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Yobetit brand ambassador proudly wears Yobetit brand
Matthew visited the Yobetit office during a quick break from training to give an update on his progress, and this is what they learnt…
Yobetit's 'Top Dog' and ambassador Matthew Abela has been playing badminton since he was 5-years-old, and it doesn't seem like he plans on stopping any time soon. During his discussion with Yobetit, Matthew shared that his badminton journey was influenced by his family.
He explained;
"My father and uncles played badminton so naturally I got into the sport,"
Matthew's love of the sport continued to grow over the years and he began competing professionally at a young age, travelling to compete internationally at just 16. During his talk with Yobetit, he expressed that badminton has helped him to mature as a person - on court and off court he is able to be more organised and focused.
In his early years of competing, Matt said he would be 'nervous' and it would affect his game. But as time passed and with more practice, he has grown more confident and developed a pre-game routine to help calm his nerves. He explained;
"The day before I compete I try to get some time to myself to be alone and find my focus so I can compete with a clear mind."
Undoubtedly, it has worked. Matthew grew to become Malta's number one badminton player, but it didn't stop there. Matthew is working hard to learn and improve as much as he can, whenever he can. He was most recently awarded a Bronze medal for his performance in the Algiers International, which was awarded to him by Joseph Muscat. And with the help of Yobetit he is able to push boundaries he wouldn't have been able to before.
How has Yobetit helped Matthew Abela so far?
Over the past year Matt has increased the number of competitions and is focusing a lot of his attention on his games thanks to the help from Yobetit. From preparing, mentally and physically to travelling to compete in the best competitions available, Matthew is loving every minute of it - and he is doing it all with the Yobetit logo sitting proudly below his right shoulder, and close to his heart.
Yobetit has helped Matthew both financially and supportively, and he is very grateful for their endeavour together. "I am proud to wear the Yobetit brand when I'm competing," he expressed.
Matthew is competing in international competitions representing Yobetit and sharing his progress on his social media platform along the way. Presently, Matthew is training for his competitions to come to ensure he has
"good physical form, enough practice and pre-season training"
What's next for Matthew?
Matthew is passionate about badminton, but it is clear that it is not just solely a personal endeavour, as he would love for the badminton presence in Malta to grow. His long-term goal is to be able to build a badminton court in Malta for all to use, and such passions are what make him such a perfect ambassador for Yobetit. He is confident and driven, the perfect qualities to represent a thriving and passionate bookmaker.
This year Matthew will be travelling to 12 different countries, and Yobetit will make sure to support the rising star throughout. His first stop is Bulgaria for the Eurasia Bulgaria Open in August, and Yobetit wishes him all the best!


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George Hughes Davis, 81, passed away on November 3, 2018.
Mr. Davis was the son of the late Hugh and Catherine Mills Davis.
Survivors include his wife, Lela Davis; children, Ledra Davis Woodlee, Stephen (Pam) Davis, Stan (Katie) Davis; brothers, Ray, Porter and Lee Davis; and grandchildren, Colin Davis, Nick Davis, Ben Davis, Pepper Davis, Annie Davis.
Memorial services will be held Wednesday, November 7, at 4 p.m. in the Smith Memory Chapel. The family will receive friends from 2 to 4 p.m. prior to the service. The Revs. Chad Mantooth and Irby Stanley will officiate.
In lieu of flowers memorials maybe made to the Winder First Baptist Church building fund.
Smith Funeral Home, Winder, has charge of arrangements.
George Davis (11-03-18)
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text: This home has it all when it comes to country style living. Welcome in to this gorgeous home on 5.8 acres with 4bed and 3.5 baths open concept ranch style home. Award winning Argyle ISD school district and amazing proximity to Highways and the University this home couldn't be situated any better. From the spacious exterior acreage to the spacious interior with split bedrooms for kids and parents on opposite sides of the home, this home really gives you a country retreat in the city. Additional Guest quarters or apartment above the barn allows for you to rent it out or use it as additional space for your needs. No HOA allows for you to add to your space as much as you need. Matterport VR tour available.


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Supplication against Showing Off in Worship (riya')
(The following supplication was mentioned by Shaikh Habib Umar DB)
Purification from showing off in acts of worship (riya')
The Prophet salAllahu 'alayhi was-salam said:
"Shirk (attributing partners to Allah) is harder to detect amongst you than the crawling of an ant but I will guide you to something which if you do it Allah will remove from you the lesser shirk and the greater shirk."
He then taught them this du`a. What is meant by the greater shirk is worshiping gods alongside Allah and lesser shirk is riya' or showing off in acts of worship, and this du`a is a protection from both types:
الَّلهُمَّ إِنِّي أَعُوذُ بِكَ أَنْ أُشْرِكَ بِكَ وأَنا أَعلَمُ وأَستَغفِرُكَ لما لا أَعلَمُ
Allahumma inni a`udhu bika an ushrika bika wa ana a`lamu wa astaghfiruka lima la a`lamu
"O Allah I seek refuge in You from knowingly associating partners with You, and I seek Your forgiveness for that which I do not know."
(3 times in the morning and 3 times in the evening)
Please feel free to benefit and share with others.
-{This Dua is found in: Ahmad 4/403. See also Al-Albani, Sahihul-Jami' As-Saghir 3/233 and Sahihut-Targhib wat- Tarhib 1/19.}


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What is OSHA and How Does it Affect Businesses?
Congress enacted the Occupational Safety and Health Act of 1970, which created the Occupational Safety and Health Administration (OSHA). OSHA's mission is to help employers and employees reduce on the job injuries, illnesses, and death by directing national compliance initiatives in occupational safety and health. OSHA, though often considered a nuisance, actually helps businesses protect their workers and reduce the number of workplace accidents. Since 1970, workplace deaths have been reduced by more than sixty percent, and occupational injuries and illnesses have declined forty percent. In addition – and what most industrial businesses fret over – OSHA has conducted close to forty thousand inspections and has issued over eighty-five thousand citations for safety violations.
Below are the ways and methods OSHA rules and regulations affect businesses:
Increased Inspections – OSHA has an exorbitant budget and has increased its hiring of inspectors over the years. In addition, the agency is shifting personnel away from its cooperative programs and toward enforcement.
Large Fines if Found Noncompliant – Even though Congress has not passed legislation to increase the maximums for OSHA fines, the agency believes it can raise fines itself by changing the way fines are calculated.
Regulation Through Embarrassment – OSHA hopes public condemnation of business activities that result in serious injury or death will act as enough of a deterrent. The agency plans to issue more hard-hitting press releases that clearly explain why an employer faced a steep fine.
Inspectors Interview Employees – During every inspection, OSHA compliance officers will converse with workers privately and confidentially in order to discover if companies are recording injuries as required.
Increased Inspections on Employee Training – OSHA says its inspectors will check whether required and necessary training is conducted by employers in a way that workers can clearly understand.
Injury and Illness Prevention Programs Required – OSHA states that workplaces in the United States need to undergo a paradigm shift, with employers going beyond merely meeting OSHA guidelines and standards. OSHA wants companies to implement risk based workplace prevention programs to uncover hazards before it lead to an injury or death.
Refined Examination of Safety Incentive Programs – OSHA fears that some employers, particularly those in high-hazard industries, have implemented programs (inadvertently or by design,) that discourage injury reporting to prevent outcomes detrimental to business. OSHA inspectors will perform stringent surveillance to discover whether such programs have caused injuries to go unrecorded.
New Regulations will Develop Faster – OSHA is researching several ways to speed development of new standards. OSHA wants to increase collaboration with other worker protection agencies to aid in quicker regulation development.
Implementation of Electronic Workplace Records – OSHA wants to transition to electronic data collection that will force companies to follow certain OSHA standards to report workplace injuries and illnesses electronically.
OSHA requirements for building safety & egress signage can vary from state to state. To learn more about how OSHA affects your business, contact GloBrite Systems.


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2008 Songs (an ongoing list)
Here's my constantly-updating long list of favorite songs of 2008. Perhaps at the end of the year, I'll put together a more concrete list.
6th Sense & Wildabeast "Arcade Fly"
88 Keys "Stay Up"
Atmosphere "Painting", "You", "Yesterday", "The Waitress"
Beck "Gamma Ray", "Modern Guilt", "Walls"
Big Boi "Royal Flush", "Some Things"
Black Keys "Psychotic Girl", "Strange Times"
Blue Scholars "Butter & Guns"
Bun B "II Trill", "That's Gangsta", "Damn I"m Cold", "Swang On Em"
Busta Rhymes "Don't Touch Me", "I Got Bass"
Cadence Weapon "House Music"
Caitlin Rose "Dead Flowers"
Cat Power "Song To Bobby"
Chester French "She Loves Everybody"*
Ciara "High Price"
Cool Calm Pete "Gitty Up Baby"
The Cool Kids "Action Figures"
Danny "I Don't Know"
Department of Eagles "No One Does It Like You"*
DJ Babu/MOP "Dearly Departed"
Duffy "Mercy"
Envelope "Looking In", "Day Dream Nation"
Estelle & Kanye West "American Boy"
The Game "Bulletproof Diaries", "House of Pain", "Dope Boys", "Letter To The King"
Gnarls Barkley "Who's Gonna Save My Soul", "Run"
Grip Grand "Remember The Time"
Guilty Simpson "I Must Love You", "Run"
GZA "Life Is A Movie"
Izza Kizza "Walk The Dawg"
Jake One/Freeway/Brother Ali "The Truth"
Jenny Lewis "Acid Tongue"
Kanye West "Love Lockdown"
Kid Cudi/Wale "Is There Any Love"
Kidz In The Hall & El-P "Drivin Down The Block"
Killer Mike "I Gotcha"
Lil Wayne "A Milli", "Shoot Me Down", "Dr. Carter", "Tie My Hands"
Man Man "Whalebone"
Morcheeba/Cool Calm Pete "One Love Karma"
Murs "Can It Be"
Mystery Jets "Young Love" (Shoes remix)
NERD "Anti Matter", "Sooner or Later"
Neon Neon "Raquel"*
Nick Cave & the Bad Seeds "Dig Lazarus Dig"
Pharoahe Monch "Broken Heart"
Portishead "Machine Gun"
Ray Lamontagne "You Are The Best Thing"
Rhymefest "Can't Make It", "Get Up", "No Sunshine"
Rick Ross "The Boss"
The Roots "Rising Down", "75 Bars", "Criminal", "Birthday Girl"
RZA "You Can't Stop Me Now", "Drama"
Schwayze "Buzzin"
Sheek Louch "Good Love"
Silver Jews "Suffering Jukebox"
Snoop Dogg "Why Did You Leave Me"
Stephen Malkmus "Baltimore"
T.I. "No Matter What"
T-Mo Goodie "Connect Like Dots"
Tobacco/Aesop Rock "Dirt"
Trina/Killer Mike "Look Back At Me"
Usher "Love In This Club"
Vampire Weekend "Cape Cod Kwassa Kwassa"
Wale/Bun B/Pusha T "Back In The Go Go"
Young Jeezy "My President"
* = may have been out in 2007


