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These days I'm working on a new collection for Daily Art. The main inspiration for the new designs was a coat I saw a couple of weeks ago.
I was looking around in a Christmas bazaar and my eye was caught by an amazing, vintage, kimono-like coat. It was made of turquoise velvet and it had gold thread embroidery all over. It was a little bit too expensive for my budget, but it stuck with me as an image, and I thought that I'm already doing embroidery, so I could just add embroidery details to pieces I already own.
Plus, when I opened my sketchbook to start designing fresh things for the brand, it came really naturally to me to create a more vintage and bohemian inspired collection.
New collection coming really soon 🙂


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Lawn Care Services
Serving Aurora, Naperville, Oswego, Batavia, Elgin, Geneva, St.Charles, Plainfield, Darien, Wheaton, Libertyville, Joliet, Schaumburg and much more in the northern and western suburbs of Chicago! View our entire service area.
The Beautiful Lawn You Always Dreamed Of – With Green T Lawn Care As part of your community, we believe in going that extra mile to keep your lawn looking great. We are very serious when we say we have the highest quality lawn care services and weed control to produce the healthiest yards in the Chicagoland area.
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Our extensive lawn fertilization program is proven to create green healthy yards every time. We carefully select the appropriate fertilizer for each season. Additionally included with our fertilization program:
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Fertilizers come in granular and liquid form. A granular fertilizer has many advantages over liquid fertilizers. The granular fertilizer is safer for lawn traffic since it doesn't require drying and it has a slower release which produces more lasting, even results.
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subset: commoncrawl


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Head over to Amazon.com where today only you can snag these Bluedio T3 Wireless Bluetooth Stereo Headphones for just $29.99 each (regularly $79.99) with FREE Super Saver Shipping!
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This Amazon deal of the day is valid February 10 only and while supplies last.


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Published on 15/03/2017 11:32:45 AM | Source: Religare Securities Ltd
Sell Engineers India Ltd For Target Rs.162.00 - Religare Sec
Engineers India Limited (ENGINERSIN)
ENGINERSIN, after the recent profit taking phase, has formed a fresh buying pivot around the sup-port area of mid-term moving average i.e.100 day EMA on daily chart. Confirmation indicators are also in the favor of rebound.
Sell Engineers India Limited @ 148-150 Stoploss 144 Target 162 CMP 148.65
To Read Complete Report & Disclaimer Click Here
For Religare Securities Ltd Disclaimer http://old.religareonline.com/research/Disclaimer/Disclaimer_RSL.html
Above views are of the author and not of the website kindly read disclaimer


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Daydreaming about things that I would rather be doing right now instead of writing papers on my day off of work. I'm starting to realize that my summer break really isn't much of a break at all | PC: @_lilwolfey_


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Welcome to Made.com Unboxed
Ever wondered how other people style their MADE pieces? Have a snoop here on Unboxed, where MADE customers share photos to inspire others. Post your own snaps, and you could win a £100 voucher.
Start exploring the world of made
Vale Adjustable Stool, Natural Ash and White
The Vale is a height adjustable stool with industrial styling. Made from natural ash wood seat and powdercoated steel legs create a stunning textural contrast.Buy Now


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This Earth Auger Bit features a replaceable fishtail point and cutting blade as well as a shock spring for ease of use. It fits all Earthquake powerheads and is available in a variety of sizes to suit your needs. Durable steel construction creates a solid, reliable design that's built to last.
- Assembled dimensions: 10 in. W x 10 in. D x 36 in. H
- Exclusive shock spring for ease of use and reducing wear and tear on transmission
- Replaceable fishtail point and replaceable blade
- Great for setting out plants
- 12 in. and 18 in. extensions available


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Grandma's Brag Book for June 11, 2014
Haley Jo, six months, tries out walking on the grass with bare feet. Parents are Todd and Laura Langdon of Duluth. Grandparents are Gary and Debbie Patrick of St. Michael, Minn., and Kimber and Bonnie Langdon of Hermantown. Great-grandparents are Muriel Zeleznikar of Duluth and Al Olson of Cross Lake, Minn.


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Jason mentioned Time Code, and
Jason mentioned Time Code, and every time I hear about the screen-split-four-ways thing I can't help but think about the camera Judith had that took four photos on one frame of 35mm film.
Only I bet the cameras used to film the movie weren't as colorful.
Sigh. I wish I'd gone to SXSW like Jason and Judith and all the other cool kids...


