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One of the informal yardsticks of financial success is to ask whether you are better off than your parents. According to a recent survey, the answer depends on whether you're a man or woman.
Women make $1.17 for every $1 their mothers earned 30 years ago but men are making 10 cents per hour less than their fathers did back then. Those are the results of a study by Young Invincibles and Demos, which examined salaries of adults age 25 to 34 in 2010 and compared them to 1980 wages.
The study concludes that the decline in manufacturing and construction, two male-dominated industries, is partly to blame for the reduction in men's wages. In the meantime, workplace conditions have steadily improved for women.
Overall, young people feel like they're facing unique challenges, including 9-percent unemployment and high student debt, and think it's more difficult to reach the financial comfort levels their parents obtained. But it's worth remembering that in 1980, the U.S. was in a recession, suffering from 11-percent unemployment as well as double-digit mortgage interest rates.
Do you think you're financially better or worse off than the previous generation?
Keep up with your wealth and mortgages and follow me on Twitter.
Get more news, money-saving tips and expert advice by signing up for a free Bankrate newsletter.


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Kalakka Povathu Yaaru 02-10-2016 Vijay TV Kalakka Povathu Yaaru 02.10.2016 Show Online | Kalakka Povathu Yaaru 02/10/2016 Vijay TV Program 02nd October 2016
Watch Vijay TV Kalakkapovadhu Yaaru 02.10.16 Game Show 02/10/16 Latest Kalakka Povadhu Yaaru Today Episode Online At Tamiltvshows.net
Kalakkapovadhu Yaaru 02-10-2016 – Vijay tv Game Show | Star vijay Tv Kalakkapovathu Yaaru 02-10-16 Program 02nd October 2016
Synopsis: Kalakka Povathu Yaaru is the famous show in Vijay Tv Channel already four season are completed.
Kalakka Povathu Yaaru produced Actor Sivakarthikeyan, Comparing Erode Mahesh, Comedia Robo Shankar and many more.
Today's Show Detail:
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Kalakkapovadhu Yaaru Season 5,Vijay tv shows
More Video's from this Category: Kalakka Povathu Yaaru Season 5 | Vijay tv Shows

subset: commoncrawl


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This is a New Year!
I am writing this blog toward all of the softball articles that talk about last years softball team well i guess what these articles are talking about Courtney Tucker she has been mentioned many times April Ayres, Kaylie Layman, and Lindsey Schoch (without really saying any names)Pretty much the girls that left the team. All i really want to say by writing this blog is if this team wants to get out of the "Barbie" name or prove to whoever that they can do better this year than the papers and the girls would be a lot better off not talking about it. I can say that i dont read the Bluffton Today very often but every time i pick it up and look in to the sports section it is either a girl on the team now in an unspoken way saying we can do better than we did last year...or saying that we dont want people to think that they are last years team and want to lose all the images that people had of the team last year...and thats fine but prove it dont talk about it. people waste too much time talking about things then doing them... i have full faith in these girls but really were all getting a little annoyed when every time we open the Bluffton Today to read about the girls that we once played on a team with to see how their doing because we care, we hear about all the things that went wrong last year... and how we wernt a team and everyone is so much closer and like it so much better playing behind Paige... thats all fine if thats how these girls feel but the seniors and courtney tried pretty hard to make our 1st year a good one... and i believe very much that we worked out a lot of kinks that started at first... but every team has there problems! well anyway its hard to open up the Bluffton Today to hear all the things that last years team did wrong... but good luck for the rest of the year!


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And so it comes to pass with every column that a decision has to be made. What shall we examine? Those of you who read and email me your comments seem as divided as I am. Some like the social aspect columns, some like the more political columns and some of you like the columns that review the latest military hardware available at discount prices. To that last group, I have forwarded those to the appropriate Pentagon sources, who you meant to contact, and they appreciate your input.
I'll be honest with you; when I weigh-out all the possibilities, those endless news developments of the day are almost too much to ignore. I mean, I want to discuss with you such crucial things such as how to find the mate of your dreams in the deodorant aisle, why adding steroids to your soup will make you strong like Popeye or even why I find the dog park the place to be if you like to pet dogs. But the news stories just keep coming and coming (like one more reality show that milks its ratings with a results show the next day), and they are all begging for just one more column's worth of attention in their greed.
I mean, how do you ignore such things as the AIG bonus payoffs? Not just that they happened; who got them, who will correct it or who will hang for it, but who do you have to know to find a job that no matter how much you wreck the paper work, the company, the investors and the planet, you will receive millions for doing so. I mean, cn u magine gittin pade milyuns fo mi callum fo mi spellen erras? Obviously I took the wrong courses in college.
Or how about that 8ctomom? I mean, how do you avoid that story? Now, you may think that Dr. Phil quite literally owns the mom, the kids and the parents like shares of IBM, and he does (common or preferred unknown) but still… how do you resist commenting anyway? I mean, there are now 14 kids running (some crawling) around, so there must be at least one story there that has not been commented on to death. And now that we have gotten an innocent neighborhood involved, the mind boggles with ideas to write about and all of them are equally boring and unimportant.
And speaking of what's all over the news, who can ignore Moneygate? The bailouts. The dispute over the bailouts. The plans. The dispute over the plans. The partisan posturing. The dispute over partisan posturing. Disputes. And the dispute in Congress over what constitutes a dispute. I mean, wow! If I was a columnist (and I am), there is enough material there to fill a newspaper.
And what about those newspapers? Used to be when they folded it was to put under your arm. Now how do you not write about that story? Once again enough material there to fill a newspaper… If it stays in business due to… the crisis's such as AIG and now we are back to their bonuses and who deserves them and who got us into this mess and…
I tell you, it's enough to divide a country. Enough to ruin a portfolio. Enough to make people angry. Which you would think would be enough to pull all of us together. Enough to make us all say "enough" and work as one so we all can have enough again. (Except for 8ctomom. She has enough already).
But it isn't. We are just fighting each other. True we almost had something with the 8ctomom, but then we thought of the children. No, we need a greater uniter. Something that will have all of us pulling the country forward again instead of pulling it apart. What we need is a common enemy that is clearly visible, and clearly the ultimate threat to all of us. What we need is a good old-fashioned interplanetary invasion.
And if that doesn't work, then deciding what to write about won't be a problem. It will be a recipe for human stew. Ahhh, back to the social columns.
Lloyd E. Flyer is a freelance writer and may be contacted through the "Tolucan Times" or at email@example.com