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Browse By
hundreds of designs to choose from!
Bring a fun playful atmosphere with you to work with these silver monkey cufflinks. Take a look at them for a moment and you'd swear that you're looking at the real thing. Sure each monkey is a classy silver tone, but you can see each of the little hairs around the animal. This set is finely crafted and built for durability. You can wear these monkeys without worrying about them wearing out. Give them as a gift to your favorite coworker, or keep these little monkeys for yourself. They even have crystal eyes that sparkle and glow in the light.
Cufflinks don't always have to be so serious. Bring a little bit of fun into a work day or a formal event with these wild silver monkeys. They have wonderful detail and twinkling crystal eyes.


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String Trick (Cats Cradle) Tutorials
Short how to do videos show you all kinds of neat string
Making a Birch Bark Basket - Video
Create a real birch bark basket for decoration.
Royal Canadian Navy Paper Model Ships
Both fun and educational, Royal Canadian Navy Paper Model Ships in Simplified and Advanced versions
A printable booklet about the pioneers for the grade three level.
Make Your Own Iyaga Game
Create a simple optical illusion
Have fun with these easy pioneer crafts
A real day, real time treasure hunt that'll keep your kids jumping...
Cut out six-sided snowflakes or make a self-sticking snowflake using real snowflake patterns.
Winter~Real Snowflake Patterns
Photographs of real snowflakes help children discover real designs for snow art.
Get an online guide to snow crystals learn to identify snowflake shapes.
The challenge helps every student brush up on knowledge, and its fun! Here are some quizzes to increase your knowledge.
Print this pretend passport for studying world geography ~ Canadian and American pretend passports
Check in with a travelling family and download printable maps of Canada
Create a little of your own weather by making this snowflake in a jar.
Donna Ward/Northwoods Press brings you tried and tested exciting geography links for games, quizzes, and great information. This will enhance every geography study including Canadian History and Geography.


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Hundreds Weigh in on FERC Grid Resiliency Pricing Proposal
The Federal Energy Regulatory Commission (FERC) has been front and center in the energy policy world since the Department of Energy utilized its authority to directly propose its Grid Resiliency Pricing Rule to the independent commission. The notice of proposed rulemaking (NOPR) was placed on the fast track and sent to FERC in late September. Public comments were due October 23 and response to comments were due November 7. FERC will make a decision on the proposal before the end of the year.
If approved, the proposal would guarantee payments primarily to coal and nuclear units with 90 days of on-site fuel storage in certain competitive wholesale markets. The rulemaking says the payments would ensure proper compensation for the reliability and resiliency attributes that these generators provide.
The NOPR has garnered much attention for the substance of the proposal and the process by which it arrived on FERC's docket. Hundreds of commenters – including power companies, elected officials, environmental groups, labor groups, market operators, and trade associations – have weighed in on the NOPR. Many of the comments fit into three main categories:
1. Opposition to the NOPR
2. Support of FERC acting quickly to value resiliency in the marketplace, but proposing a different remedy
3. Support of the NOPR
Opposition to the NOPR
A tranche of comments were firmly against the FERC NOPR. Opposition united some unlikely interests, with groups like the American Petroleum Institute and the Natural Resources Defense Council, all filing comments urging FERC to reject the proposal.
Common themes among this set of commenters includes:
1. The need for FERC to more clearly define resiliency and the problem that the NOPR seeks to address,
2. The concern that cost-of-service payments will cause serious harm to the wholesale markets,
3. The lack of opportunity for meaningful stakeholder involvement due to the expedited rulemaking process,
4. The concern that the Department of Energy's proposal would raise costs for consumers and increase air pollution,
5. The question of whether supporting on-site fuel storage is the best way to improve reliability and resiliency on the grid, and
6. The argument that the NOPR does not meet the legal standard for action
Many commenters opposed to the proposal urged FERC to deny the NOPR, and instead, study and define resiliency on the grid.
We strongly encourage the Commission to use this opportunity created by the Secretary to identify attributes of the current competitive market system that need to be improved, to crisply define them and either modify the current published proposal or initiate regional proceedings to examine resilience issues and consider the need for market rule changes.
-Group of Eight Former FERC Chairs and Commissioners
This DOE NOPR would distort the markets and support power generators that cannot compete with the superior economics of natural gas generation, citing a reliability 'emergency,' even though one has not been shown to exist.
-American Petroleum Institute
…the proposed rule is misguided and fundamentally flawed and represents nothing more or less than corporate welfare that will result in massive harm to American consumers and the American economy.
-Electric Power Supply Association
Support the Problem Statement, Not the Proposed Remedy
Another group of commenters agreed that resiliency should be valued in the wholesale electricity marketplace, that the need for this market reform is urgent, and that FERC is the correct venue for action. However, these commenters did not give a blanket endorsement for the Department of Energy's proposal to ensure cost-of-service payments to certain generators. Instead, many of these commenters offered up alternative solutions or substantive additions to the NOPR's proposed remedy.
For example, ClearPath Foundation proposed two new market-based mechanisms to allow generators with certain resiliency attributes to receive compensation.
Another example is Exelon Corporation, which listed a series of actions that it called on FERC to undertake. This includes:
1. Correcting energy price formation in PJM;
2. Issuing a policy statement declaring that nuclear units that benefit from state programs designed to preserve their operation will not have their offers mitigated in FERC's markets;
3. Directing organized markets to report on other market-based reforms that could help foster resiliency; and
4. Requiring the covered markets to submit detailed information that can be used to develop a richer understanding of where our grid's vulnerabilities lie, how those vulnerabilities match up against the intelligence community's threat assessments, and what steps must be taken to ensure a sufficient degree of resiliency to protect the nation.
(The Secretary of Energy) is asking whether wholesale markets in PJM, NYISO, and ISO-NE – which are designed to ensure we have enough megawatts to serve load- should also be designed to ensure we have the right megawatts to serve load.
Allowing the current situation to continue risks a more vulnerable United States power grid.
-ClearPath Foundation
Support of the NOPR
Finally, a smaller group of commenters came out in support of the FERC NOPR. These commenters agreed that resiliency attributes need to be immediately valued in the wholesale marketplace and that ensuring cost-of-service payments to generators with on-site fuel storage would solve the problem.
Common themes among this set of commenters includes:
1. The argument that today's markets are not pure and are constructed to achieve certain policy goals,
2. The assertion that current rates are not just and reasonable,
3. The finding that fuel-secure generators will continue to retire without urgent FERC action, and
4. The conclusion that the retirement of fuel-secure units will make the grid less resilient and reliable
For example, First Energy's comments call for FERC to direct covered markets to adopt tariff changes that would ensure resilient generators receive a payment each month the covers the gap between what the unit earns in the capacity, energy, and ancillary markets and their full costs of operation and service. In exchange, the units must remain in operation and provide energy and ancillary services when called upon.
Several labor groups, including the Utility Workers Union of America, also came out in support of the NOPR. The Utility Workers Union of America said without FERC action the nation is at risk of losing coal and nuclear plants that provide critical reliability and resiliency attributes.
Getting these markets right is not simply a matter of sound policy, it impacts our members' jobs and communities.
–Utility Workers Union of America
Simply put, the imminent closure of resilient generation presents a clear and present danger to the Nation.