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Test Items tests a selected item to determine if its values test True for the values specified in an expression.
Insert a new or existing expression into the Expression Editor.
ExampleA computer distributor may have one or more computer items with 17" monitors listed on a Bill of Materials (BOM).
An expression can be written that enables you to test a selected computer item to determine if its BOM includes a17" monitor.
Click Test Item.
An Item ID dialog box opens.
Select an item from the drop down list.
If the item:
Fulfills the expression criteria, a message notifies you the item matches the expression.
Does not fulfill the expression criteria, a message notifies you that the item does not match the expression.
Click OK.
Result: The message closes and the Expression Editor displays.
Note: Expressions that are valid for Test Item should also be valid in List Items .
Step 6. Test the expression.


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Greetings from Melbourne! After a three month road trip across America and two months in Saigon, I am finally back in Australia. I spent a week in Melbourne in late August prior to leaving for America and couldn't wait to … Read all about it!
Category Archives: Vietnam
This is the second successive year that I've returned to Vietnam. The first stint lasted nearly nine months that took me from the north to south; with my recently stay only lasting a quick two months. What can I say – I just love the place! Vietnam is a popular … Read all about it!
As a child, every year we always celebrated Tet (Vietnamese Lunar New Year) as it was the most important date in the yearly calendar. It was also be a date that I would dread yet enjoy at the same time. The day would start my … Read all about it!
Vietnamese food is simple, yet exciting and loved by millions around the world – me especially. After the first year of travel primarily through Latin America, I felt that I should spend the majority of the second year in the country of my heritage. What I … Read all about it!
"Is this a restaurant or somebody's home?" I asked a stranger inside as I stood at the apartment doorway. He looked at me oddly and replied that it indeed was somebody's home. From the sounds of the conversations echoing from inside, deep down, … Read all about it!
I recently wrote a story for AWOL about the Vietnamese foods that you may not have heard of, but should try. As I was going through my long list, I realised that it was quite a challenge to not include too many Vietnamese noodle soups into the list. … Read all about it!
Food is one of the reasons as to why we travel. It's one of life's pleasures that all of us can relate to, provide a window into a local culture and has the power to connect us with new people … Read all about it!
When I initially settled in Saigon in September, people would ask me what was there was to do here? My response then, was that there wasn't too much to do except eat – a lot. I'd spend most late afternoons in search of … Read all about it!
When I was a kid, our family would visit the local fast food chain called Henny Penny which specialised in fried chicken. It wasn't as popular as Kentucky Fried Chicken (now known as KFC), however, it was the main sponsor of the local football … Read all about it!
Whilst I was travelling through Central and South America last year, there was one thought that would plague my mind on a regular basis: Vietnamese food. Not a day would go past as I was sitting at a restaurant and eating a menu … Read all about it!


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MVP Shock
View Single Post
* Ace Member *
Join Date: Jan 2010
Location: MI
Posts: 3,314
Niced 2 Times in 2 Posts
I've been away from the CPU for a bit so I haven't read much of this thread...Here is my quick review of the Shocks I received:
I have 2 early run Shocks and 2 "improved" Shocks which benefited from considerable tinkering on the part of MVP (that is going to have an impact on all of their drivers).
The two original Shocks fly a lot like my good Volts, only a bit straighter/more line-locking. I like them a lot as they are less affected by the wind than my Volts and because I've always been more a TB guy rather than an Eagle guy. Besides that they aren't incredibly impactful if you already have some Volts that you like.
The two new Shocks I received are a totally different animal...I'm not sure what Mike and ZJ are seeing with theirs as they have more power than I do, but I'm not getting any turn out of mine, even into the wind. I love these and they are honestly what I've been waiting for since before MVP ever even made a driver. They are VERY much like a good stable S or CPD for me, so far seemingly interchangeable. I used these in the wind today and they were awesome.
Over the past week I've gotten 2 packages from MVP...The new Shocks and the Tangents, and they are EXACTLY what I wanted most from them.
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Results 1 to 1 of 1
11-29-05, 07:36 #1Registered User
- Join Date
- Oct 2005
- Posts
- 87
Unanswered: Default Number of records in continuous form
Hello, i have a question,
I have Main form, and Subform (which is continuous form). Now when i open main form (or even subform itself) i see continuous form, and two empty rows.Whenever i fill first row and press on second, third row appears, and so on.
Can i set somewhere to show me only 1 empty row on this continuous form, and when i fill it, second row appears, and so on. E.g. is there any options for customizing how many empty rows are displayed and the begining of continuous form?
And how "saving of records" work here, because if i fill one row, it won't save anything....it will save it only when i press on other row (when third row creates)
Thanks for your help