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The Dutch government on 15 September 2015 presented its main plans for the year ahead during the annual "Prince's Day" (budget day). Included in the proposals is a new section to be added to the Dutch corporate income tax law for additional transfer pricing documentation requirements—i.e., country-by-country (CbC) reporting and documentation requirements, essentially incorporating the OECD's base erosion and profit shifting (BEPS) Action 13.
In addition, the Netherlands would add more stringent documentation requirements for multinational enterprises (MNEs) that have annual consolidated group turnover greater than €50 million. The proposed changes are expected to be enacted and effective beginning 1 January 2016.
The proposed CbC requirements would be a change from the current legal requirements under article 8b of the Dutch corporate income tax law (known in English as the "Corporate Income Tax Act 1969"). Not only would the proposed legislation provide more detail on the documentation required as such, but it also would introduce a penalty regarding CbC reporting and a strict filing deadline for documentation.
A key objective of the BEPS Action 13 is to increase transparency through improved transfer pricing documentation standards, including through the use of CbC reporting. As such, CbC reporting requires multinational enterprises (MNEs) to provide tax administrations information annually, in each jurisdiction where the MNEs do business, relating to the global allocation of income and taxes paid, together with other indicators of the location of economic activity within the MNE group.
According to the current wording of the proposed law in the Netherlands, as from 1 January 2016, parent companies of Netherlands based multinationals with an annual turnover of a minimum of €750 million would be required to file the new CbC report within 12 months following fiscal year-end close. The first CbC reports would be filed in 2017, and could be filed in either English or Dutch language.
The proposed law generally is in line with the CbC reporting implementation package, issued by the OECD in June 2015. This requires taxpayers to disclose per country information on revenues, profit before income tax, corporate income tax paid, corporate income tax as included in the annual accounts, stated capital, accumulated earnings, number of employees, and tangible assets other than cash and cash equivalents.
Also, the Dutch proposal would require the following information to be provided for all the constituent entities of the MNE group:
Additional guidance is expected, concerning the form and content of the CbC report.
BEPS Action 13 proposes the automatic exchange of the CbC reports filed in the jurisdiction of the (surrogate) parent with the tax authorities of all jurisdictions in which the MNE operates. In line with the recommendations in BEPS Action 13, the proposed Dutch law would require constituent entities in the Netherlands to file the CbC report for the entire MNE group if the CbC report were not to be exchanged with the Netherlands by the country of the (surrogate) parent.
Penalties would be imposed in instances of intentional non-compliance or "serious misconduct" of the reporting entity regarding its obligation to file the CbC report, with the penalty amount being up to €20,025 as well as possible criminal prosecution.
In addition to the introduction of CbC reporting, the Dutch government announced more stringent documentation requirements for MNE group entities that are tax resident in the Netherlands and have a turnover exceeding an annual threshold of €50 million. The group entity would be required to file a master file that provides an overview of the MNE as a whole, including the nature of its activities, its general transfer pricing policy, and its global allocation of income and economic activities.
A local file would also need to be provided and reflect information relevant for transfer pricing analysis relating to transactions between taxpayers and related parties in other tax jurisdictions. Both files would be filed in either English or Dutch.
The current wording of the proposed Dutch law is in line with the master file and local file standards, as described in the BEPS Action 13 report, but with additional guidance regarding the form and content of the documentation. An important and new requirement would be that the master file and the local file would need to be part of the entity's administration prior to filing the tax return. This would be a change from current practice which requires the taxpayer to provide transfer pricing documentation within two months after a formal request has been issued by the Dutch tax administration.
An important and new requirement would be that the master file and the local file would need to be part of the entity's administration prior to filing the tax return. This would be a change from current practice that requires the taxpayer to provide transfer pricing documentation within two months after a formal request has been issued by the Dutch tax administration. As before, noncompliance with the documentation requirements would result in a reversal of the burden of proof.
Entities that form part of an MNE group and have a turnover exceeding the €50 million threshold need to consider preparing for the upcoming changes in the documentation requirements. Furthermore, MNEs with a turnover exceeding €750 million need to be ready to file CbC reports. To assist multinationals in preparing to comply with the proposed CbC reporting and documentation requirements, the KPMG member firm in the Netherlands (Meijburg & Co) has developed a process and diagnostic review.
Read a September 2015 report [PDF 36 KB] prepared by the KPMG member firm in the Netherlands.
For more information, contact a tax professional with the KPMG member firm in the Netherlands:
Jeroen Dijkman | +31-88 909 2543 | email@example.com
Jaap Reyneveld | +31-88 909 1114 | firstname.lastname@example.com
Eduard Sporken | +31-88 909 1618 | firstname.lastname@example.com
Maurits Stuyt | +31-88 909 1061 | firstname.lastname@example.com
The KPMG logo and name are trademarks of KPMG International. KPMG International is a Swiss cooperative that serves as a coordinating entity for a network of independent member firms. KPMG International provides no audit or other client services. Such services are provided solely by member firms in their respective geographic areas. KPMG International and its member firms are legally distinct and separate entities. They are not and nothing contained herein shall be construed to place these entities in the relationship of parents, subsidiaries, agents, partners, or joint venturers. No member firm has any authority (actual, apparent, implied or otherwise) to obligate or bind KPMG International or any member firm in any manner whatsoever. The information contained in herein is of a general nature and is not intended to address the circumstances of any particular individual or entity. Although we endeavor to provide accurate and timely information, there can be no guarantee that such information is accurate as of the date it is received or that it will continue to be accurate in the future. No one should act on such information without appropriate professional advice after a thorough examination of the particular situation. For more information, contact KPMG's Federal Tax Legislative and Regulatory Services Group at: + 1 202 533 4366, 1801 K Street NW, Washington, DC 20006.
KPMG International has created a state of the art digital platform that enhances your experience, optimized to discover new and related content.


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Gem.Prijs: BRL 92,00 - 260,00
Klasse: 0 stars
Featuring free WiFi, a restaurant and a children's playground, Hotel do Santuário offers pet-friendly accommodation in Nova Trento. Guests can enjoy the on-site bar. Free private parking is available on site. All rooms include a TV. For your comfort, you will find free toiletries and a hairdryer. You will find a 24-hour front desk at the property. You can play table tennis and billiards at the hotel. Bombinhas is 46 km from Hotel do Santuário , while Balneário Camboriú is 42 km away. The nearest airport is Navegantes - Minister Victor Konder International Airport, 50 km from the property. meer
Gem.Prijs: BRL 114,00 - 360,00
Klasse: 0 stars
Offering a restaurant, Natalina Pousada & Restaurante is located in Nova Trento. Free WiFi access is available throughout. Featuring simple décor and furnishing, each guestroom boasts a private bathroom with free toiletries. Extras include bed linen. At Natalina Pousada & Restaurante , guests can find a shared kitchen to prepare homemade dishes. The property offers free parking. Hercilio Luz International Airport is 57 km away. meer
Gem.Prijs: BRL 80,00 - 200,00
Klasse: 0 stars
Featuring an outdoor pool, Pousada Portal do Vigolo is located in Nova Trento and offers a continental daily breakfast. WiFi is free in all areas. The rooms come with tiled floors and large windows. Each is equipped with a private bathroom. The on-site restaurant serves traditional foods. Guests can also enjoy a shared lounge and a games room. There is a playground for children. São João Batista is a 15-minute drive from the property, while Tijucas is 35 km away. meer
Gem.Prijs: BRL 110,00 - 265,00
Klasse: 0 stars
Featuring free WiFi and a spa centre, Pousada do CEIC offers pet-friendly accommodation in Nova Trento, 46 km from Bombinhas. Free private parking is available on site. Rooms come with a private bathroom. A flat-screen TV is offered. You will find a shared kitchen at the property. Balneário Camboriú is 44 km from Pousada do CEIC , while Itapema is 38 km away. Navegantes - Minister Victor Konder International Airport is 53 km from the property. meer


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|Sonic State Studio / Effects Units /
|Roland SDX-330 At a Glance Roland News(489) Streaming Video (108)
|Released: early 90's? Version: 0.00
|Rated: Not Reviewed Add review: (0)
|Linkssubmit a link
|JD writes:
Wow~ this unit is really good, abiet specialized. It does chorus, flange, detune and LFO functions. Although certain settings can "act" like a delay, this is not a good unit for delay/reverb/etc. The sound quality, even at audio of 16 bit, is very, very good and relatively low-noise. It's the world's coolest chorus/flange box....and there is a blow-out price on this unit of $US 229 at Synthony.com. This is a professional piece in all respects, the original MSRP was around $US 800. For slightly more than the price of a cheap chorus pedal, you can own what might be the world's best dedicated chorus/flanger unit.
Good Points
Sound quality and variety. This unit really offers everything from deep, dark chorusing to shimmery vibrato. Sound quality will *kill* the cheap Zoom/DOD/Boss unit you own. It is programmable in the way I never thought chorusing could ever be. Want an eight voice chorus? Okay. You can, if you have the stamina, individually program the LFO characteristics, detune, level, dynamic response, etc.....for each single voice of your eight voice chorus! A little over the top, probably....but truly a cool unit. The manual is not as bad as most Roland gear, but not really good for pointing out which parameter manipulations are good for what. On the other hand, the preset names give you a good place to start. The best "good point" of this unit: it really does chorus/flanging f/x as good and detailed and programmable as I've ever heard. For me, it's good enough that I can reliably free up my mult-fx units (Lex MPX-1, MPX-100, Ensoniq DP/4 for pure reverb emulations.
Bad Points
I wish it had balanced ins/outs or digital ins/outs. At the same time, the noise specs are very good. While the manual is not nearlt as bad as most Roland units, it's not really good, either.
Roland SDX-330 Specifications:
Digital IOs:
Analog IOs:
2 / stereo unit unbalanced
Midi IOs:
1 in/1 out/1thru
Maximum Resolution:44.1 @ 16 bit
see description
Software supported:
SDX-330 Links
Roland Vintage Effects This site contains information about early Roland effects including Space Echoes, Roland Rack and early Roland pedals.
Try the Effects Units links page for more..


text: The New York Times writes about Palm's recent hire of Paul Mercer, a former Apple engineer, who most recently had founded Pixo. Pixo was a software that served as the basis for the original Apple iPod. The article suggests that Mercer's work at Palm will involve some form of response to Apple's iPhone announcement. Palm is one of the companies that is felt to be most affected by a succesful launch of the Apple iPhone.