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EAST RUTHERFORD, N.J. -- It's come to this for the New York Jets. The team that will say (almost) anything has undergone a metamorphosis. These Jets will try anything. Almost anything.
"They threw the kitchen sink at us," Houston Texans coach Gary Kubiak said, following Monday night's 23-17 win.
If you're Rex Ryan, why not? Ryan is desperate to save a season that's spiraling down, and he decided to let it fly. A devil-may-care onside kick? After the Jets had closed within six points? Late in the ... third quarter?
Yes. The answers were yes.
Did the Texans recover? And turn the short field into points? Those answers, too, were yes.
Ryan had no regrets. "That was me all the way," he said. "I came here to win. That's it. Whatever it takes. Faking a punt in your own territory, going for it on fourth down in your own territory -- I came to win."
There was another story on Monday night, about the team that did win. The undefeated Texans didn't play great, but they have two great players: running back Arian Foster and defensive end J.J. Watt. The Jets have no one on their roster to rival either.
What they have is a mistake-prone quarterback, Mark Sanchez, who was described last week by offensive coordinator Tony Sparano as "a piece of the puzzle." (Oh. Now they tell us.) And they have a backup quarterback, Tim Tebow, whose role remains a closely guarded secret, including to him.
"No," Tebow replied after the game when asked if he has a clear understanding when and how he will be used. He added that he's always ready when his number is called.
Except for his role on punt team -- no one executes a better fake -- the Jets utilize Tebow almost begrudgingly, as if he were forced upon them. One play here. Two there.
Consecutive carries by Tebow in the red zone for 16 yards ... and off the field he goes. Two Sanchez incompletions follow. And a 21-yard field goal. So much for continuity, imposing of will or rhythm.
The Jets are funny. Out of necessity, they put players like Jeff Cumberland, Jason Hill and Chaz Schilens in position to win or lose plays that will determine the outcome of a game.
They aren't, as of now, willing to do the same with Tebow.
He threw the prettiest pass of the game by a Jet -- make that one of the prettiest passes of the season by a Jet -- on the team's second possession. (Hill, signed last week, couldn't make the catch.) Yet Tebow didn't make another throw in the game.
Sanchez's completion percentage -- already lowest in the league among starters and falling -- has dropped to a pin-the-tail-on-the-donkey 48.4 percent. And the storyline is still that Tebow can't throw?
These Jets are in danger, serious danger, of being defined by their bad luck and considerable failings.
Perhaps you've heard, they've lost Darrelle Revis and Santonio Holmes for the season. That's unlucky.
The Jets can't run the ball or stop the run. And neither looks like it's going to change anytime soon, especially when you consider that Monday night's effort represented considerable progress: After being outrushed by the San Francisco 49ers by 200 yards in Week 4, they were outgained by 100 by the Texans.
Outrushed by an even 300 yards in the past two weeks. That's failure.
Jets coaches spent last week looking for solutions, and the answers Monday came with gambles that paid off -- the fake punt by Tebow and the quarterback sneak by Sanchez in their own territory.
They got the rare combination, for this group, of a dynamic play with perfect execution on a 100-yard kickoff return by Joe McKnight. That's the kind of spark that often fuels an upset.
Instead, Ryan went with the onside kick.
The Jets did show some moxie, making good on Ryan's vow that they would "fight like underdogs." Effort wasn't the issue. Reality was.
The Jets have fallen on the wrong side of .500, and their next two games are against Andrew Luck's Indianapolis Colts and at the rival New England Patriots.
The Jets might see tight end Dustin Keller and rookie receiver Stephen Hill return soon from hamstring injuries. So, there's that. But these are still desperate times. And it's time for more Tebow. Maybe he can rekindle the magic. Maybe he can still win.
Really, what would it hurt? What could it hurt? For those answers, we're still waiting.
Follow Kimberly Jones on Twitter @KimJonesSports.


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Wednesday, December 1, 2010
2010 KBBC: Week 3, Day 2 | Der Evangelische Theologe
Be sure to check out the new KBBC post. Mike Jimenez has written a nice article on Barth and Badiou followed by a fine response by Geoff Holsclaw.
Mike attempts to show the relationship between Barth and Badiou's understanding of "event" particularly as it relates to the "Christ event," for Barth, and knowledge and truth of the "event," for Badiou, which produces a type of de-theologized universal truth empowering a radically non-conformist conviction.
Geoff's response is quite appreciative, but finds Mike's reliance upon Badiou's book "St. Paul," to be a bit narrow. Geoff believes the real point of conversation takes place between the ontologies of the two--a suggestion that I agree with.
Another excellent paper and response for this years KBBC. Remember, Travis and David are turning this years conference into a book, so, if you feel so obliged, please donate (there is a link at the bottom of each post).
Posted by Andrew Esqueda at 10:50 AM No comments: Links to this post
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Receiving an order from a customer depends on either the schedule of the sales representative visiting the customer, or receiving a phone order. It involves manual work such as writing down the order, entering it into a system, checking the stocks, confirming delivery dates, confirming prices, etc.
My Booking Solution's web booking form can be placed in any website to allow customers to place a booking instantly. Having a "Book Now" button on the website will increase the potential of a website visitor making a booking instantly, resulting in increased sales.
The website forms require further manual work to check and confirm orders, send emails with payment details, send manual reminders prior to bookings, and may lead to human error. Staff time spent on manual work can be diverted to customer service.
My Booking Solution provides complete automation, from an order placement to invoicing. The system follows leading best practice methods, automating your business operations and completely eliminating human intervention in back office functions.
Many booking systems do not automate the complete booking to invoicing process. It requires staff time that can be diverted to core business activities to increase customer service, marketing activities, or to expand the service offering. Time to process orders manually will result in delays and human errors, and increased cost of staff payment.
My Booking Solution provides complete automation. The delays in getting back to the customers can result in lost sales. Our intelligent booking processing logic displays only the available booking slots to your customers. The system takes care of booking cancellations, online payments, invoicing, receipts, and sending booking reminders to your customers. The daily performance of the business is displayed in a graphical form with key performance indicators.
It takes thrice the cost to find a new customer when compared to making repeat sales to an existing customer. Many service businesses let go of this opportunity. The booking forms do not provide the ability to offer gift vouchers, discounts, and package deals.
My Booking Solution opens up whole new avenue of sales opportunities to your existing customers. You will be able to offer gift vouchers, discounts and package deals to encourage repeat visits.
There is no one setup fits all model for a service business. Every business has its own specific requirements.
My Booking Solution allows businesses to set up its services, pricing, business operational hours, and cancellation policy to suit its own requirements.
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+61 8 6113 1284
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Phone: 08 6113 1284
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April Flower EveningsPosted: April 17, 2018 Filed under: 1970s, belinda bellville, bill gibb, Gina Fratini, Inspirational Images, john bates, oliviero toscani, Rayne, Richard Sharah, Sue & Helen, thea porter, Toscani, Uncategorized, Vintage Editorials, Vogue, yves saint laurent, zandra rhodes 1 Comment
Delicate flower evening dresses, in silks and chiffons… Beauty far beyond the English flower garden…
Photographed by Toscani. Make-up by Richard Sharah.
Scanned from Vogue, April 1975.
Inspirational Images: Fresh Woods and Pastures NewPosted: April 8, 2012 Filed under: 1960s, belinda bellville, jean varon, john bates, Justin de Villeneuve, twiggy, Vintage Editorials, Vogue 1 Comment
The most Easter-themed spread I could come up with at short notice. Happy Easter and hello Mr Spring, I've missed you so!
Prints by Bernard Neville for Liberty. Photos by Justin de Villeneuve. Vogue, May 1969.
Scanned by Miss Peelpants


text: A little over a year ago I married a photographer. Jerry came complete with fantastic gear, knowledge, experience and a heart to teach me. This time a year ago I never could have predicted we would be shooting so many weddings, families and portraits. For this we are both very thankful. Even though we are second-shooters for most of the weddings, we are gaining a massive amount of experience for our future brides and grooms. Every wedding we attend, it's as if they were our family and we do our best to catch the moments they will treasure. It's fun to think what we will be doing this time next year. Maybe we'll be hiring third shooters to help us with our own. In the meantime Jerry and I promise to bring out the best in all our clients.