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JOB Adverts
Vacant posts exist in an innovative readership promotion facility and literaryspace in Dar es Salaam Tanzania. Applicants that wish to be considered must first and foremost be avid reader and/or persons who appreciates literature and literary discourse; with excellent sales, marketing and people skills. Knowledge and exposure to the book trade, marketing of intellectual and cultural products and a track record of quantifiable achievements in past endeavors will be given special consideration.
1. Bookshop Sales & Marketing Executive (tenable in January, 2016)
· Create, lead and motivate a slim sales team to meet set sales targets (incl. expanding a customer base and maintain a high level of customer service, organizing and managing day-to-day bookshop routine-- daily sales, maintaining an attractive and accessible shop flow design, managing stocks and sales accounts, sourcing books locally and internationally).
· Develop and implement creative sales strategies (incl. mapping customer needs, creating new markets, retain existing customers, developing special packages e.g. book exhibitions & book events, family days and children's corner).
· Maintain and foster business relationships with book suppliers and book chain practitioners (incl. developing special/customized readership cum book sales packages to educational, literary and cultural organizations and networks—and for their clientele).
· Initiate and execute PR & marketing initiatives so as to drive and create awareness of Bookshop stock and Soma Book Café Brands (incl. designing and implementing book promotion packages—e.g. book clubs and membership packages, online marketing, regular compilation and disseminating customer info packages, etc.).
· Build a programmatic team and create inter-departmental synergy (incl. smooth relations with co-workers, participation in planning and appraisal meetings, sharing tasks and lending a joint advertising, sales and PR packages-- exhibitions, events, theme days, database management & sharing, etc.).
· A College education in business communication related fields with interest in sales and marketing of books and allied intellectual and cultural products.
· At least 2 years working experience in sales/marketing environments.
· A reader, book lover, creative, innovative and performance oriented.
· Competitive, self-driven with strong human relation skills.
· A team player, able to work under pressure with high level of integrity.
Negotiable, according to qualifications and experience.
2. Assistant Communication Officer (intern--tenable in February 2016)
· Coordinating Soma storytellers (physical) Hub, activities and events (incl. PR and media liaison, literary events organizing, promoting and scheduling , establishing and maintain updated databases of key resource people, partners and audiences, maintain a cutting edge reference resource corner and group process facilities at the Hub);
· Day-to-day maintenance of E-platforms and media presence (incl. regular updating of Soma Webpage and other e-forums and platforms; writing, soliciting and uploading/posting news stories, events schedules, customers info packs, reports, dialogues and resource inputs on the web facebook, twitter, Whats-Up, Instagram etc. with links to relevant social media platforms, and monitoring and reporting on usage data and statistics).
· Assist in marketing and pushing Soma Brands (incl. originating PR/advert material content + coordinating design, printing and dissemination; assist in developing and running PR campaigns and drafting press releases for events/activities; collecting, documenting and sharing for appraisal audiences/participants' feedback /opinions and change stories).
· Building new and consolidating existing strategic partnerships and networks (incl. monitoring, negotiating drafting MoUs with existing readership clubs/groups/forums hosted at and/or sharing platform creating mapping and outreach
· College education (minimum Diploma) in Mass Communication or PR and Marketing or related field with knowledge and skills on how to navigate the cyberspace/social media savvy.
· Proficient in Kiswahili and English.
· A good communicator (ability to tell stories in different hues and media: text, images and sound); avid reader and skilled writer with good taste and humor.
· A team player, persuasive, result oriented, able to work under pressure
· A good listener, open minded and innovative and with integrity.
Negotiable, according to qualifications and skills development arrangements.
*If you meet the required criteria for any of the posts, send us a copy of your personal profile (CV) and a motivational letter/mail addressed to: THE ADVERTISER, P. O. Box 4460 Dar Es Salaam; or email@example.com telling us why you and how you will add value to the organization).