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Fukushima: One year later
Mar. 12, 2012 / Posted by: Erich Pica / Categories: Blog, Climate and Energy
One year ago I, like many people across the United States and around the world, watched as the horrible images flooded in from Japan and the Fukushima Province after the 9.0-magnitude earthquake and resulting tsunami devastated the coastline. News...Read More »


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"Few organizations help us fulfill the American Red Cross mission to prevent and alleviate human suffering like Wawa, led by Howard Stoeckel," says CEO of American Red Cross Southeastern Pennsylvania. The American Red Cross Southeastern Pennsylvania (SEPA) Chapter honored Wawa's CEO, Howard Stoeckel, with the 2012 Citizen of the Year Award during its 30th annual
Red Cross Names Wawa 2012 Citizen of the Year
CITGO Supports Local Red Cross
Nine locally owned CITGO stations in Robeson and Scotland Counties, N.C., are supporting the local Red Cross chapter through fundraising efforts and two community blood drives. From Aug. 3 to Sep. 6, these CITGO stations are selling $1 paper blood droplets to raise money for the many community, disaster, military and health assistance programs provided
Sheetz And Customers Raise 56,000 for Haiti
Sheetz and its customers are donating more than $56,000 to help victims of the Jan.12 earthquake in Haiti. During the month of February, customers gave $28,359.37 to the relief effort. Sheetz is matching that total, bringing the final figure to $56,718.74. All proceeds are going to the Red Cross. The donations were collected in special


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VERGENNES — In a wide-ranging discussion with locals at the Legislative Luncheon in Vergennes on Monday, Gov. Peter Shumlin defended his stance on the Addison-Rutland Natural Gas Project.
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VERGENNES — The Vergennes Union High School board at a special meeting on Tuesday decided to put a two-tiered budget proposal before voters on May 5.
The first article on the ballot will ask Addison Northwest Supervisory Union residents to back a spending plan that includes about $156,000 of cuts from the $10.47 million proposal that lost on Town Meeting Day, 831-718.
VERGENNES — The latest Boys & Girls Club of Greater Vergennes Youth of the Year had several goals in mind when she decided to compete for the honor.
Some were practical — if Vergennes resident Ericka DeLisle, 18 on April 1, wins the Vermont Youth of the Year competition in Montpelier on April 9, she will earn scholarship money to help her attend the Massachusetts College of Liberal Arts this fall.
DeLisle would also like to have a higher profile for her primary message — against bullying.
UPDATED: VERGENNES — Someone robbed the People's United Bank on Main Street in Vergennes on Friday afternoon, Vergennes police said.
VERGENNES — Vergennes aldermen on Tuesday confirmed their support for an East Street preschool playground, an action taken despite a Town Meeting Day vote against the project.
All five aldermen at the meeting said the 303-202 tally on March 3 on the $42,000 project was not representative because the petitioned language on the article failed to make clear that residents would not pay to build the playground.
VERGENNES — The Vergennes Union High School board on Monday took steps toward an April 14 budget revote and picked a new chairperson. But, despite debate among its members and the 20 attendees, board members did not settle on a new spending plan.
In a paper ballot of the board members, Addison representative to the VUHS board Laurie Childers unseated sitting chairman Kurt Haigis, one of two VUHS directors from Ferrisburgh, as the board's new leader.
VERGENNES — In addition to deciding to move ahead with a city park for preschoolers, Vergennes aldermen at their meeting Tuesday evening also:
•Elected Renny Perry as senior alderman. Perry will stand in as mayor if needed at meetings when Mayor Bill Benton is absent. Randy Ouellette held the post in recent years, but chose not to run for another term.
VERGENNES — While the annual March municipal meeting in Vergennes does not include the typical Town Meeting Day votes on municipal and road budgets — the city council sets those spending plans in June — this week saw a lot of action in the Little City on Town Meeting Day.
VERGENNES — About 5,000 visitors come to Brandon for its annual community-wide yard sale, an event coordinated by that town's chamber of commerce, which in turn reaps close to $1,000 for promoting and organizing the day.
That success caught the attention of downtown Vergennes merchant Linda Cook, owner of Linda's Apparel and Gifts on Main Street.
Cook brought the idea of trying to duplicate those results to someone who knows the idea works in Brandon: new Addison County of Chamber Executive Director Susan Hoxie, who is a Brandon resident.
DANVILLE — Former Vergennes Union High School Co-Principal Edwin Webbley has been cited by Vermont State Police for allegedly taking cash and checks out of a safe at The Danville School. Webbley has served as the Danville School co-principal since this past summer.
VSP cited Webbley, 60, to appear in Caledonia Court on March 23 to answer to the charge of embezzlement.
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Energetic pandas kept awake by unseasonably warm weather have been showing off their acrobatic skills at the world's oldest zoo.
Helmut Pechlaner, director of the Schoenbrunn Zoo in Vienna said: "The bears are only young and love climbing the trees, but I've never seen one do a handstand at the top of a tree before.
"Normally they slow down and sleep a lot at this time of year, but it has been so warm in Austria lately that they've been more active than usual."
Female bear Yang Yang and her partner Long Hui were presented to Schoenbrunn Zoo two years ago by the Chinese government following a personal request from Austrian Chancellor Wolfgang Schuessel.
The young pair will stay in the Austrian capital for 10 years to raise awareness of endangered species before returning to their homeland in 2013.
There are only an estimated 1,600 Giant Pandas left in the wild.
The pair become an instant hit in the Alpine republic, quickly becoming one of the most visited attractions at the 18th century zoo.
Yang Yang and Long Hui are also under constant observation by zoo scientists as little is known about the habits of the Giant Panda.
It is hoped the two will mate and return to China as a family group but zoo keepers say that despite their best efforts the pandas are simply much more interested in bamboo than sex.


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Schools will have to make up for 4 days of fun
Posted January 31, 2014
Fayetteville, N.C. — At the Ramsey Street YMCA in Fayetteville Friday, kids were literally climbing the walls. That way of burning off excess energy was a welcome respite for some parents who were dealing with children on an unexpected mid-winter vacation.
Cumberland County's 52,000 public school students have had four days off, the result of a snowstorm that dumped about 3 inches of snow on the area and the freezing temperatures that followed.
Y instructor Sharon Smith brought her son and grandson along to work with her Friday.
"They might as well come to the YMCA and work out," she said. "We have lots of fun here, do lots of exercise, have a great time."
Not all parents were lucky enough to be able to take their children to a place like the "Y." Real estate agent Marva Moore had to schedule appointments around caring for and entertaining her son, Tyler.
"It's tough," Moore said. "Luckily, my other two went to school today. They go to private school."
School systems around the area were working on plans Friday to make up the missed time. In Cumberland County, the fact that students attend an extended-day schedule means they have hours in the bank.
"I think we will probably lose some teacher work days," said school board member Michael Boose. "But I don't think that ultimately we're going to have to make up but a day or two."
In Wake County, make-up days were supposed to begin Saturday for year-round students, but the school district canceled the session because road conditions remained hazardous.


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County Premier
Minehead 2, Bridgwater Town Res 0
BRIDGWATER Town Reserves started the new season with a 2-0 defeat at Minehead on Saturday.
Minehead, who finished sixth in the division last season, took the points courtesy of goals from Aaron Deeks and Patrick Reed.
Town will be looking to bounce back tomorrow night when they host Wrington Redhill at Fairfax Park before a local derby clash with Berrow on Saturday.
The Robins finished mid-table last season and will be hoping to improve on that.