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According to EY's Renewable Energy Country Attractiveness Index (RECAI), the UK's appeal as a destination for renewable energy investment is now at its lowest level for almost five years.
The sector is currently weighing the impact of a recent consultation on solar subsidies that will see the UK Government withdraw Renewables Obligation (RO) support for solar projects above 5MW two years earlier than planned, according to professional services firm EY.
In addition, the Government has allocated the majority of the funding available to support renewable energy projects through to 2020.
EY said competition is also intensifying internationally and new dynamic emerging markets are increasingly threatening the UK's ability to attract investors.
For example, India's new Modi government is overhauling its energy sector to incite public and private renewables investment.
Brazil, Chile, South Africa and Kenya are developing deployment pipelines and consistent policy support.
EY environmental finance leader Ben Warren said: "What we are seeing is a 'perfect storm' of reasons prompting a fall in the appeal of the UK's renewables market.
"The booming UK solar sector, one of only six markets globally to surpass the 5GW installed capacity, was caught by surprise by the Government's consultation in May. Legal challenges and investor petitions have been launched in response, urging the Government to give the sector more time and greater policy stability to compete with conventional fuels.
"At the same time there is simply not much left in the pot. 60% of the funding available has already been allocated leaving investors and developers concerned about budgetary constraints for future projects.
"To continue to compete for international capital, the UK's market reform and upcoming Contract for Difference (CfDs) regime will have to go a long way to repair the damage or recent policy mishaps."
China returns to the top for the first time since May 2013 while Europe and the US continue to lose ground to emerging markets, according to the RECAI, which ranks 40 renewables markets on their attractiveness in the eyes of investors.
The latest report highlights that Europe is currently at an inflexion point, striving to become a global sector leader but facing strained infrastructure and supply capabilities.
Mr Warren concluded: "Consumers, including home owners, commercial businesses and corporations, are becoming more empowered to take control of their own energy supply and demand.
"As a result, investors are also becoming increasingly motivated and empowered. This is not only driving the democratisation of energy, but is also channeling significant volumes of capital to where they are most needed.
"Looking forward, advancements in technology, changes in policy, and continuous reduction in cost will enhance the new energy landscape and drive affordable, reliable and low carbon energy in more areas around the globe."
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Table of Contents
At Betterment, we think a lot about how people manage their unused cash. After all, unused cash is often the money you could be using to pursue your financial goals through investing, but instead, you're keeping it liquid. We know from talking to our customers that holding cash isn't always intentional; it's a choice by default—not knowing how, when, or why to put your money to work.
So, when we talk about unused cash, it doesn't look the same for every investor; it's simply the money that you haven't yet spent and you haven't yet invested for a purpose. As your advisor, our ultimate recommendation is for you to identify the purpose of that money and to plan to save and invest for future expenditures. Until you identify that purpose, our advice for managing unused cash aims to achieve several priorities:
- Protect the principal balance
- Generate as much yield as possible to mitigate inflation (keeping costs low)
- Retain liquidity—i.e. access to the money—without penalty or extraneous restrictions
A starting point for evaluating cash savings products is to first make sure your principal balance is well protected, looking for ultra low-risk solutions. From there, evaluate expected yields, opting for a high yield relative to available options. Next, consider any minimum deposit amounts, fees, penalties, and tax consequences of the cash savings product. And finally, evaluate any product-specific risks.
Here, we'll compare Smart Saver with other products using this approach. As you'll see, no one solution offers ideal principal protection, yield, and liquidity. However, understanding the tradeoffs can help you make smart choices about managing your unused cash.
Evaluate Yield: Smart Saver vs. Savings Accounts
A historical convention for many Americans is to maintain unused cash in a savings account at a bank (or credit union) earning interest; often with the hope of combating inflation. Because of their widespread use, savings accounts are a likely comparison for individuals evaluating Smart Saver in place of a cash savings product.
Among savings accounts, rates in the form of annual percentage yield (APY) are set by the bank based on the margins earned on money the bank loans out and the bank's business circumstances. In contrast, Smart Saver's expected yield rate (a composite 30-Day SEC Yield) is based on the recent dividends, interest and expenses from ultra low-risk, short-term bonds that the cash is invested in. Learn more about how the yield is calculated in our methodology for Smart Saver's underlying investments. Both a savings account's APY and Smart Saver's expected yield approximate how much income a deposit could generate in a year, but there are important differences in how the numbers are determined, which should affect your degree of confidence in whether the expected yield will match the actual yield. Of course, historical performance, even very recent historical performance like the most recent 30 days of yield, is not an absolute indicator of future performance.
In the case of a savings account, APY is a pre-defined number, rather than a calculated one. Working within the margin earned from loaning your money out, banks can raise or lower their accounts' APY to attract new business. This can even occur within a year. A bank might raise rates to attract new customers, or lower rates to manage business operations. In addition, a bank can reset the structure of their yields based on deposit size.
In contrast, Smart Saver's yield, a composite of 30-Day SEC yields for the portfolio's underlying bond funds (net of fund fees and Betterment's 0.25% management fee), are set by the market and cannot be adjusted by Betterment (unless Betterment changes its management fee). Smart Saver is structured to generate a yield that correlates to federal interest rate changes, as the underlying bonds are sensitive to federal interest rates. The assumption underlying the 30-Day SEC yield expectation is that each bond in the funds will be held to maturity. In reality, the bond funds underlying Smart Saver are not held to maturity, as to enable liquid access to your money, but they have historically had ultra low price volatility and relatively low turnover, leading to our expectation that the 30-Day SEC yield is a fair estimate of future yield.
While banks' rates for loaning money are also sensitive to federal interest rates, they have some discretion for how much of the margin they pass to savings account holders in increased interest. Hence, when evaluating the average savings account APY in recent history, most bank APY rates have not risen as quickly as national metrics like the Federal Funds Rate.
As shown in Figure 1, we can assess what the typical savings account APY looks like using the Federal Deposit Insurance Corporation's "Weekly National Rate," a simple average of rates paid by U.S. depository institutions (which does not include credit unions, but does include any bank's branch-specific rates). We use the rate for deposits below $100,000. As of April 1, 2019, the Weekly National Rate is 0.10%. Access the FDIC's weekly update.
As a simple average, you should know that FDIC National Weekly Rate does not account for each institution's total assets under management or number of customers, and thus, it may not reflect the actual savings account APY that customers are receiving in the marketplace. However, given that customers do not have access to all possible rates, it's a reasonable definition of the typical savings account APY available in the United States. The highest yields are often well above the FDIC rate, so it may also be worth comparing Smart Saver to a select group of higher-yield savings accounts.
Hypothetical Historical Performance:
Smart Saver vs. the Average Savings Account
In this chart, we compare Smart Saver versus the Average Savings Account in relation to national interest rates, illustrated by the Fed Funds.
The above chart shows the hypothetical growth of $10,000 deposited in Smart Saver, as if the account was available starting in 2016, which we use as the marker for the recent period of rising federal interest rates. The chart shows Smart Saver's hypothetical performance (using data from Xignite), net of fund fees and Betterment's 0.25% management fee. This backtest of performance assumes daily rebalancing and reinvestment of all yields. Both "Fed Funds" and the "Average savings account" represent theoretical accounts. In the case of "Fed Funds," it's not possible to invest in the Federal Funds Rate; this chart illustrates account growth if it were possible, using the national interest rate. The average savings account also represents a hypothetical savings account based on the average of savings accounts nationwide. The source for both "Fed Funds" and "Average Savings Account" is the Federal Reserve.
Similar to this chart, Betterment provides a comparison between the weekly national rate and the expected yield for Smart Saver as a fair benchmark of potential yield for Smart Saver customers. At present, this comparison shows that Smart Saver's expected yield of 2.00% is about 20 times the FDIC Weekly National Rate. We update this comparison on a quarterly basis, using the FDIC National Weekly Rate and Smart Saver yield.
The key learnings from this comparison are that the typical savings account has a much lower yield than Smart Saver, and also has a yield that tends to lag actual interest rate changes, which profits the bank assigning these yields at their customers' expense.
Protect the Deposit: Smart Saver vs. Bank Accounts
When considering how well protected your cash deposit is in any account, many customers will again turn to the products banks offer, including savings accounts, checking accounts, money market accounts, and CDs. Some customers may also compare Smart Saver to products such as a cash management account or a debit account, depending on their desire to spend the deposit into the future.
We recommend considering several variables when evaluating the safety of any amount of unused cash:
- The risks involved in what kind of institution you use to hold your money
- The risks involved in how an institution uses your money
- Any insurance that applies to the account
To start, your choice of institution matters for how safe a deposit is. Putting money in a bank involves different risks than brokerages, which involve different risks than financial advisors. It's worth noting, of course, that all of these options' cash savings products typically involve less risk than holding on to cash outside of an account. For example, a bank has a regulated responsibility to protect your money, but banks are not typically required by regulation to have a holistic fiduciary responsibility to provide you with advice in your best interest. Similarly, depositing your money with a broker-dealer (even one tied to a financial advisor) involves different risks than putting your money with a bank. A bank account balance may be insured, while an account balance at a broker-dealer rarely is.
Any institution could become insolvent, in which case, the risk to your money largely depends on how the institution has used the money. In the case of bank savings accounts, deposits are loaned to other customers, which means that in the case of bank insolvency, your money is in use elsewhere. (For this main reason, banks are covered by FDIC insurance, which we explore in depth below.)
With Smart Saver and some kinds of money market accounts, your money is put in underlying investments that seek to generate yield. In the case of the firm's insolvency (i.e., the firm holding your investments), your money would then still be invested in the underlying vehicles.
Cash savings may be protected to varying degrees by certain types of insurance coverage, depending on the type of firm. Because banks loan money out to other individuals and entities, their deposits are generally insured by the Federal Deposit Insurance Corporation (FDIC) up to $250,000. This includes savings accounts, most money market accounts, and CDs. Accounts at Betterment are not FDIC insured. Broker-dealers, including Betterment Securities (which provides brokerage services to clients of Betterment), are required to be members of the Securities Investor Protection Corporation (SIPC), which provides up to $500,000 in protection for securities customers of its members if the member faces insolvency. However, SIPC insurance does not protect changes in the value of those deposits, or in the case of fraudulent changes to an account. For details, visit SIPC.
Keep Money Accessible: Smart Saver vs. Money Market Accounts and CDs
Once you've assessed the potential yield and level of protection in potential cash savings products, you'll likely find that a pattern emerges between how accessible your money is and the other two variables we've explained. In particular, some products can provide premium yield in exchange for little to no access to your money for a given period of time—most often years.
The paramount example of how you can seek higher yields for less liquidity is a certificate of deposit (CD) at a bank. CDs may offer high yields for extremely low risk, but in exchange, the certificate holder agrees not to withdraw the deposit for the term of the certificate. If customers do withdraw from CDs, they are usually subject to high penalties.
An important feature of Smart Saver is the ability to access any amount of your cash, without penalty, while still seeking a high yield. While there are CDs with higher yields than the expected yield of Smart Saver, they usually come with terms that far exceed the amount of time we would suggest leaving cash unused. Most high-yield CD terms are only advisable for those customers who are extremely averse to taking on any level of risk over a period of time.
A less extreme example than CDs are money market accounts and some savings accounts that restrict the number of transactions you can make in or out of the account. If you plan to use your unused cash in a variety of ways, then a restrictive number of transactions in and out of the account may pose a challenge to you. Similar to CDs, making more than the allotted number of transactions can lead to penalties.
Since Smart Saver pursues its yield by investing your money in ultra low-risk funds, access to withdrawals is not limited to a certain number of transactions. Rather, the main limitation is the amount of time it takes to process a withdrawal. In the case of moving your unused cash into goal-oriented investments, this process simply requires trading into the proper allocation, which can happen within the same day. To withdraw money for cash spending, it takes approximately 4-5 days to sell out of the funds and electronically move your money to a linked transaction account.
Smart Saver is one of many available cash savings solutions. Know the tradeoffs.
In this paper, we outlined the importance of evaluating cash savings solutions based on their ability to protect the principal balance, generate as much yield as possible, and help you retain access to your money. As you consider Smart Saver and other products, you can review the acceptable reasons Betterment customers might use Smart Saver, as well as how we developed Smart Saver's underlying portfolio. As with any financial product, we encourage you to explore the tradeoffs of Smart Saver, ask us questions, and decide whether it's the right solution for you.
Explore your first goal
Safety Net
This is a great place to start—an emergency fund for life's unplanned hiccups. A safety net is a conservative portfolio.
Whether it's a long way off or just around the corner, we'll help you save for the retirement you deserve.
General Investing
If you want to invest and build wealth over time, then this is the goal for you. This is an excellent goal type for unknown future needs or money you plan to pass to future generations.
Smart Saver
You could earn 20X more than a typical savings account with our low-risk investing account for your extra cash.


