / July 2, 2012

In this photo made June 28, Paula Coppersmith holds a lobster at Dock's Seafood restaurant and market in South Portland, where they're selling five lobsters for $24.

Robert F. Bukaty/AP

Enlarge

A glut has driven down?lobster?prices in Maine ? bringing cheer to lobster-loving consumers at the start of the state's tourist season but gloom among lobstermen.

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Retailers have been selling small soft-shell?lobsters?in the Portland area for an unusually low $3.79 to $4.99 a pound. At those prices,?lobsters?have been selling for less than the per-pound price of bologna at many supermarket deli counters.

Zain Nemazie, of Austin, Texas, was expecting low?lobster?prices ? but not this low ? while on vacation in Maine with his family.

"This is as good as it gets," Nemazie said late last week after paying $4.59 a pound for large 1 1/2-poundlobsters?at a seafood shop on Portland's waterfront. "We're from Texas, where we'd be paying at least $12 a pound."

At Docks Seafood in South Portland, owner Bob Coppersmith said customers were eating up the low prices, including a deal where he was selling five small live?lobsters?for $25. He later dropped it to five for $24.

"One gentleman came in and said, 'So I get five?lobsters?for $25. What's the catch?'" Coppersmith said. "I said there's no catch. He said, 'You're going to put five?lobsters?in a bag and not weigh them and give me them to me for 25 bucks?' He just couldn't believe it."

The Fourth of July represents the unofficial start to Maine's tourist season, when out-of-state visitors begin arriving in earnest.

Typically, Independence Day also is when Maine's?lobster?catch begins picking up as?lobsters?begin shedding their hard shells in favor of new soft shells. Soft-shell?lobsters?have less meat than hard-shell ones, but they are easier to crack open ? it can be done by hand, no claw cracker needed ? and sell for a lower price.

This year, though, soft-shell?lobsters?began showing up in abundance in fishermen's traps weeks earlier than normal.

Most of those?lobsters?usually go to Canadian processors. But the processors haven't been able to handle the Maine catch because Canadian lobstermen had such strong catches during their spring season, resulting in a backlog, said Neal Workman, head of The Fisheries Exchange, a Biddeford company that tracks prices, catches and other market information for the?lobster?industry.

Supply right now far exceeds demand, resulting in a "perfect storm" for the industry, he said.

"Things are plugged up," Workman said.

Virtually all soft-shell?lobsters?are sold to processors or on the local market, because they're too fragile to ship long distances. The?lobsters?sold at retailers outside of New England are most often hard-shell?lobsters, which command a premium price and are hardy enough to be shipped long distances.

For now, the excess supply in Maine has driven retail prices to under $4 a pound for the smallest of the soft-shell?lobsters. Larger?lobsters, and those that still have hard shells, are more expensive.

While consumers may be smiling, lobstermen are smarting because of the low prices ? between $2.50 and $3 a pound ? they're getting for their catches.

The fishing season is young and lobstermen are hopeful prices soon will rebound to their normal levels, said Patrice McCarron, executive director of the Maine Lobstermen's Association.

"The Fourth of July is a big boom in demand for us," she said. "We're going to see some?lobsters?move through the system, so there's hope that we'll see a balancing in the market once we get through the holiday demand and get back on track for a typical season.

"But there's definitely a lot of angst among harvesters."

With Independence Day around the corner, Pete McAleney of New Meadows?Lobster, a?lobster?dealer in Portland, was using the low prices as a marketing opportunity.

"To heck with hot dogs and hamburgers, eat a?lobster," McAleney said. "They're very affordable."

Source: http://rss.csmonitor.com/~r/feeds/csm/~3/SAsHX9rIkOs/Lobster-glut-drives-price-per-pound-lower-than-bologna

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Monday, July 2, 2012

Researchers block pathway to cancer cell replication

Researchers block pathway to cancer cell replication [ Back to EurekAlert! ] Public release date: 2-Jul-2012
[ | E-mail | Share Share ]

Contact: Debra Kain
ddkain@ucsd.edu
619-543-6163
University of California - San Diego

NOTCH1 signaling promotes T-cell acute lymphoblastic leukemia-initiating cell regeneration

Research suggests that patients with leukemia sometimes relapse because standard chemotherapy fails to kill the self-renewing leukemia initiating cells, often referred to as cancer stem cells. In such cancers, the cells lie dormant for a time, only to later begin cloning, resulting in a return and metastasis of the disease.