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Braxton Family Values reality star Traci Braxton has she a lot of weight over the last couple of seasons.
During an episode of Braxton Family Values on season 2, the sisters all sat down with Dr. Sherri to discuss ways to improve their relationship. When it was Toni Braxton's time to share her thoughts on the relationship between the sisters, she started by telling Traci that she wanted her to "lose 20-40 pounds immediately." Traci got very offended at Toni's comment and eventually stormed out of the meeting, but later on during the season, you saw her and Tamar join the gym and workout with a trainer.
Since then, Traci has lost a whopping 64 pounds and has been keeping it off. During a recent interview on NewsOne Now with Roland Martin, Traci dished on how she actually gained weight and how she lost it and is keeping it off.
[I dropped 64 pounds] in two years. When it came down to eating, I just basically ate anything I wanted to eat and I just thought it was okay. It's fine, it's healthy. I didn't have my mind right. I was angry at myself for gaining the weight and I didn't feel as sexy as I wanted to feel, and I didn't give my family my all.
On taking two years to lose the weight
When you lose it quickly, you fail, but failure is not an option for me. I'm like 'okay Traci, you need to show the world that you're not the underdog, that you're likable too and that you can do it for yourself. You're not doing it for your sisters because your sisters are hounding you.' I was really skinny when I was growing up. They used to call me "big bird" because I was so tall and real lean and thin. I had to get it together and for these people that are taking these diet pills thinking 'okay, I'm gone get it together,' uh-huh.
Traci went on to give her workout regimen saying she worked out three times a week in the gym anywhere from 1-2 hours at a time depending on how much she ate. She also dished on being a diabetic and losing the weight for health reasons.
Congrats to Traci on her weight loss. I for one know the weight loss struggle as I am trying to lose half of my current body weight as well. I appreciate her for sharing her story because it is very motivating.
If you missed Toni telling her that she wants Traci to lose weight, watch it below [5:55 mark]:
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When was the last time you ever heard of anyone wanting to boycott a company because they wanted to bring a new product to market?
Well apparently this is the situation that Valve is finding itself in with some pretty serious gamers who are really angry that the company is bringing the next version of the popular game to market only a year after the original Left 4 Dead was released. They have even set up a Steam Group within the Steam (Valve's game store and community) Store community pages.
The opening paragraph of their statement to both the gaming community and I would image to Valve itself is this
The Left 4 Dead 2 Boycott is a group of individuals who have pledged to boycott Valve's upcoming release of Left 4 Dead 2 on November 17th, 2009. We have assembled a manifesto outlining the basic concensus of many members of our community. (Note: this manifesto is a new version, which we have recently posted to keep our manifesto in line with the middle ground of our members. This is the correct group for the boycott)
They go on to list out their whole – for a lack of better words – manifesto.
-Valve is a company with financial needs and cannot be expected to survive without the release of new games.
-Judgment cannot be passed on the quality of Left 4 Dead 2 until its release.
-Left 4 Dead was, and is, a quality game which deserves the praise of the entire gaming community.
-To holding Valve to its promise of free, continual updates to Left 4 Dead in order to build and sustain the community.
-To keeping the Left 4 Dead community together in order to improve the quality of online gaming.
-To supporting the model of continual updates Valve has set forth with its staple products like Team Fortress 2.
-The release of Left 4 Dead 2 as a stand-alone sequel will split the communities and decrease the quality of multiplayer gaming.
-The announced content of Left 4 Dead 2 does not warrant a stand-alone, full-priced sequel and should instead become updates (free or otherwise) for Left 4 Dead.
-Left 4 Dead has not yet received the support and content which Valve has repeatedly stated will be delivered.
-The release of Left 4 Dead 2 will make Left 4 Dead an obsolete purchase and inferior piece of software after only one year since release.
-That Valve honor its commitment to release ongoing periodic content for Left 4 Dead.
-That Left 4 Dead 2 not be released as a stand-alone, full-priced sequel but as either a free update to Left 4 Dead or an expansion with full compatibility with basic Left 4 Dead owners.
-That Left 4 Dead owners be given discounts for Left 4 Dead 2, should it be released as premium content.
Therefore, we – the members of this Left 4 Dead 2 Boycott – promise to abstain from the purchase of Left 4 Dead 2 until our requests are addressed.
I got to admit this is the first time I have ever heard of anything like this – especially when it comes to gaming. Talk about passionate.
[hat tip to Technologizer]


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BookCreator Tool v3.5
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Device: Galaxy S, Nook w/CM7
Originally Posted by
Hey "X" if you're still around. Firstly of course I'll echo everyone's gratitude for the nice toolset you've handed us. Unfortunately I'm mostly here to whine about a problem I'm having though. Similarly to a few others I've seen on my skim through the thread, I'm on Windows 7 and Office 2010, using the 2007 template, and Word crashes during the export. It seems to crash at the instant that a second instance of Word opens. Unlike some others though, nothing is created for me. I would just move on and use something else but I've prepared 100 files before realising that export doesn't work! (Woe is me!) So, I'd prefer to find out how to get it working.
I thought maybe permissions or somesuch was at fault. I stored my template file on the desktop (because I'm lazy and messy) and I thought maybe that was it. So I copied it to a "normal" folder and tried a brand new fresh new file but still no luck. I'm using all the proper buttons to set title, author. Mostly using the magic chapter finder (I love you so much for this, btw). Alas nothing works.
Any ideas, anyone?
I'm still around, though I hardly visit the site anymore.
I'm not sure what problem you are seeing is. The issue did exist for everyone at one point but I rewrote the 2007 template to resolve that defect. Since then I've not seen or have been able to reproduce the problem.
My configuration is very similar to yours, I have Windows 7 and office 2010. The way I start a word doc is to double click on the template (I actually have gravitated to putting a shortcut on my task bar since I use it so often).
Some data that might help me resolve this issue is to enable the debug flag, it's on one of the tabs on the "create eBook" dialogbox. It will produce a "debug.txt" file in the same location of the word doc. Also show a screen shot of the error if an error is being shown.
Btw your welcome, hopefully we can get this issue resolved for you so you can keep on enjoying the tool.
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text:
Cumberland (6-7-2) ends the season after winning for the first time in the conference tournament since 2005 when the Bulldogs won the regular season and the tournament.
Bethel (14-0-3), the defending national champion, moves on to the tournament finals this Friday.
The Wildcats outshot CU, 18-4, in the match, though CU keeper Michael Michailidis made seven saves to keep it close. Thirteen of Bethel shots came in the second half after a scoreless first period.
Karaoglan put Bethel on the board in the 66th minute on an assist from Dawyne Smith and Eric Rosas, and Orozco's tally in the final two minutes came from Felix Obilo.


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I'm sure I've posted about my 'fake chicken pie' as Jim likes to call it. When I told him we were having it for dinner he actually did a little dance in the kitchen!
I didn't use packaged fake chicken this time, I just cut up the last two Fat Free Vegan seitan cutlets into pieces and threw them in with whatever vegetables looked pie worthy (looks like there's carrots, leeks and mushrooms in there this time, I can't recall). The pastry is packaged, it's Sainsburys pre-rolled puff pastry, although it didn' t puff very much.
In the background are the first roasted brussel sprouts of the season, so damn yummy. I've eaten roasted sprouts two or three more times since then and I don't get tired of them. I don't recall where I read about putting barbecue sauce on them but I tried it the other night and oh my god it was amazing, I'm salivating thinking about eating them that way again, but sadly there are none in the fridge at the moment…
Both the boy wolfed down everything but the sprouts, although Jim and I have come to an agreement that as he's 7 he has to eat 7 sprouts when I serve them. I forced Piggle (who's 3) to eat 4, luckily he doesn't know how old he is yet!
Next up I will probably be posting about our Thanksgiving dinner which we're not having until Saturday so we can have it with my whole family (my Dad and I are the only Americans but apparently everyone else likes Thanksgiving dinner too!). I'll be making the stuffing and a pie, hopefully both will come out ok as they're both new recipes.


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Last updated: 26 May 2016
Jennifer Barker was the (now retired) Executive Director of the Eastern Oregon Renewable Energies Association nonprofit, and the organizer of SolWest Fair in John Day, Oregon. She is the author of The Morning Hill Solar Cookery Book, Morning Hill Cookbook, and Solar Poetry from SolWest Fair. She has been cooking with the sun since 1992.
- Fall 2015: SolWest Fair is now being hosted by Oregon Rural Action. It is held each June in La Grande, Oregon, and includes a solar cookery class and demonstration. SolWest is a three-day, annual education-oriented regional event. Business vendors will reach an educated crowd interested in renewable energy and sustainable lifestyles. Homeowners will take the message home and apply it in their lives. For more details, check out their website at http://www.solwest.org.
External links
- https://www.facebook.com/morninghillforestfarm/
- http://www.solwest.org
- Jennifer's Solar Cookery Page offers a Philosophy of Cooking, links to web pages, articles and media, and an order form for The Morning Hill Solar Cookery Book.
- SolWest Renewable Energy Fair, a renewable energy event held each June in La Grande, Oregon with over 30 workshops on renewable energy topics (including solar cooking).
- July 2003: Jennifer Barker is interviewed on The Splendid Table on NPR
Jennifer Barker
EORenew/SolWest Fair
PO Box 485
Canyon City OR 97820
Tel.: +1 541-575-3633
Email: firstname.lastname@example.com


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ATTLEBORO – An amendment to city law that will "let businesses make money and prevent thieves from stealing it," was approved by the city council Tuesday.
The law allows jewelry makers to get a waiver from rules that require a 14-day waiting period before they can alter precious metals and jewels given over to them for reworking into new pieces.
The 14-day waiting period in the city's pawn shop law was intended to make it harder for crooks to dump stolen valuables. The two weeks gave cops and victims time to check the stores and catch up to them.
But the law unintentionally was applied to small manufacturers as well, which delayed their work and encouraged customers to seek other shops outside the city.
Under the new law approved Tuesday on an 11-0 vote, jewelry shops such as Attleboro Jewelry Makers will be able to apply for waiver from the 14-day wait.
If the jewelry is turned over to them for remanufacture, the shop won't have to wait at all to start work. However, if someone sells them something, that piece can't be altered or resold for 14 days.
Councilor Richard Conti originally initiated the effort to make a change in the law by changing the 14 days to eight days, but he likes the latest version. "It's a better idea," he said.
Meanwhile, Councilor Jay DiLisio summed up the change.
"This makes it easier for businesses to make money and harder for thieves to steal yours," he said.
GEORGE W. RHODES can be reached at 508-236-0432 or at email@example.com.