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Research Project
Grant-in-Aid for Scientific Research (C)
Vacuolar-type HィイD1+ィエD1-ATPase in multinucleated osteoclastic cells is the most important enzyme for demineralization of apatite crystals in bone and teeth. We localized the expression of vacuolar-type HィイD1+ィエD1-ATPase in osteoclasts and odontoclasts during bone and root resorption. Most of these multinucleated osteo/odontoclasts exhibited well-developed ruffled borders and clear zones, and HィイD1+ィエD1-ATPase was localized along the limiting membranes of pale vacuoles and along the ruffled border membranes. We further clarified the effects of administering bafilomycin A1 on the bone resorbing activity of osteoclasts during experimental movement of rat molars. To generate orthodontic force, an elastic band was inserted between the upper first and second molars of rats for 7 days. After elastic band application, bafilomycin A1 solution was administered daily intraperitoneally, and the structural changes and the expression of HィイD1+ィエD1-ATPase in osteo/ odontoclasts were examined. In bafilomycin A1-administered rats, most osteo/ odontoclasts had lost their intact ruffled borders and associated cytoplasmic vacuoles and showed decreased expression of HィイD1+ィエD1-ATPase. These results suggest that bafilomycin A1 administration is an effective biological means to inhibit osteoclastic bone resorption and odontoclastic root resorption via a mechanism involving impairment of the structure and function of the ruffled borders in osteo/oodontoclasts.
Published : 1998-04-01
Modified : 2016-04-21
User Guide
Terms of Use
Attribution of KAKENHI


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VINTON, Iowa -- Several animals seized from a home in Vinton will be returned to their owners.
The Vinton Police Department served a search warrant at the home last month and found roughly 700 rabbits, guinea pigs, birds, and reptiles. Police say many of the animals were being housed in small cages and in filthy conditions.
During a hearing on Thursday, a Benton County judge ruled 10 rabbits or guinea pigs, one turtle, and three lizards should be returned to their owners, Barbara and Marshall Galkowski. The pair is also required to reimburse area animal shelters for the cost of caring for the animals.
The remaining animals will eventually be put up for adoption.