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Lewisburg Tennessee in Marshall county.
Lewisburg, Tennessee is located in Marshall county within the zipcode 37091. With a total of 2 golf courses in Lewisburg, it lies at an elevation of 741 feet above sea level. The current date and time in Lewisburg Tennessee is November 19, 2017, 4:07 pm. Add a course for free by clicking here or contact us here.


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In order to get a little more control over our analytics, I am hand-tagging our URLs through Google URL builder. But something weird was happening where the tags weren't being recorded in GA. Diving in, I saw that we still have GA integration turned on and that was giving us URLs with two utm_campaign, utm_source, etc.
So I turned off GA integration and tested it. Somehow, I'm still seeing utm_campaign and utm_content being added to all my URLs.
Is there a way to turn this off? Shouldn't shutting off GA integration done that? What am I missing?
Thanks for you help.
Hey James,
When removing the GA integration you'll want to reimport any campaigns from before that was turned off or reimport the templates (if the draft is old). Did you try that?
From Australia to Zimbabwe, and everywhere in between, companies count on Campaign Monitor for email campaigns that boost the bottom line.Get started for free


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March 8, 2017 - 5:00 pm
March 8, 2017 - 8:00 pm
The Simmons College of Kentucky Falcons Basketball Team will be featured by NBA Television on Wednesday, March 8, 2017, doors open at 5PM EST. The documentary will air at 6PM. The event will be held at DiOrio's Pizza and Pub. The restaurant is located at 919 Baxter Avenue, Louisville, Kentucky 40204.
This fun-filled evening will feature great food and drinks, exciting raffles, prizes and much more. We will chat about the making of the film and answer your general questions. We hope you will consider participating in this event. The admission cost is $5.00 for students and $10.00 for everyone else. Food and drink is not included in admission cost. Proceeds benefit Simmons College Athletics Department.


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Water quantity FAQ Frequently Asked Questions
The question library on water related issues
How much water is there on earth?
How much of the water can be found in oceans?
As oceans are very wide and there are multiple to be found on earth, oceans store most of the earth's water. This is apparently 97% of the total amount of water on earth, 2% of which is frozen.
How much freshwater is available?
Of all the water on earth, which is 97,14% of the total amount of surface water, only 2,59% is freshwater. Of this 2,59% another percentage is trapped in ice caps and glaciers, which is about 2%. The rest of the freshwater is either groundwater (0,592%), or readily accessible water in lakes, streams, rivers, etc. (0,014%)
How much water is suitable for drinking water?
How much of the human body consists of water?
Humans mainly consist of water; it is in all our organs and in is transported throughout our body to assist physical functions. When a human does not absorb enough water, dehydration is the result. This is not very surprising, given that 66% of the human body consists of water.
What causes fresh water shortages?
There are four different causes of water scarcity: a dry climate, drought (a period in which rainfall is much lower and evaporation is higher than normal), drying of the soil due to activities such as deforestation and overgrazing by livestock and water stress due to increasing numbers of people that rely on limited levels of run-off.
How can water supplies be increased?
There are five ways to increase water supplies in a particular area: build dams and reservoirs to store run-off, bring in surface water from another area, withdraw groundwater, convert salt water to freshwater (desalination) and improve the efficiency of water use. These methods all have their pros and cons.
What are the causes and effects of flooding?
For more specific questions on water quantities, move to our specific water quantity questions
For water terminology check out our Water Glossary or go back to water FAQ overview
Feel free to contact us if you have any other questions also on the cost of water
About Lenntech
Lenntech BV
Distributieweg 3
2645 EG Delfgauw
tel: +31 152 610 900
fax: +31 152 616 289
e-mail: firstname.lastname@example.com
Copyright © 1998-2017 Lenntech B.V. All rights reserved


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Developed and created by Ferrari Middle East and Africa specifically for the regional market, the California T Deserto Rosso has been previously presented to the entire world.
Now the regional division of Ferrari Middle East and Africa has decided to follow up with another clip in the same vein – footage took during the first California T owner's meeting that took place over the span of a weekend. This was an exclusive event as it was only attended by a "handpicked selection" of Ferrari owners and connoisseurs who were invited to have a taste of the Arabian Desert glory and also enjoy some relaxing events during private parties. Ferrari of course claims the event was hugely successful as it "paid tribute to one of the most successful Ferrari models ever and its proud customers." The Deserto Rosso experience, according to the company, offered an immersive experience into the "unique characteristics" of the California T.
Just as a quick reminder, the California T has been introduced to the worldwide audience during the 2014 Geneva Motor Show and it brought the first turbocharged powertrain to the Prancing Horse brand as it uses a turbocharged 3.8-liter V8 engine that churns out 560 horsepower and 557 pound-feet of torque. It has been linked to a seven-speed dual-clutch automatic gearbox that helps the convertible reach 62 mph in 3.6 seconds and a maximum speed of 196 mph.