text: Capoeirista 3266 Report post Posted April 20, 2013 (edited) Hi there! I'm building a 2D editor at the moment (using Monogame) and was wondering about the best way to blend render targets. Each scene in the engine is composed of three layers, background, central and foreground... that way I can add objects to a particular layer, apply the effects and lighting I want on said layer without affecting objects in other layers. Until recently I've been using a single render target to draw the scene (and a light map render target, blending the two together using a simple shader), but since I want lights to take affect in their assigned layer (not across the entire scene) I'm going to have to use separate render targets for each layer, and do a lighting pass for each one. So at the end of this I'm going to be left with three render targets (lighting + objects in the layer) that I need to apply any post processing effects to, and then blend in to the final scene... and was wondering about the best way to go about this. I assume the only way to really do this is using a pixel shader (to sample each render target and blend the result), but wanted to get suggestions before I go ahead with this. Also, is this complete overkill? I've not really built a 2D rendering system before, so I'm kind of winging it. I intend to add dynamic shadows on a per-layer basis as well. Thanks for the help! Edited April 20, 2013 by Orangeatang 0 Share this post Link to post Share on other sites


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Roma style tomatoes. Packed in USA.
Tomato Puree (Tomato Paste, Water), Sea Salt, Contains Less than 2% of the Following: Spices, Olive Oil, Garlic Powder, Natural Flavor, Citric Acid, Romano Cheese Made from Cow's Milk (Cultured Milk, Salt, Enzymes), Sugar.
Always refer to the actual package for the most accurate information


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Rev. William Hampton
b.abt 1659 Probably at Bletchingley, Surrey, England
d.abt 17 May 1745 Worth, Sussex
Family tree▼
m. 25 Feb1657
m. 24 Oct 1688
Facts and Events
William Hampton was the eldest sonS2 of Charles Hampton by his wife, Katherine née Parker, who were married 25 Feb 1657 at Bletchingley, Surrey.S3 And if William's age at his death, on or shortly before his burial on 17 May 1745S5, S11 was, as stated so precisely, "aged 86 yrs 3 mths," he should have been born about the middle of February of 1659 - which would perfectly coincide with the 12 Feb 1659 date of his christening on the I.G.I.S1 But according to both the I.G.I.S7 and Collections of the Surrey Archæological Society, Vol. IX, part I, p. 300,S8 his brother and the presumably second son, Charles Hampton was born at Worth, Sussex just a few days later, on 21 Feb 1659 – and apparently baptised there sometime that same year. There is no mention of either the birth or baptism of William Hampton in the latter work.S8 So one must assume, given this birth of the second son, Charles, early in 1659, that the eldest, William, was really born at least the year before, unless of course they were actually twins, born on the same day and someone inverted the number 12 for 21 in Charles' case or vice-versa in William's case! Failing this hypothesis, we might have to wonder if he or someone else had miscounted his years at the end - and he actually died after 87 years and 3 months - not 86 and 3...?
Of course this must have been a very exciting time for their father, the Reverend Charles Hampton (1630-1704). His wife had just given birth to his first born son and very shortly after to his second – and he had just been appointed Rector of Worth (15 Dec 1658 – instituted 6 May 1662).S2 Meanwhile he obviously maintained his close ties to Bletchingley, of which he was also the rector from 1678 until his death in 1704. His grandfather, William Hampton (1597-1677) was rector there (as well as at Plumpton in Sussex) from 1635 until his death in 1677.S4
There is also some possible confusion over the Rev. William Hampton's date of death. The aforementioned Collections of the Surrey Archæological Society,S5 as well as the National Burial Index for England & Wales,S11 have him buried on 17 May 1745, while the CCEd - Clergy of the Church of England DatabaseS10 has him 'vacating' his office of 'rector' at Worth, owing to his 'natural death' on 3 Oct 1745 - and even more confusingly - at Plympton (sic), owing to his 'natural death' on 20 Oct 1745! One may sincerely hope that these CCEd dates actually refer to the official notifications of his vacation of the office of rector, at those respective parishes, rather than to his date(s) of death. — Robin Cary Askew, 15 August, 2009


text:
But fear not - there is plenty to explore...Shop all Mini Logo Shop sale Mini Logo
Black is back and Mini Logo knows how to make black ride as badass as it looks. The Mini Logo 100 K12 Skateboard Deck is lightweight with an extra deep concave while still providing excellent pop and response for all your skating needs.
The Mini Logo K12 deck has a double kick nose with extra deep concave that adds significant stiffness to the deck. The deck is lighter and thinner, but doesn't lose any pop or response. The deck also features a steep, flat nose and tail.
Nose 6.875 in/ /Tail 6.625 in
|Size (in)
|31.875 x 8
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Available Colors
- Black
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Click here to view an image of each option.
Aduro Facio iPad Case and Bluetooth Keyboard
A colorful folio case opens up to reveal a snugly cradled iPad and wireless keyboard or a ransom note explaining that both items have been kidnapped. The Bluetooth keyboard is removable, allowing users to type at a comfortable distance from the screen or take the keyboard out entirely to transport the iPad alone.
- Durable iPad case folds up into a stand
- Bluetooth wireless keyboard for comfortable typing
- Keyboard is removable, unlike the memory of your first goldfish, Ariel, a dreamer who longed to be part of your world
- Case comes in five colors
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- Fits iPad 2, 3, and 4
- Includes a USB charging cable
How to get your goods: by purchasing this Groupon and providing your name and shipping address, your order is complete!
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Architecture Major
My favorite Marywood moment was the first weekend of freshman year!
see all Ambassador profiles »
Nutrition and Dietetics Alum
Working for Powerbar, I've met many professional and world-class athletes. I then started my own software company, Visual Veggies Software.
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Dan Schauer
Program Coordinator
Phone: 503-846-6287
Email: firstname.lastname@example.com
Carol Renaud
Program Specialist
Phone: 503-846-6286
Email: email@example.com
Dan Schauer and Carol Renaud are transferring to Washington County and remain on CPO staff. The CPO office will continue to be located at the County Public Services Building, 155 N. First Ave, Suite 200, Hillsboro, OR 97124. After July 1, Web content will begin moving to the Washington County site. Later in 2016, the Washington County Public Services Building seismic retrofit construction project will involve relocating all employees, in phases. Stay tuned.
Change for Beth St. Amand: Beth, CPO Coordinator from June 2014 to May 2016, became the STEM Beyond School Outreach Coordinator with OSU Extension Service-Washington County. Phone: 503-821-1114, Email: firstname.lastname@example.com.