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Phosphatidylinositol 3-kinases (PI3K) constitute important regulators of various signaling pathways with relevance in cancer. Enhanced activation of p110α, the catalytic subunit of PI3K, was found in a high proportion of many human tumor types. We generated a mouse model in which PI3K is activated by forced recruitment of p110α to the membrane. Different transgenic lines expressing myristoylated p110α protein under the control of the epithelial-specific mouse mammary tumor virus promoter were selected according to different levels of PI3K activity and characterized. Delayed mammary gland involution and morphologic changes of the mammary ducts could be detected in young transgenic female mice. These changes were more pronounced in old animals, especially in mutiparous females, in which we observed increased ductal branching, alveolar hyperplasia, and intraductal neoplasia. We also observed a small percentage of mammary tumors. Crosses of myrp110α transgenic mice with heterozygous p53(+/−) knockout mice resulted in neither enhanced tumorigenesis nor in a stronger mammary gland phenotype. However, the CDK4 activating mutation (R24C) lead to increased tumorigenesis in transgenic myrp110α mice, emphasizing the postulated perturbation of the interaction of the CDK4/Rb/E2F cascade and the PI3K signaling in many human cancers. Interestingly, in tumors of myrp110α transgenic mice, we observed an increased phosphorylation of the estrogen receptor-α, a typical feature of human breast cancer. The model presented here will help to discover additional factors which influence the progression of preneoplastic lesions to tumors in the mammary gland and to explore antitumor therapies based on PI3K or estrogen receptor-α pathway inhibition. [Cancer Res 2008;68(23):9643–53]
- Akt
- tumorigenesis
- mouse model
- mammary gland
The family of phosphatidylinositol 3-kinases (PI3K) plays a central role in transducing a variety of extracellular stimuli into a wide range of cellular processes, including cell cycle progression, cell growth, survival, cell adhesion, and cell motility. When activated by cell surface receptors, PI3K regulates the phosphoinositide lipid metabolism and the production of phosphatidylinositol 3,4,5-triphosphate (PIP3) at the plasma membrane. The production of PIP3 facilitates the recruitment of AKT via its pleckstrin homology domain, leading to its phosphorylation at Thr308 and Ser473. As the primary downstream mediator, AKT transmits the PI3K signal to a large number of molecules thereby diversifying the PI3K signal into various functional outcomes. PTEN is a dual protein/lipid phosphatase, the main substrate of which is PIP3, the product of PI3K. Loss of PTEN function results in the accumulation of PIP3, mimicking the effect of PI3K activation.
The PTEN/PI3K pathway is highly involved in cancer. PTEN activity is lost by mutations, deletions, or promoter methylation at high frequency in many primary and metastatic human cancers ( 1, 2). Germ line mutations of PTEN are found in Cowden, Bannayan-Riley-Ruvalcaba, and Proteus-like syndromes, all of them familial cancer predisposition syndromes ( 1, 3). Recently, many activating mutations in the PI3KCA gene (coding for the catalytic subunit of PI3K, p110α) have been described to be present in human tumors ( 4).
Studies in genetically modified mice showed that mice with only one functional PTEN allele develop tumors in several organs ( 5). Moreover, heterozygous PTEN knockout mice crossed with mouse mammary tumor virus (MMTV) promoter Wnt1 transgenic mice develop mammary tumors earlier in life than the parental strains ( 6). In conditional models, PTEN loss resulted in the generation of tissue-specific tumors. Elimination of PTEN, specifically in mammary glands, originates excessive side branching, accelerated ductal extension, and mammary tumors with metastatic properties ( 7). Similar tumorigenic properties have been observed in other tissues after PTEN conditional excision. In these models, conditional PTEN depletion also resulted in developmental defects, highlighting the importance of PTEN for normal differentiation.
However, despite its proposed relevance in the PTEN pathway, no equivalent results have been found in mouse models with activated AKT transgenes. Several independent groups have generated transgenic mice expressing constitutively active AKT in mammary glands ( 8– 11). Activation of the AKT pathway led to involution defects, consistent with the phenotype in Pten conditional knockout mice. However, no major differences could be observed in ductal growth and epithelial differentiation when comparing transgenic and wild-type females, despite the high expression levels of the constitutively active form of AKT ( 9, 11).
It has been proposed that the phenotypical differences between the PTEN and AKT mouse models could be due to a signaling pathway bifurcation between the PI3K/PTEN level and AKT ( 3). For the study presented here, we generated a mouse model for constitutive PI3K activity. To this end, we expressed the catalytic subunit of PI3K, p110α, fused to a Src myristoylation sequence, under the control of the mammary-specific MMTV promoter ( 12). Membrane localization of p110α is sufficient to trigger downstream responses characteristic of growth factor activation, including the stimulation of p70S6 kinase (S6K), Akt, and c-Jun-NH2-kinase (JNK; ref. 13). Also, expression of myristoylated p110 isoforms significantly reduces caspase-3–like activity and correlates with the increase in Akt phosphorylation. Membrane-targeted p110α shows higher catalytic activity similar to the active mutants E542K, E545K, and H1047R ( 14, 15), also correlating with higher capability to activate AKT and transforming potential ( 14, 16– 18). Therefore, membrane-targeted forms of p110α could act as constitutively active PI3K and are sufficient to stimulate several downstream kinases and confer transforming capabilities to cultured cells.
Here, we describe the phenotype of three transgenic mouse lines which express different levels of a constitutively active p110α, under the control of the mammary gland–specific MMTV promoter. In all three lines, increased branching and preneoplastic lesions of the mammary gland ducts were found. Furthermore, we describe the increased susceptibility to mammary proliferative lesions when crossed with CDK4(R24C) knock-in mice, but not with p53 heterozygous knockout mice.
Materials and Methods
Cloning of the p110α transgene. First, a myristoylated version of the vector pMB was generated by introducing the human Src myristoylation sequence. Next, the cDNA for murine PI3KCA, coding for p110α, was inserted in phase into the myristoylated version of the vector pMB.
Generation, handling, and analysis of transgenic mice. All animal experiments were done under the experimental protocol approved by the Institutional Committee for Care and Use of Animals of the Spanish National Cancer Research Centre which complies with European legislation on the care and use of animals, NIH guidelines for the use of laboratory animals, and related codes of ethic practice. Transgenic mice were generated by microinjecting the 3.2 kb fragment of pMMTV-MYRp110-α into the pronucleus of single-cell embryos isolated from superovulated B6/CBA mice. The embryos were implanted into pseudopregnant females and allowed to develop to term. The genotype of transgenic mice was assessed by PCR (forward primer, 5′-TGAATTGGCCGCTCGCGAATC-3′; reverse primer, 5′-CACTGGCATGCCAATAAC-3′). Western blot analyses were performed as reported in Supplementary Data 10.
Murine tissue immunohistochemistry. Mammary glands were fixed in 10% buffered formalin and embedded in paraffin. For histopathologic analysis, they were sectioned (3 mmol/L) and stained with H&E. Slides were baked overnight at 56°C, deparaffinized in xylene, rehydrated, and washed with PBS. Epitope retrieval was performed in sodium citrate (pH 6.5). Endogenous peroxide activity was quenched with 1.5% hydrogen peroxide in methanol for 10 min and incubation (40 min) with the primary antibodies: phosphorylated S473-AKT1 (Epitomics), phosphorylated S1108-eIF4G (Cell Signaling Technology), Cytokeratin 6 (Covance), phosphorylated estrogen receptor-α (ERα; 1/25 dilution; Cell Signaling Technology), p53 (Novocastra), cathepsin D (Santa Cruz Biotechnology), phosphorylated c-Jun (Ser73; Cell Signaling), and phosphorylated SAPK/JNK (Thr183/Tyr185; Cell Signaling). After incubation, immunodetection was carried out with the peroxidase-based PAP system (DAKO) using diaminobenzidine as substrate. Incubations omitting the specific antibody were used as a control of the technique. Statistical analyses were performed as reported in Supplementary Data 11.
Generation of transgenic mouse lines expressing an epithelial-specific myristoylated p110α gene. To investigate the effect of an enhanced PI3K activity in the epithelial cells of mammary glands, we constructed transgenic mice which express the cDNA of the murine p110α under the control of the epithelial-specific MMTV promoter. The SRC myristoylation sequence was fused to the NH2 terminus of the p110α protein, which leads to its localization to the inner leaflet of the plasma membrane and the constitutive activation of the kinase. We identified 18 founder mice which transmitted the transgene to their progeny. Among them, 13 expressed the transgene. We selected three lines (ED1, ED3, and ED1003) with different levels of activated AKT in the epithelial compartment of the mammary glands, as determined by Western blot analysis and immunohistochemistry using a phosphospecific AKT antibody ( Fig. 1A and B ).
We analyzed the tissue distribution of transgene expression in these three lines by immunohistochemistry (antibodies against phosphorylated AKT and p110α) and Western blot (phosphorylated AKT antibody). Besides mammary glands, transgene expression was found in the testis of all three lines (Supplementary Data 1). Additionally, strong expression was detected in the prostates of the lines ED3 and ED1003 (Supplementary Data 2); a milder expression was seen in the epididymis of these two lines and in the seminal vesicles of line ED3. Although no expression could be detected in the uterus of females of all three lines, transgene expression was observed in the ovaries of ED1 and ED3 mice. Expression in additional organs was detected only in line ED1 (the results are summarized in Supplementary Data 3 and 4).
For virgin females, multiparous females (four pregnancies), as well as males, no significant difference in life span could be detected between the wild-type mouse cohort and the three transgenic mouse lines (Supplementary Data 5; data not shown). The virgin and multiparous female mouse colonies were macroscopically analyzed after death or humane end point, sacrificed and examined for pathologic features. These results are summarized in Supplementary Data 6.
Functional expression of the transgene in the mammary gland. The expression of the transgene in epithelial cells of mammary glands of these mouse lines was analyzed by immunohistochemistry using an antibody against phosphorylation of AKT at Ser473 ( Fig. 1B).
The line ED1 showed a weak elevation of AKT-phosphorylation, followed by ED1003 with a stronger AKT-phosphorylation, whereas mice of the line ED3 displayed the strongest level of AKT-phosphorylation in 9-week-old mammary glands ( Fig. 1B), suggesting that the overexpression of myrp110α led to a net increase of PI3K catalytic activity. To confirm this data, we analyzed other markers of PI3K activity in normal ducts of transgenic animals ( Fig. 1C). We have assayed S6K, eIF4G, and JNK phosphorylation as markers for AKT activation, and c-Jun phosphorylation as a marker for JNK activity. Normal mammary glands showed the enhanced activity of these markers, demonstrating the activation of the transgene. To prove that this increase was indeed due to PI3K activity, we injected i.p. the PI3K-specific inhibitor LY294002 or only the solvent agent in two transgenic littermates of the ED3 cell line. After 12 hours, the mice were sacrificed and their mammary glands analyzed for AKT phosphorylation. The immunohistochemical analysis showed a clear reduction of AKT phosphorylation after treatment with LY294002 ( Fig. 1C). Moreover, we have observed that inhibition of PI3K reduced the levels of phosphorylation of the rest of downstream markers of PI3K confirming the functional relationship between PI3K activation by myrp110α and the activation of the pathway as shown by immunohistochemistry.
Next, we examined whether the elevated PI3K activity in transgenic mice resulted in increased epithelial proliferation. Indeed, a higher percentage of cells stained for the proliferation marker Ki67 could be observed in ducts of transgenic mice of line ED3 than in wild-type littermates ( Fig. 1D).
Upon weaning (cessation of lactation), wild-type mammary glands, which had proliferated massively during pregnancy and lactation, regressed into a virgin-like state, a process called involution. Because it has been described that AKT activation leads to delayed mammary gland involution ( 10, 11), we investigated if the elevated PI3K activity in our transgenic mouse lines had similar functional consequences. We studied whether the involution process was altered by comparing transgenic and wild-type mammary glands 3 days after weaning. Involution was greatly delayed in all three transgenic mouse lines, as can be seen in whole-mounted mammary glands stained with red carmine ( Fig. 2A, left column ) and in histologic sections stained with H&E ( Fig. 2A, middle column).
We quantified the effect on mammary gland involution by comparing the numbers of mammary epithelial cells present 3 days after weaning in each mouse line ( Fig. 2B). To this end, we examined the mammary glands of two mice of each transgenic mouse line and wild-type controls. All three transgenic lines showed higher numbers of cells as a consequence of PI3K activation. The immunohistologic staining for phosphorylated AKT ( Fig. 2A, right column) revealed a stronger phosphorylation in transgenic glands than in wild-type controls, thereby suggesting the implication of the transgene in the process of involution. Altogether, our data confirm that the transgene is expressed, active, and functional at the physiologic level.
MMTV myrp110α transgenic lines show proliferative lesions in the mammary glands. We determined the morphologic differences between the transgenic lines and wild-type mice by closer histologic examination of the mammary gland ducts of young 9-week-old virgin females. First, we assessed the average number of epithelial cell layers of the mammary ducts for each mouse line. To this end, the layers at the opposite points of the longest diameter and of the opposite points of the perpendicular axis were counted ( Fig. 3B, red bars in f ). The average number of epithelial cell layers was increased in the transgenic mouse lines, albeit only slightly in line (ED1003; Fig. 3A). To avoid bias from the form of the duct cut, we also counted the number of epithelial cell layers at the thinnest point of each duct ( Fig. 3B, black bars in c). Again, there was a significant difference between the transgenic lines ( Fig. 3B, b and e) and the wild-type cohort ( Fig. 3B, a and d), indicating that the transgenic mice had a higher number of cell layers per duct. Third, we determined the percentage of mammary intraepithelial neoplasias (MIN; Fig. 3B, c). As obligatory features for a MIN structure, we selected more than one layer of atypical cells with hyperchromatic nuclei, little cytoplasm and increased mitotic activity with variable pleomorphism (see Fig. 3B, c, arrows; ref. 19), and epithelial growth into the lumen of the ducts. More MIN structures were found in transgenic mammary glands than in wild-type glands (represented in Fig. 3B, b versus a). Of each mouse cohort, more than 60 mammary gland ducts were examined. We observed a statistically significant increase in all three transgenic lines ( Fig. 3A). These results show that morphologic abnormalities can be observed in the mammary glands of very young virgin female mice of the myrp110α transgenic mice.
Increased incidence of ductal ramification, alveolar hyperproliferation, cystic dilation, and neoplastic alterations in myrp110α transgenic mice. After the death or humane end point sacrifice of the animals, we analyzed the phenotypes of their mammary glands. All mammary glands analyzed could be assigned to one of the following categories: (a) normal structure similar to the one of young virgin female mice, (b) increased number of ramifications and slightly increased alveolar size, (c) increased number of ramifications and strongly increased alveolar size, (d) extreme alveolar hyperproliferation covering the space between the ducts to <70%, (e) ductal cystic dilation (ectasia) of more than 10 times and increased alveolar size. All three transgenic mouse lines displayed stronger pathologic alterations than the wild-type cohort ( Fig. 3C and D). The strongest effect could be observed in the virgin female cohort of line ED3 and in the multiparous female cohorts of all three lines.
Due to the abnormalities observed in the ducts of young myrp110α transgenic mice, we decided to analyze microscopically the mammary glands of the transgenic line ED3 in comparison with wild-type animals. As shown in Fig. 4A , 12% of virgin transgenic females had tumors, all of them adenosquamous carcinomas, whereas no tumors were observed in wild-type females. Among multiparous myrp110α transgenic females, 28% showed tumors. Of those, 66% had microscopic adenosquamous carcinomas, commonly in several mammary glands. The other 34% had macroscopic carcinomas. Only 5% of multiparous wild-type mice showed tumors, all of them adenosquamous carcinomas. All tumors from transgenic mice showed strong AKT-P and eIF4G-P staining ( Fig. 4B), indicating that they proceeded from epithelial cells with increased PI3K signaling ( 20). To confirm this point, we analyzed the phosphorylation and activation of other markers of PI3K pathway activation. JNK and S6K phosphorylation as well as c-Jun phosphorylation, as a marker of JNK activation, were increased in these tumors ( Fig. 4C).
Most human tumors assessed were positive for ERα, a primary factor for its classification according to current clinical outcomes ( 21). To establish the molecular correlates between the human tumors and our mouse model, we analyzed the levels of ERα phosphorylation in MIN and tumors. We observed that all proliferative lesions from transgenic animals showed strong ERα phosphorylation ( Fig. 4B). Moreover, cathepsin D, a marker of ERα activation, is also increased in transgenic tissue ( Fig. 4C). Thus, functional activation of PI3K might trigger ERα phosphorylation, being a growth advantage for ductal cells and a common feature of human breast cancer. To fully confirm this functional relationship, we measured ERα phosphorylation and cathepsin D expression in the ducts of healthy transgenic animals treated with the PI3K inhibitor LY294002 ( Fig. 4D). We observed that transgenic animals expressing myrp110α have high levels of ERα phosphorylation and increased cathepsin D expression, and both are reduced under PI3K inhibition, confirming that ERα is phosphorylated and activated by PI3K contributing to the tumorigenesis observed in these mouse models.
The phenotype of myrp110α transgenic mice does not change in p53(+/−) heterozygous background. Thus, activation of the PI3K by membrane binding of p110α predisposes to neoplastic transformation. However, a large percentage of virgin and multiparous transgenic females did not bear tumors, and others had only microscopic ones.
It has been proposed that PI3K activation triggers senescence in primary cells and that this tumor suppressor mechanism is dependent on the presence of p53 ( 22– 24). To explore whether this mechanism plays a role in our experimental system, we first checked the status of p53 protein in the neoplastic transformations found in myrp110α mice. We analyzed p53 stabilization as a correlate for p53 mutation using immunohistochemistry because it has been observed that most p53 mutations appear as strong nuclear p53 staining. Especially in p53 heterozygous mouse models, loss of heterozygosity generally occurs by p53 mutations. We observed that macroscopic carcinomas showed p53 mutations reflected by the high levels of nuclear p53 expression ( Fig. 5A ), whereas in MINs and adenosquamous carcinomas, nuclear p53 staining was barely detectable, correlating with wild-type p53. These results point to the existence of a tumor progression barrier established by wild-type p53, like the one suggested in senescence. To check the influence of this barrier in our experimental system, we crossed the transgenic line ED3 with p53(+/−) heterozygous knockout mice. We did not observe any influence of the loss of one p53 allele on the mammary gland morphology of myrp110α transgenic mice ( Fig. 5B). Even the higher incidence of preneoplastic lesions in the mammary glands which we had previously observed in the ED3 line was not further elevated by the loss of one p53 allele (data not shown). The survival curves of the virgin and multiparous females and the male mice of the crosses did not differ from the respective p53(+/−) colonies ( Fig. 5D; data not shown). Altogether, these data indicate that the loss of one allele of p53 does not cooperate with the elevated PI3K activity in our experimental model. On the other hand, homozygous p53-null background mice die too early of leukemia and sarcoma, not allowing for the analysis of its cooperation on mammary tumor development (data not shown).
To study whether mammary epithelial cells from myrp110α transgenic mice entered senescence earlier, we isolated and cultured epithelial cells from these mammary glands. Cells from transgenic mice showed similar proliferative capabilities and entered senescence with similar kinetics to wild-type cells ( Fig. 5C).
Taken together, our experiments suggest that although tumor proliferation may be blocked by the presence of wild-type p53, p53-dependent senescence might not be the only tumor suppressor mechanism impeding tumorigenesis in the mammary glands of myrp110α transgenic mice. It is also possible that loss of heterozygosity of p53 is influenced by PI3K activation in a tissue specific manner. In this regard, the mouse strain C57BL6 is resistant to breast tumorigenesis, and this might influence the outcome of our experiments.
Alteration of the pRb pathway by the R24C mutation of CDK4 enhances the preneoplastic predisposition of myrp110α mice. The CDK4/Rb/E2F pathway regulates the expression of genes important for cell proliferation, as well as genes that trigger apoptosis. Recently, it could be shown that PI3K/AKT signaling blocks E2F1-induced apoptosis during normal cell proliferation ( 25). To assess the balance between the CDK4/Rb/E2F axis and the PI3K signaling in our mouse model, we crossed the ED3 cell line with the CDK4(R24C) mutant knock-in line ( 26, 27). We observed a clear increase of mice with mammary lesions ( Fig. 6A ). The incidence of tumor-bearing mice increased to 50% of the cohort ( Fig. 6A). The analysis of tumors showed that CDK4(R24C) mice only developed small (<1 mm) adenosquamous carcinomas, whereas the same mice developed a broader spectrum of mostly malignant tumors ( Fig. 6B) when they expressed additionally the myrp110α transgene. However, the overall survival was not significantly altered (Supplementary Data 7).
There are, however, some differences between virgin and multiparous females. Although virgin mice carried mostly malignant tumors, multiparous females also developed a high percentage of adenosquamous carcinomas ( Fig. 6B).
The analysis of MINs and tumors showed an increased AKT activation in all tumors of epithelial origin, indicating that the PI3K activation might have contributed to tumorigenesis ( Fig. 6C). Because the transgene has been expressed specifically in epithelial cells, it is likely that the sarcomas had arisen spontaneously. Consistently, the levels of phosphorylated AKT were very low if at all detectable. These data were confirmed by the analysis of S6K, JNK, and c-Jun phosphorylation as different markers for PI3K pathway activation (Supplementary Data 8).
Because ERα might be activated by the transgene and contribute to tumorigenesis, we analyzed the levels of ERα phosphorylation ( Fig. 6C). Again, ERα was phosphorylated in all cases bearing activated AKT, but not in sarcomas, highlighting the different cellular origins of the sarcomas and the rest of the lesions. Finally, we analyzed the status of the p53 protein. We found mutated p53 only in sarcomas ( Fig. 6C). Our results suggest the spontaneous origin of sarcomas, whereas the rest of the epithelially derived lesion originated from transgene cooperation.
Here, we describe three transgenic mouse lines with enhanced p110α expression accompanied by high levels of AKT activity. All the transgenic mouse lines showed delayed mammary gland involution. Phenotypically, transgenic lines present morphologic changes of the mammary gland characterized by increased proliferation of epithelial cells. We observed a mild increase in preneoplastic lesions and tumors in the membrane-bound p110α transgenic mice, however, they mostly fail to progress to carcinoma, unlike the lesions of mice with specific PTEN deletion in mammary glands ( 7). The difference cannot be explained by insufficient levels of activated AKT because the growth-regulatory and signaling properties of the three most frequently observed PI3K mutations, E542K, E545K, and H1047R, have been determined and compared with membrane-targeted PI3K (myrp110α). They show similar catalytic activity ( 14) and similar capability to activate AKT ( 16). Moreover, myrp110α also seems to have oncogenic activity at the same level as the PI3K mutants ( 17, 18). However, it is possible that the subcellular localization of PIP3 or its substrate specificity play an up to now undervalued role in PTEN/PI3K signaling ( 16). Alternatively, the data presented here might suggest that an additional PI3K/AKT-independent mechanism contributes to PTEN-induced tumorigenesis, providing a signal for the transition from premalignant or benign lesions to carcinoma (see ref. 3 for a review).
Several examples of AKT-independent PTEN signaling have been reported ( 28– 33). Furthermore, PTEN is found in the nucleus in a number of different normal and tumor cell types. Nuclear localization of PTEN may contribute to its tumor suppressor activity ( 3, 34), perhaps in a phosphatase-independent manner ( 35, 36). These findings underscore the complexity of PTEN functions at distinct subcellular compartments and imply that the tumor suppressor and/or proapoptotic functions of PTEN rely, at least in part, on actions executed by PTEN in the cell nucleus ( 35). Therefore, it is possible that positive cooperation between PI3K and another PTEN target is necessary to provide full transforming activity. Previously published data and those presented here suggest that p53 might be this second target. P53 activation by PTEN is nuclear and independent of PI3K signaling ( 35, 36). Moreover, p53 is induced by PI3K activation ( 24) imposing a senescence blockade to tumorigenesis induced by PTEN loss in vivo ( 23). In our work, the analysis of p53 showed an interesting pattern when comparing tumors from myrp110α transgenic mice alone or in CDK4(R24C) background. Mammary carcinomas from myrp110α transgenics showed mutated p53, whereas premalignant lesions did not. This suggests that p53 blocks tumorigenesis in myrp110α transgenics. However, in our model, elimination of one or two alleles of p53 does not alter the range or number of lesions observed in myrp110α transgenic mice nor the overall survival. Furthermore, transgenic breast epithelial cells senesce with similar kinetics to wild-type cells. On the other hand, in double myrp110α;CDK4(R24C) mice, neither premalignant/malignant nor benign lesions showed p53 mutations. Only a few of the sarcomas found showed AKT, ERα, and p53Mut phenotypes, indicating a different, perhaps spontaneous, origin, and confirming the above observations. These data suggest that the tumor suppressor mechanism induced by PI3K activation might be overcome by mutating either p53 or pRb pathways, indicating that senescence may not be the only tumor suppressor mechanism acting at the physiologic level.
The CDK4/Rb/E2F pathway regulates the expression of genes important for cell proliferation, as well as genes that trigger apoptosis. Recently, it could be shown that PI3K/AKT signaling blocks E2F1-induced apoptosis during normal cell proliferation ( 25). PI3K and AKT inhibit cellular apoptosis by regulating the activity of apoptotic proteins such as BAD, caspase-9, and Mdm2 ( 37, 38). It has also been reported that the presence of the E2F1 apoptotic program in breast and ovarian tumors coincides with a good prognosis ( 25). These facts suggest that, in a normal cell, the balance between the E2F-induced genes and PI3K signaling is tightly controlled, and that this balance might be disturbed during tumorigenesis. Myrp110α transgenic expression in a CDK4(R24C) mutant background produces an increase in preneoplastic lesions and in tumor formation. Also, the types of tumors found was influenced by the mutation of CDK4: although many tumors in the myrp110α transgenic mice and all of the heterozygous CDK4(R24C) control cohort were adenosquamous carcinomas, we did not find these kinds of tumors in virgin mice of the crossed cell lines, but papillary and complex adenocarcinomas with variable glandular, acinar and solid areas, and ductal and undifferentiated carcinomas. In the multiparous cohort of double CDK4(R24C);myrp110α, we found a mix of tumors with and without a squamous component. A squamous component is rarely observed in malignant human breast cancer but the mammary epithelium of older mice under chronic prolactin stimulation commonly has squamous metaplasias ( 39). In human breast tumors, activation of cyclin D1 is a common event. Amplification of the gene has been detected in ∼15% of breast cancers, whereas overexpression of cyclin D1 at mRNA and protein levels is seen in up to 50% of primary tumors, mostly ER-positive and well-differentiated tumors ( 40, 41). Furthermore, joint overexpression of cyclin D and PI3K pathway activation, either directly or indirectly through membrane receptors, is a common event described in human tumors ( 42– 44). In our model, R24C mutation blocks the binding of INK4 inhibitors to CDK4, maintaining unregulated kinase activity, similar to the effect induced in CDK4 by cyclin D overexpression. We have found that although normal ducts or tumors from R24C mutant mice do not have PI3K pathway activations, tumors from myrp110α;CDK4(R24C) mice have strong activations of the PI3K pathway (Supplementary Data 9). This might suggest an additive effect between both pathways in tumorigenesis.
For the construction of mouse models which resemble tumorigenesis in humans, the shift of small adenosquamous carcinomas towards malignant carcinomas is of great importance. We also observed a shift in the type of tumors between virgin and multiparous females, reminiscent of the different types of tumors found in similar comparisons of virgin versus multiparous human female tumor patients.
Most human breast cancers (70%) are ER-positive and estrogen-dependent ( 45). Only 50% of all ER-positive tumors are responsive at first presentation to antiestrogens such as tamoxifen; furthermore, at least in the metastasis setting, initially responsive tumors eventually become resistant to endocrine treatment, leading to tumor progression and death ( 46). Therefore, a better knowledge of the factors influencing tumor sensitivity to various types of endocrine therapies is needed. The analysis of MIN and tumors showed concomitant AKT and ERα activation in all tumors of epithelial origin, indicating that the PI3K activation might have contributed to tumorigenesis by turning on ERα. It has been described that constitutively active AKT may phosphorylate ERα, resulting in the alteration of gene expression and activity independently of estrogen ( 47, 48). Recent studies showed a positive correlation between activating PIK3CA mutations and ER expression in mammary tumors ( 49). Alternatively, ERα might reflect the origin of tumors from ERα+ progenitor cells. Either way, the animal model presented here recapitulates the important features of human cancer, i.e., activation of PI3K signaling, involvement of the CDK4/Rb/E2F axis, and phosphorylation of ERα. Therefore, these transgenic lines will be of high value to investigate the concerted action of the different signaling pathways involved in breast cancer and to develop, respectively, tailored therapies.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Grant support: Spanish Ministry of Health (FIS-02/0126), Fundacion Mutua Madrileña, Spanish Ministry of Science and Technology (SAF2005-00944), and Eli Lilly.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
The authors acknowledge Dr. M. Barbacid for the CDK4(R24C) knock-in mice, the Comparative Pathology Unit of the CNIO for the histologic and immunohistochemical work, the Trangenic Unit at the CNIO for the pronuclei microinjection, and the Animal Facility Unit, specially Yolanda Cecilia, for the maintenance and care of the mice. Thanks to Francisco Real for critical reading of the manuscript.
Note: Supplementary data for this article are available at Cancer Research Online (http://cancerres.aacrjournals.org).
- Received April 24, 2008.
- Revision received July 31, 2008.
- Accepted September 5, 2008.
- ©2008 American Association for Cancer Research.