One such type of cancer is called pediatric T cell acute lymphoblastic leukemia, or T-ALL, often found in children, who have few treatment options beyond chemotherapy.

A team of researchers led by Catriona H. M. Jamieson, MD, PhD, associate professor of medicine at the University of California, San Diego School of Medicine and Director of Stem Cell Research at UC San Diego Moores Cancer Center studied these cells in mouse models that had been transplanted with human leukemia cells. They discovered that the leukemia initiating cells which clone, or replicate, themselves most robustly activate the NOTCH1 pathway, usually in the context of a mutation.

Earlier studies showed that as many as half of patients with T-ALL have mutations in the NOTCH1 pathway an evolutionarily conserved developmental pathway used during differentiation of many cell and tissue types. The new study shows that when NOTCH1 activation was inhibited in animal models using a monoclonal antibody, the leukemia initiating cells did not survive. In addition, the antibody treatment significantly reduced a subset of these cancer stem cells (identified by the presence of specific markers, CD2 and CD7, on the cell surface.)

"We were able to substantially reduce the potential of these cancer stem cells to self-renew," said Jamieson. "So we're not just getting rid of cancerous cells: we're getting to the root of their resistance to treatment leukemic stem cells that lie dormant."

The study results suggest that such therapy would also be effective in other types of cancer stem cells, such as those that cause breast cancer, that also rely on NOTCH1 for self-renewal.

"Therapies based on monoclonal antibodies that inhibit NOTCH 1 are much more selective than using gamma-secretase inhibitors, which also block other essential cellular functions in addition to the NOTCH1 signaling pathway," said contributor A. Thomas Look, MD of Dana-Farber/Children Hospital Cancer Center in Boston. "We are excited about the promise of NOTCH1-specific antibodies to counter resistance to therapy in T-ALL and possibly additional types of cancer."

In investigating the role of NOTCH1 activation in cancer cell cloning, the researchers showed that leukemia initiating cells possess enhanced survival and self-renewal potential in specific blood-cell, or hematopoietic, niches: the microenvironment of the body in which the cells live and self-renew.

The scientists studied the molecular characterization of CD34+ cells a protein that shows expression in early hematopoietic cells and that facilitates cell migration from a dozen T-ALL patient samples.

They found that mutations in NOTCH1 and other genes capable of promoting the survival of cancer stem cells co-existed in the CD34+ niche. Mice transplanted with CD34-enriched NOTCH1 mutated T-ALL cells demonstrated significantly greater leukemic cloning potential than did mice without the NOTCH1 mutation. The mutated cells were uniquely susceptible to targeted inhibition with a human monoclonal antibody, according to the scientists.

###

Additional contributors to the study include Wenxue Ma, Daniel J. Goff, Ifat Geron, Anil Sadarangani, Christina A. M. Jamieson, Angela C. Court, Alice Y. Shih, Qingfei Jiang, Christina C. Wu, Kristen M. Smith, Leslie A. Crews, Ida Deichaite, Sheldon R. Morris and Dennis A. Carson, UC San Diego Department of Medicine and Stem Cell Program, UC San Diego Moores Cancer Center; Alejandro Gutierrez, Dana-Farber/Children Hospital Cancer Center in Boston; and Kang Li, Ping Wei and Neil W. Gibson, Oncology Research Unit, Pfizer Global Research and Development, La Jolla Laboratories, San Diego.

This work was supported by the Ratner Family Foundation, the Leichtag Family Foundation, and Moores Cancer Center Donor Funds; grants from the National Institute of Health (1K08CA133103 and 5P01CA68484); the William Lawrence Foundation, and the American Society of Hematology-Amos Medical Faculty Development program. Dr. Jamieson's work was supported by the California Institute for Regenerative Medicine (CIRM).


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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.