text:
Excessive sodium reabsorption by the kidney has long been known to participate in the pathogenesis of some forms of hypertension. In the kidney, the final control of NaCl reabsorption takes place in the distal nephron through the amiloride-sensitive epithelial sodium channel (ENaC). Liddle's syndrome, an inherited form of hypertension due to gain-of-function mutations in the genes coding for ENaC subunits, has demonstrated the key role of this channel in the sodium balance. Although aldosterone is classically thought to be the main hormone regulating ENaC activity, several studies in animal models and in humans highlight the important effect of vasopressin on ENaC regulation and sodium transport. This review summarizes the effect of vasopressin V2 receptor stimulation on ENaC activity and sodium excretion in vivo. Moreover, we report the experimental and clinical data demonstrating the role of renal ENaC in water conservation at the expense of a reduced ability to excrete sodium. Acute administration of the selective V2 receptor agonist dDAVP not only increases urine osmolality and reduces urine flow rate but also reduces sodium excretion in rats and humans. Chronic V2 receptor stimulation increases blood pressure in rats, and a significant correlation was found between blood pressure and urine concentration in healthy humans. This led us to discuss how excessive vasopressin-dependent ENaC stimulation could be a risk factor for sodium retention and resulting increase in blood pressure.
- water conservation
- antidiuresis
- sodium excretion
- collecting duct
vasopressin was first identified as a pressor hormone and later recognized to be also a potent antidiuretic hormone. Today, these early historical discoveries have been explained by the identification of different receptor types. V1a receptors (V1aR), abundantly expressed in vascular smooth muscle cells, and signaling through calcium and phosphatidylinositol transducer pathways, are responsible for the pressor effects. V2 receptors (V2R), expressed mainly in principal cells of the renal collecting duct (CD), and signaling through cAMP, mediate the antidiuretic actions of the hormone (113).
Vasopressin is elevated in some forms of human hypertension (26, 92, 111) and in animal models of hypertension (see reviews in Refs. 91 and 108). This hormone has long been suspected to play a role in blood pressure control because of its vasoconstrictive effects, well demonstrated in vitro. However, the studies trying to evaluate the contribution of V1aR-dependent effects in hypertension are inconclusive [either in favor of (27, 35, 70) or against (59, 98)].
Excessive sodium reabsorption by the kidney is known to participate in the pathogenesis of some forms of hypertension. Among the genes responsible for monogenic forms of blood pressure disorders identified to date, the majority either mediate renal sodium transport in the distal part of the nephron or are involved in its regulation. Loss of function of the corresponding proteins leads to salt-wasting states with hypotension (48), and gain of function to salt-retaining syndromes and hypertension. Liddle's syndrome, a severe and hereditary form of early onset hypertension, is due to gain-of-function mutations in the genes coding for either the β- or γ-subunits of the epithelial sodium channel, ENaC (41, 93). Patients exhibiting this syndrome have strongly increased ENaC activity (53, 82). If a permanent activation of ENaC is sufficient to induce severe hypertension, more subtle stimulation of ENaC by hormones or mediators could participate in essential hypertension (77).
ENaC is expressed in several excretory organs including the salivary glands, colon, and kidney. In the salivary glands and colon, aldosterone is the main hormone regulating ENaC abundance and activity. However, in the principal cells of the CD, vasopressin regulates ENaC activity, in addition to aldosterone. Vasopressin and V2R agonists thus not only increase water permeability of the CD but also stimulate sodium reabsorption (88, 90, 99). Accordingly, excessive vasopressin-dependent ENaC stimulation could potentially be a risk factor for sodium retention and an increase in blood pressure. This sodium-retaining effect of vasopressin may probably be additive to that occurring upstream, on the Na-K-Cl cotransporter (NKCC) in the thick ascending limb and on the Na-Cl cotransporter (NCC) in the distal convoluted tubule (31, 64, 65, 74). The hormone levels required for these actions in the different parts of the distal nephron may differ and may exhibit significant species differences (5, 55). Moreover, even if vasopressin also influences NKCC and NCC activity, ENaC in the CD is the last transporter where a final regulation of sodium excretion can occur.
Vasopressin and aldosterone are released in response to different stimuli and act in different ways. The action of aldosterone is obviously linked to the need to conserve sodium. The renin-angiotensin-aldosterone system (RAAS) is stimulated by a low-sodium diet, and aldosterone increases sodium reabsorption in the distal nephron, as it does in the gut. In contrast, vasopressin is not known to be secreted in response to low sodium intake. It is secreted in response to increases in plasma osmolality, and mostly to hypernatremia, usually indicating a water deficit. Thus, why is renal ENaC regulated and activated by vasopressin? This review presents experimental and clinical data demonstrating the role of renal ENaC in water conservation at the expense of a reduced ability to excrete sodium and explains how this vasopressin-dependent function might contribute to salt-sensitive hypertension.
Vasopressin, ENaC, and Urinary Sodium Excretion
In the rodent and human kidney, ENaC is most abundantly expressed in the luminal membrane of connecting tubule cells and in principal cells of the CD, mainly in its cortical and outer medullary parts. The activity of this channel is considered to be the limiting step for sodium reabsorption in these segments. In the rodent and human kidney, the same cells express the V2R on their basolateral membrane, and aquaporin-2 (AQP2), the vasopressin-regulated aquaporin, on their luminal membrane (Fig. 1A). This coexpression of V2R, AQP2, and ENaC is also observed in the amphibian urinary bladder, often used as a model of the mammalian CD. A number of other mediators possess specific receptors and have been shown to act specifically on the same cells, including prostaglandins, dopamine, bradykinin, endothelin, and α2-adrenergic agonists.
Different time course and mechanism of vasopressin and aldosterone effects on ENaC.
The major action of hormones involved in ENaC regulation is an alteration in channel density at the apical membrane (20). Most of the effect of aldosterone on sodium membrane transporters occurs over hours and involves the synthesis of specific proteins. Acute aldosterone-mediated ENaC activation by rapid, nongenomic mechanisms has been observed in isolated rabbit principal duct cells (112) and cortical CD cell lines (see review in Ref. 43), but the relevance of these effects in vivo are unknown. On the contrary, the rapid effects (minutes) of vasopressin on its target tissues are well established and can be reversed quickly because of the short biological half-life of the hormone. Sustained high vasopressin levels (for days) may also induce a long-term regulation of ENaC as explained below.
In several cell and tissue models, the addition of vasopressin or cAMP agonists induces a rapid increase in ENaC activity. The increase in sodium transport occurs mainly by increasing channel density at the apical membrane through targeting and fusion of ENaC-containing vesicles (21). The translocation of ENaC to the apical membrane is facilitated by a vasopressin-induced increase in expression of an ubiquitin-specific protease (Usp10) that stabilizes sorting nexin 3 (18). On removal of a V2R agonist, ENaC is endocytosed from the membrane surface and reorganized into recycling vesicles, with a mechanism similar to that described for AQP2 regulation (21). Aldosterone also increases the abundance of ENaC at the apical membrane, mainly by decreasing ENaC internalization through the synthesis of SGK1, a kinase that negatively modulates the action of Nedd4–2 (28, 36, 96). Recent data suggest that the regulation of sodium transport is probably not only accounted for by changes in apical channel density but also by proteolytic maturation of its subunits and changes in open probability of the channel (19, 50, 83). The present models of proteolytic regulation of ENaC comprise intracellular action of furin and furin-like convertases at the Golgi and final activation by membrane-bound proteases or soluble proteases present in the extracellular milieu (49, 83). Furin and prostasin have been identified as activators of ENaC by releasing inhibitory peptides from the α- and γ-subunits that increase the channel open probability. Additional proteases can process the γ-subunit (CAP2, kallikrein, elastase …). However, the identification of tissue-specific proteases and the mechanisms of regulation of these proteases remain to be elucidated (50). It has been shown that aldosterone reciprocally regulates the expression of prostasin and protease nexin-1, an endogenous prostasin inhibitor (66). Our recent findings suggested that prostasin could be involved in the effect of vasopressin on ENaC (87), favoring the increase in channel open probability observed by Bugaj et al. (19) in the isolated murine CD.
In addition to the differing kinetics of the action of aldosterone and vasopressin, these two hormones also differ by their long-term effects on the abundance of ENaC subunits. In most aldosterone-sensitive tissues, aldosterone regulates the abundance of ENaC subunits at both the mRNA and the protein level (4, 32, 79). Surprisingly, however,, in the kidney aldosterone does not increase the abundance of β- and γ-subunits (the 2 subunits in which gain-of-function mutations induce Liddle's syndrome) and has only a very modest effect on the α-subunit (4, 32, 58, 106). In contrast, administration of vasopressin or the V2R agonist dDAVP in rats has been shown to increase significantly the abundance of the mRNA coding for these two subunits and of the corresponding proteins (Fig. 2, A and B) (30, 34, 68, 87). Salt-sensitive Sabra (SBH) rats, known to have higher vasopressin secretion and higher urine osmolality than their salt-resistant counterparts (108, 109), also have a higher abundance of β- and γ-subunits in kidney cortex (67). Moreover, changes in dietary salt intake in SBH rats did not modify ENaC subunit abundance, while an increase in water intake significantly lowered ENaC expression (67) (Fig. 2C) without affecting serum aldosterone level (67, 87). As shown in Sprague-Dawley rats, the vasopressin-induced increase in ENaC subunit abundance allows more intense sodium reabsorption in the CD upon acute stimulation by dDAVP (68) (Fig. 3A).