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October 06, 2011
Miracle Worker
So I think I can speak for both myself and Sami in saying…I feel rubbish! There is nothing like a bad dose of the sniffles to really get you feeling bleh. Resulting in a very red-nosed me huffing and puffing about feeling sorry for myself. So in a desperate attempt to make myself feel human again (and to somehow stop my whining), I fell back on an old favourite of my grannies, a right good menthol steaming!
Nothing gets me cleared out and freshened up like this.
However, this is not for the faint hearted expect lots of sweat, pores and well um, snot.
Sometimes simple works best, basically all you need is boiling water in a large bow pop in some menthol crystals/oil or in my desperate case mix in some good old vics vapour rub. Then simply pop your head over the bowl and cover with a towel to lock in the steam.
This is when the magic happens, not only does the steam draw all the impurities from your pores, but the menthol will help clear your sinuses making you feel a lot clearer and better.
Keep your head rested over the bowl for a good 10-15 minutes breathing deeply and obviously not getting too close so you dont burn your face in the water!
Afterwards give your skin a good splash of cold water and use some toner to tighten your pores again, and perhaps in my case give your nose a good blow?
My grannie will be very pleased I'm sharing this little tip with you so I hope you all try it out the next time you're feeling under the weather.
In other news I'm looking forward to a little trip to Newcastle on Saturday, it's always nice to get a change of scenery and Newcastle is packed full of lovely little boutiques and vintage shops, so I'll be sure to share any bargains with you all.
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ABC News reports on a work world with "no commute, no corporate headquarters and perhaps not even an office in the physical world at all." The 2-minute video clip says it all . . .
Having a big desk as a sign of status with lots of family photos and you know, carpeting that's fluffy and nice, that is a vision of the past," said Hoffman, executive vice president of Accenture.
42 percent of IBM's 350,000 employees rarely come into an IBM office.
With no corporate headquarters, if you need a work space, you reserve it like a hotel room — checking in and out at a kiosk.
This forecast presents a challenge to traditional high schools that are charged with preparing students for the future workplace. That is . . . unless we embrace, promote, even mandate on-line learning as part of a comprehensive high school educational experience.
In our school system, we have around 40 students taking 22 on-line classes through the North Carolina Virtual Public High School. The one early guarantee I am coming away with is that these classes are rigorous. It has been an eye-opener for some students.
The on-line educational model is fairly new terrain for these students and their guidance counselors. I applaud them for "jumping off the cliff." I am confident that our local support team and the provider support team can enhance their experience for a safe landing.
This NCVPS experience will give these trailblazing students a leg up in their quest for a place in the future of work.
For more, check out the News-Times article on Virtual Courses.