Researchers block pathway to cancer cell replication [ Back to EurekAlert! ] Public release date: 2-Jul-2012
[ | E-mail | Share Share ]

Contact: Debra Kain
ddkain@ucsd.edu
619-543-6163
University of California - San Diego

NOTCH1 signaling promotes T-cell acute lymphoblastic leukemia-initiating cell regeneration

Research suggests that patients with leukemia sometimes relapse because standard chemotherapy fails to kill the self-renewing leukemia initiating cells, often referred to as cancer stem cells. In such cancers, the cells lie dormant for a time, only to later begin cloning, resulting in a return and metastasis of the disease.

One such type of cancer is called pediatric T cell acute lymphoblastic leukemia, or T-ALL, often found in children, who have few treatment options beyond chemotherapy.

A team of researchers led by Catriona H. M. Jamieson, MD, PhD, associate professor of medicine at the University of California, San Diego School of Medicine and Director of Stem Cell Research at UC San Diego Moores Cancer Center studied these cells in mouse models that had been transplanted with human leukemia cells. They discovered that the leukemia initiating cells which clone, or replicate, themselves most robustly activate the NOTCH1 pathway, usually in the context of a mutation.

Earlier studies showed that as many as half of patients with T-ALL have mutations in the NOTCH1 pathway an evolutionarily conserved developmental pathway used during differentiation of many cell and tissue types. The new study shows that when NOTCH1 activation was inhibited in animal models using a monoclonal antibody, the leukemia initiating cells did not survive. In addition, the antibody treatment significantly reduced a subset of these cancer stem cells (identified by the presence of specific markers, CD2 and CD7, on the cell surface.)

"We were able to substantially reduce the potential of these cancer stem cells to self-renew," said Jamieson. "So we're not just getting rid of cancerous cells: we're getting to the root of their resistance to treatment leukemic stem cells that lie dormant."

The study results suggest that such therapy would also be effective in other types of cancer stem cells, such as those that cause breast cancer, that also rely on NOTCH1 for self-renewal.

"Therapies based on monoclonal antibodies that inhibit NOTCH 1 are much more selective than using gamma-secretase inhibitors, which also block other essential cellular functions in addition to the NOTCH1 signaling pathway," said contributor A. Thomas Look, MD of Dana-Farber/Children Hospital Cancer Center in Boston. "We are excited about the promise of NOTCH1-specific antibodies to counter resistance to therapy in T-ALL and possibly additional types of cancer."

In investigating the role of NOTCH1 activation in cancer cell cloning, the researchers showed that leukemia initiating cells possess enhanced survival and self-renewal potential in specific blood-cell, or hematopoietic, niches: the microenvironment of the body in which the cells live and self-renew.

The scientists studied the molecular characterization of CD34+ cells a protein that shows expression in early hematopoietic cells and that facilitates cell migration from a dozen T-ALL patient samples.

They found that mutations in NOTCH1 and other genes capable of promoting the survival of cancer stem cells co-existed in the CD34+ niche. Mice transplanted with CD34-enriched NOTCH1 mutated T-ALL cells demonstrated significantly greater leukemic cloning potential than did mice without the NOTCH1 mutation. The mutated cells were uniquely susceptible to targeted inhibition with a human monoclonal antibody, according to the scientists.

###

Additional contributors to the study include Wenxue Ma, Daniel J. Goff, Ifat Geron, Anil Sadarangani, Christina A. M. Jamieson, Angela C. Court, Alice Y. Shih, Qingfei Jiang, Christina C. Wu, Kristen M. Smith, Leslie A. Crews, Ida Deichaite, Sheldon R. Morris and Dennis A. Carson, UC San Diego Department of Medicine and Stem Cell Program, UC San Diego Moores Cancer Center; Alejandro Gutierrez, Dana-Farber/Children Hospital Cancer Center in Boston; and Kang Li, Ping Wei and Neil W. Gibson, Oncology Research Unit, Pfizer Global Research and Development, La Jolla Laboratories, San Diego.

This work was supported by the Ratner Family Foundation, the Leichtag Family Foundation, and Moores Cancer Center Donor Funds; grants from the National Institute of Health (1K08CA133103 and 5P01CA68484); the William Lawrence Foundation, and the American Society of Hematology-Amos Medical Faculty Development program. Dr. Jamieson's work was supported by the California Institute for Regenerative Medicine (CIRM).


[ Back to EurekAlert! ] [ | E-mail | Share Share ]

?


AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.


Source: http://www.eurekalert.org/pub_releases/2012-07/uoc--rbp070212.php

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