Studies of in vitro perfused cortical CD or of cell lines derived from amphibian bladder have shown that vasopressin and aldosterone exert synergistic actions on ENaC-mediated sodium transport (19, 22, 44, 78, 102). As illustrated in Fig. 3, B and C, the acute effect of vasopressin on sodium reabsorption in cortical CD from rats or mice is markedly potentiated by chronic stimulation of mineralocorticoid receptors (19, 90). The different mechanisms of action described above could account for at least some of the synergism between aldosterone and vasopressin. Moreover, it was shown in vitro that phosphorylation of Nedd4–2 by SGK1 or PKA, triggered by aldosterone or vasopressin, respectively, is a central point of convergence for ENaC regulation by the two hormones (94, 95). In this review, we purposely focused mainly on the influence of vasopressin on ENaC. However, because of the synergism observed in vitro, vasopressin may have only a modest effect on ENaC activity in vivo in situations in which aldosterone levels are very low.
Effects of ENaC stimulation by vasopressin on renal sodium excretion in vivo.
Could the V2R-mediated effects on ENaC and sodium reabsorption demonstrated in vitro contribute to sodium retention in vivo? A theoretical calculation suggests that it should, as explained in Fig. 1B. Recent observations in vivo confirm that vasopressin significantly reduces sodium excretion. The acute administration of the potent and selective V2R agonist dDAVP not only increased urine osmolality and reduced urine flow rate but also reduced sodium excretion in rats (75) and humans (10) (Fig. 4). In patients with nephrogenic diabetes insipidus (DI) due to loss-of-function mutations of either AQP2 or V2R, dDAVP was unable to increase urine osmolality. However, it reduced sodium excretion in those with AQP2 mutations but not in those with nonfunctional V2Rs (10) (Fig. 4). In the isolated erythrocyte-perfused rat kidney (allowing good oxygenation of the medulla and thus operation of the concentrating mechanism), addition of dDAVP to the perfusate increased urine osmolality and decreased both urine output and fractional sodium excretion (52). This suggests that the effect observed in vivo is due to an intrarenal mechanism. The effect of dDAVP on sodium excretion is probably due, in large part, to a V2R-dependent ENaC-mediated increase in sodium reabsorption in the CD because prior administration of amiloride prevented the antinatriuretic but not the antidiuretic effect of dDAVP in water diuretic healthy subjects (16).
Besides these recent demonstrations of a direct negative V2R influence on natriuresis, several previous studies in normal rats and healthy humans showed that sodium was excreted faster or with a higher fractional excretion rate when hydration and thus urine flow were increased above normal, suggesting that a low urine flow impaired sodium excretion to some extent (2, 3, 12, 17, 23, 51, 63) (Table 1).
The effect of vasopressin on sodium reabsorption probably requires a higher hormone concentration than the effect on water reabsorption and is detectable only when urine osmolality reaches a certain threshold, as observed in vitro and in vivo in rats and humans. In the isolated, perfused rat cortical CD, a relatively high vasopressin concentration in the bath was needed to significantly stimulate sodium flux while water flux responded to much lower concentrations (Fig. 5A) (5, 90). In normal rats, acute V2R antagonist administration increased urine flow rate and sodium excretion dose dependently, but the effect on sodium was of much lesser magnitude than that on water and required a higher drug concentration (Fig. 5B) (75). In healthy humans undergoing water diuresis, a very low infusion rate of vasopressin reduced only the urine flow rate whereas a larger infusion rate (still within physiological limits) reduced both urine flow rate and sodium excretion (3).
In normal life (without any intervention), a fall in sodium excretion or fractional excretion is observed only when urine osmolality rises above a certain threshold (∼500–600 mosmol/kgH2O) (Fig. 6) (12, 63), suggesting that in humans also, a higher level of vasopressin is required to influence sodium reabsorption than water reabsorption. Moreover, these data reveal that a reduction in the efficiency of sodium excretion with increasing urine concentration occurs in about one-third of the urine samples obtained from healthy individuals in their usual lives.
When vasopressin levels reach pharmacological levels or are inappropriately high, a natriuretic action progressively compensates and even largely overcomes the antinatriuretic V2R-mediated effect. This vasopressin-induced natriuresis is mostly due to V1aR-mediated actions (5, 47, 75). This explains why vasopressin has often been described to be natriuretic. However, the level of vasopressin required to induce this V1aR-dependent natriuretic effect is probably not often reached in normal conditions (75).
It is important to stress that the intensity of the urine concentration process resulting from vasopressin action on the CD does not depend solely on the plasma level of vasopressin. Several hormones and mediators are known to interfere with the cellular effects of vasopressin by acting on phosphodiesterases that promote the degradation of cAMP in CD cells (Fig. 1A) (5). Thus, for a given vasopressin level, the intensity of vasopressin's effects on water and sodium reabsorption will depend on the level of all other mediators acting simultaneously on the same cells. For example, it is well established that prostaglandins counteract the antidiuretic action of vasopressin, whereas nonsteroidal anti-inflammatory drugs (NSAID) potentiate it. Although less often mentioned, these mediators also influence its antinatriuretic action in the same way. This may, at least in part, explain the well-known sodium retention induced by NSAID in vivo (42) as also observed in the isolated kidney in vitro (52). Activation of V1aR in the apical membrane of CD principal cells and in interstitial medullary cells is known to stimulate prostaglandin production and may thus attenuate V2R-mediated effects (5, 75). Bradykinin has also been shown, both in isolated, perfused rat CD and in transgenic mice, to attenuate vasopressin action on water and sodium transport (99) and urine concentration (1).
Water Conservation at the Expense of Less Efficient Salt Excretion
Sodium and water conservation or excretion are often associated. A highly effective control mechanism keeps sodium concentration in plasma and extracellular fluids within narrow limits. Vasopressin is a critical hormone in this homeostatic regulation because the osmoreceptor neurons that influence vasopressin release are most sensitive to extracellular sodium concentration. An increase in plasma sodium concentration will stimulate vasopressin release, which will in turn promote water reabsorption, but also impair to some extent the ability of the kidney to excrete sodium because of vasopressin's effect on ENaC. This regulatory pathway is counterbalanced by the pressure-natriuresis mechanism. An increase in extracellular fluid volume due to water and sodium retention induces an increase in blood pressure, which, in turn, reduces isosmotic sodium and water reabsorption in the kidney and allows readjustment of the extracellular fluid volume. Note that during pressure-natriuresis, sodium and water excretions are increased simultaneously and to the same extent (83). This pathway brings sodium balance back to normal, at the expense of an increase in blood pressure (40). All individuals are not equally sensitive to salt excess. "Salt-sensitive" subjects exhibit larger changes in blood pressure than "salt-resistant" subjects when submitted to abrupt changes in salt intake (62, 105). Presumably, the osmoreceptor-vasopressin-thirst system may play a role in the magnitude of salt-dependent changes in blood pressure. The influence of aldosterone on ENaC activity in both the colon and kidney suggests a role for this channel in sodium conservation. However, the fact that, in the kidney, ENaC is also regulated by vasopressin suggests that ENaC may, in addition, play a role in water conservation.
As explained above, low levels of vasopressin probably act only, or mostly, on water permeability, whereas with higher levels of vasopressin, sodium reabsorption is also stimulated and promotes additional water reabsorption. These differences in vasopressin's influence on water and sodium handling may be due to the different distribution of AQP2 and ENaC along the CD. Even modest increases in water permeability will favor water reabsorption along the entire CD, including its medullary portion lying in a hyperosmotic environment. However, in the cortex, osmotic equilibration with the surrounding interstitium likely occurs relatively early along the collecting system (connecting tubule and initial cortical CD). Thus, in later sections of this collecting system within the cortex and outer medulla, more water can be reabsorbed only if solutes are reabsorbed (89). ENaC-mediated sodium reabsorption creates an osmotic driving force that allows an additional (isosmotic) reabsorption of water (89). Such isosmotic water and sodium reabsorption in the cortex leaves sodium concentration in the lumen unchanged (68) but concentrates all other solutes in the tubular fluid and thus favors final urine concentration. As recalled earlier, vasopressin is not secreted in response to a sodium deficit. Thus its ability to regulate ENaC activity and abundance is not likely related to the need to conserve sodium. Rather, based on the observations listed above, we propose that the action of vasopressin on ENaC is intended to conserve water by allowing more water to be reabsorbed from the CD, thus enhancing the concentration of other solutes and reducing the amount of water required for their excretion. Water conservation is favored at the expense of less efficient sodium excretion.
Interestingly, a similar improvement in water conservation occurs with urea (Fig. 7). Although the kidney needs to excrete a relatively large daily load of urea (on a normal protein intake), the vasopressin-dependent urea transporter UT-A1, located in the terminal inner medullary CD (54), allows significant amounts of urea to be reabsorbed. This improves urea accumulation in the medullary interstitium and favors overall urine concentration (33), but results in less efficient excretion of urea (like for sodium with the effect on ENaC), as illustrated by the fall in fractional excretion of urea with declining urine flow rate (8). Thus vasopressin's actions on ENaC in the cortex and outer medulla, on the one hand, and on UT-A1 in the inner medulla, on the other, can be viewed as two independent and additive means to improve water conservation (Fig. 7). The less efficient urea excretion due to vasopressin action is compensated for by an increase in plasma urea level that allows more urea to be filtered (8, 17). The less efficient sodium excretion may secondarily induce pressure-natriuresis. This concept is also supported by the finding of reduced blood pressure dipping at night (hence a relative nocturnal hypertension) in subjects in whom sodium and water excretion during the daytime is an abnormally low fraction of the total 24-h excretion (6, 7, 37). When subjects are in a steady state, the influence of urine flow rate on diuresis/natriuresis is not discernable in 24-h urine because the nighttime period compensates for changes occurring during the daytime period (or vice versa in rats which are active mostly during the nighttime).