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Outstanding opportunity to move up in desirable McKenzie Lake. Walk to school, shopping & the beach from this fully developed & well-maintained 2 storey walkout on a quiet close. Newer flooring throughout & newer appliances in the bright kitchen with a lake view & access to the elevated deck w/ NG hookup for your BBQ. Main floor also features a large living room & dining room, family room warmed by the wood fireplace, as well as a 2 pc powder rm & large laundry rm leading to the insulated attached double garage. Upstairs, your family can retreat to their large bedrooms, while you relax in your expansive, private master suite. Developed basement features a large recreation rm with gas fireplace, leading directly out to the covered stone patio & mature landscaped private yard. There's also a large den, easily converted to the 4th bedroom, 3 pc bath. Make this bright, open home your executive enclave in one of Calgary's most sought-after lake communities. Outstanding value! Even more outstanding opportunity! Both HWT's replaced 2016 and furnace serviced in 2017; newer toilets and kitchen appliances.
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The company has been awarded $10 million worth contracts to supply its PX pressure exchanger and pump technologies for water projects in Saudi Arabia
May 2018
Energy Recovery, a leader in pressure energy technology for industrial fluid flows based in California, US, said it has been awarded $10.1 million contract to supply its PX pressure exchanger, and pump technologies for water projects in Saudi Arabia.
The orders are expected to ship in the second and third quarters of 2018.
As per the deal, Energy Recovery will supply its PX-Q300 pressure exchangers, VPXP circulation pumps and AquaBold high pressure pumps for multiple desalination facilities, which will produce up to 470,000 cubic metres of water per day.
Energy Recovery estimates the PX devices will reduce the facilities' power consumption for all projects by 50 MW, saving over 431 GWh of energy per year, and helping them avoid over 258,000 tonnes of CO2 emissions per year.
On the contract win, president and CEO Chris Gannon said: "Megaprojects and the Middle East remain key indicators as to the health of the overall water market, and we see continued strength throughout 2018 and into 2019."
"We remain focused on maximising customer value with end-to-end recovery solutions that combine our PX pressure exchanger and pump technologies," stated Gannon.
Rodney Clemente, Energy Recovery's VP (Water) said: "Historically, the Saudi Arabian market was difficult for membrane desalination technologies to penetrate as low-cost, local power enabled technologies such as thermal desalination to initially gain majority market share. Due to advancements in seawater reverse osmosis technologies and increased awareness in energy preservation, there has been a shift from thermal desalination to seawater reverse osmosis solutions."
"We first deployed our PX pressure exchanger technology into Saudi Arabia in 2013, and over the past five years we have captured eight mega project references," stated Clemente.
"Energy Recovery is positioned to unlock emerging market opportunities and remains focused on maintaining market position in critical countries like Saudi Arabia," he added.


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Property Management
At Renfrow Realty, we deliver turn-key commercial property management solutions founded on our principles of dependability, honesty, and excellence. From warehouses to restaurants, retail spaces to office buildings, we actively engage on your behalf to improve occupancy, boost net operating income and maximize your asset's value and performance.
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Coming soon! We have been out busy clicking away but we promise we have lots to say about that as soon as we get a little break! Check back soon for all kinds of shenanigans involving our many adventures and Milly the Dog!
In the meantime check out Nikki's super world famous amazingly awesome blog of randomness here


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The lovely ladies at Cake Break have welcomed a (roughly) monthly reading group.
Each month over tea and cake, we will be chatting about our chosen book. You can read our latest newsletters (and find out what we'll be talking about at our next meeting – albeit loosely), click on the link in the scroll down menu, or below.