Water Conservation and Blood Pressure: Pathophysiological Observations
The data reported above demonstrate that vasopressin's effects on ENaC result in better water conservation but less efficient sodium excretion. This effect of vasopressin on sodium reabsorption could influence blood pressure in the long term, as described below.
Effects of V2 agonist or antagonist on blood pressure.
Several observations in rats suggest that long-term V2R agonist stimulation in vivo induces a rise in blood pressure. In Brattleboro rats with central diabetes insipidus, DOCA-salt administration induces an increase in blood pressure only if AVP or the selective V2 agonist dDAVP is infused, and the degree of hypertension is proportional to the dose of dDAVP (14, 86). In Brattleboro rats, blood pressure rises less after induction of "one kidney-one clip" hypertension than in control Long-Evans rats, a difference abolished by chronic dDAVP infusion (107). In normal Sprague-Dawley rats, long-term infusion of dDAVP has been shown to raise blood pressure by ∼10 mmHg without significant change in volemia (34, 60, 61) and to aggravate DOCA-salt hypertension (34) (Table 2). This blood pressure effect is favored by unilateral nephrectomy or saline infusion and is potentiated by inhibition of the renin-angiotensin system (13) (Table 2). In rats with adriamycin-induced nephropathy, with DOCA-salt hypertension, or a combination of both, treatment with a selective, nonpeptide V2R antagonist for 10 wk significantly reduced or entirely prevented the rise in blood pressure usually seen in these models (70–72).
Complexity of vasopressin action on blood pressure.
The effects of V1a on vascular smooth muscle are thought to raise blood pressure. However, in the hypertensive rat model induced by nitric oxide (NO) inhibition, in which vasopressin levels are known to be elevated, chronic treatment with a selective V1aR antagonist unexpectedly increased blood pressure further (56). This antagonist probably inhibited the natriuretic V1aR-mediated effect and unmasked the antinatriuretic V2R-mediated effect (75). This study suggests that, when endogenous vasopressin secretion is elevated in some pathological situations, V1aR-mediated effects may counteract the V2R hypertensive effects. Other mechanisms favoring natriuresis could also counterbalance the antinatriuretic V2 effects, including suppression of plasma renin activity or aldosterone secretion and increase in plasma atrial natriuretic peptide, as observed in the syndrome of inappropriate secretion of antidiuretic hormone (80). Moreover, complex specific tissue interactions were shown between V2 and V1a effects, at the epithelial and vascular levels (25). Acute regional vasodilator and hypotensive effects of dDAVP mediated by endothelial V2R and NO production have been reported in healthy humans and animals (15, 45, 97, 101, 103).
In summary, several local or peripheral compensatory mechanisms may offset the vasopressin/ENaC-mediated effect on blood pressure. The resulting increase in blood pressure is likely small and does not reach pathological values. However, in the presence of other aggravating factors, vasopressin could contribute to sodium retention and become one of the multideterminants of salt-dependent hypertension.
Vasopressin and blood pressure: effects of gender, ethnic background, and geographic location in humans.
Men are known to be more susceptible to hypertension than women. Studies have shown that men have higher vasopressin levels than women and that the antidiuretic effect of a given dose of vasopressin is stronger in men than in women (76). This could contribute to their greater susceptibility to hypertension.
It is conceivable that a higher urine concentration, especially during the daytime, may induce a temporary sodium and water retention that favors a rise in blood pressure. In young normotensive Americans (age range 18–40 yr), a significant positive correlation was observed between systolic or pulse pressure and mean 24-h urine concentration in men but not in women (11) (Fig. 8). Over the whole range of urine concentration, systolic and pulse pressure were significantly higher in African Americans (AA) than in European Americans (EA) (Fig. 8). Now, AAs show a greater susceptibility to develop hypertension than EAs. Some studies suggest that they have higher vasopressin levels and/or higher urine osmolality (11, 24) and are less able to dilute urine after a water load (104). AAs also have a less active RAAS. This has been proposed to be part of corrective mechanisms involved in maintaining sodium balance in response to sodium retention (85). As proposed earlier, there may be a balance between the RAAS and the osmoreceptor-vasopressin-thirst system, with a stronger influence of the latter in AAs than in EAs (11, 57).
In a large worldwide association study, significant associations were found between blood pressure and ecological variables such as latitude, temperature, and rainfall, explaining worldwide variation in heat adaptation, as defined by functional alleles in five genes involved in blood pressure regulation (one of the alleles coding for β-ENaC) (110). This suggests an association during evolution between better water conservation (an essential function in heat adaptation) and higher blood pressure. Nephrolithiasis has been repeatedly found to be associated with high blood pressure (69), suggesting that a common factor such as high urine concentration favors the simultaneous occurrence of the two diseases. Smoking is known to be an aggravating risk factor for high blood pressure and cardiovascular events. A rise in vasopressin levels may be partially responsible for some of these adverse effects because nicotine is a potent stimulator of vasopressin release (46, 84).
Taken together, these observations regarding gender and ethnic differences, and associations of high blood pressure with climate, urolithiasis, or smoking, support the notion that hypertension is favored by high urine concentration and hence by the balance between the antidiuretic/antinatriuretic action of vasopressin and the counteracting effects of other humoral factors acting on the CD.
Water conservation and blood pressure: evolutionary aspects.
In ancestral times, salt intake was low and it was appropriate to conserve simultaneously salt and water. Reabsorbing sodium to conserve water had no adverse consequences. The present Western-type diet provides significantly more sodium and less potassium than prehistoric food. The typical balance between the RAAS and the thirst-vasopressin system is still the same although water conservation is no longer crucial. To date, conserving water and sodium simultaneously is less necessary, at least in Western countries. Moreover, natural selection during human evolution may have favored the survival and expansion of subjects with a good ability to conserve water, even if the price to pay was a poor, or rather a delayed capacity to excrete sodium. Poor water conservation increases the risk of dehydration and death within a few days, whereas a poor sodium excretory capacity has only long-term adverse effects by raising blood pressure and favoring cardiovascular diseases later in life, usually after the age of reproduction, thus without influence on natural selection.
Moreover, changes in diet from the hunter-gatherer civilization to present living conditions probably makes aldosterone and the renin-angiotensin system less important than it was in primitive humans. In this context, and without enough time for significant evolutionary changes, we hypothesize that the osmoreceptor-vasopressin-thirst axis has reached a greater influence in the overall regulation of water and salt homeostasis.
In conclusion, the studies reviewed above suggest that the effects of vasopressin on renal ENaC abundance and activity are part of a mechanism that contributes to water conservation at the expense of less efficient sodium excretion. Vasopressin, which is elevated in some forms of hypertension, could contribute to a rise in blood pressure, not by its V1aR-mediated effects (that actually facilitate sodium excretion) but by its V2R-mediated effects. High salt intake would probably not affect blood pressure in salt-sensitive individuals did the kidney dispose of larger amounts of water to excrete the salt. In Western countries, with a long life expectancy, relatively high levels of salt intake and less risks of dehydration, it might be appropriate to reduce, even if only modestly, the spontaneous tendency to conserve water (i.e., to concentrate urine) that occurs at certain times of the day, to accelerate sodium excretion after each intake. It is, however, difficult to increase fluid intake deliberately above what natural thirst commands. Even subjects with recurrent, painful nephrolithiasis often do not succeed in raising their urine output above the recommended amount of 2 liters/day (9, 73). In this context, it will be interesting to see whether newly designed "aquaretics" (selective vasopressin V2R antagonists) (29, 38) are able to reduce salt-sensitive hypertension with fewer side effects than classic diuretics. Interestingly, V2R antagonists have been shown to increase sodium excretion in cirrhotic patients (39). It is conceivable that hyponatremic heart failure or cirrhotic patients, resistant to classic diuretics, may increase their sodium excretion if the diuretic is associated with a small dose of a vasopressin receptor antagonist, promoting a moderate increase in urine flow rate. Finally, it will be interesting to see whether tolvaptan treatment in patients with polycystic kidney disease (100) will prevent or retard the development of hypertension, in addition to reducing cyst expansion.
No conflicts of interest, financial or otherwise, are declared by the authors.
The authors thank Tilman B. Drueke (INSERM ERI-12, Amiens, France) and Dominique Guerrot (INSERM U702, Paris, France) for valuable discussions and editing of the manuscript.
- Copyright © 2010 the American Physiological Society
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VOICES Ideas and Insight From Explorers
Tag archives for honey
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