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Vault Guides are THE source for insider insight on career information and employer reviews. Shop Vault Guides
Newfield Exploration explores for new fields of oil and natural gas reserves but is happy with old reserves too. The independent oil and gas exploration and production company drills in the Mid-Continent (Anadarko and Arkoma Basins), the Rockies (Uinta and Williston Basins), and the Gulf Coast region of Texas. The company seeks to hedge its exploration and production bets by exploiting assets outside of the US, primarily in China and Malaysia. In 2015 Newfield Exploration reported proved reserves of 509 million barrels of oil equivalent (41% oil, 16% NGLs, and 43% natural gas).
While Newfield Exploration only has operations in the oil and gas exploration and production industry, it is organizationally structured in geographic operating segments: the US and China.
In 2015 the company had 5230 gross wells (net 3,280).
Geographic Reach
Newfield Exploration has oil and gas assets in the US (Mid-Continent, the Rocky Mountains and onshore Texas), and China. US operations accounted for 83% of the company's revenues in 2015, while China accounted for the remainder.
Sales and Marketing
Oil, natural gas and NGLs are sold at market-based prices to a variety of purchasers, primarily under short-term contracts and long-term contracts in the Uinta Basin at market-based prices. China National Offshore Oil Corporation Ltd., MidCon Gathering LLC, and Sunoco Logistics Partners Operations GP LLC accounted for 13%, 11%, and 10%, respectively, of the company's total revenues in 2015.
Financial Performance
In 2015 Newfield Exploration's decreased by 32%.
The drop in revenues from domestic operations was attributable to lower oil prices. Domestic liquids production increased year over year, reducing the impact of lower commodity prices by $236 million. The proved reserves in 2015 were negatively impacted by the significant drop in commodity prices. Due to price-related revisions, domestic liquids reserves decreased 21% year-over-year.
Revenues from China increased due to production from the Pearl development.
In 2015 net loss decreased by 474% due to the presence of a ceiling test and other impairments as the result of a net decrease in the discounted value of its proved reserves and a drop in net sales.
Cash from operating activities decreased by 13%.
Despite a reduced capital budget in 2015 that reflected the current price environment, the company's primary, long-term goal continues to be delivering stockholder value through consistent growth of cash flow, production and reserves. Over the past several years, it has focused its investments on oil and liquids-rich resource plays in the US. It operates in several US basins with the primary growth area being the Anadarko Basin. Key components of Newfield Exploration's business strategy includes: focusing on organic opportunities through disciplined capital investment; continuously improving operations and returns; preserving a strong and flexible capital structure; maintaining a diverse asset base with ongoing portfolio management; and executing select, strategic acquisitions and divestitures.
In 2016 more than 80% of its capital investment was focused on the SCOOP and STACK. Outside of the Anadarko Basin, the company planned to invest $125 million the Williston, Uinta and Arkoma basins. It planned to complete 12-15 wells in the Williston Basin.
That year Newfield Exploration sold its Texas assets for about $380 million.
In 2015 the company reduced it capital investments by 26% and re-directed capital to their highest return region - the Anadarko Basin of Oklahoma. It also divested non-strategic assets of $2.2 billion from 2012-2015 and used the proceeds for drilling and reduce borrowing. As part of their cost saving measure, the company reduced workforce by more than 20%.
In 2015, the company acquired various other oil and gas properties for approximately $125 million.
In the US, Newfield Exploration has steadily shifted its exploration and production focus from the Gulf Coast and Gulf of Mexico to the Mid-Continent and Rocky Mountain regions. In particular, it is targeting unconventional oil shale plays, where due to recent improvements in drilling technology it can access a higher return on investment. It is also developing its international assets, including its holdings in the Pearl field in the offshore China.
To raise cash in order to pay down debt and fund capital expenditures, in 2014 the company sold it Granite Wash assets, located primarily in Texas, for $588 million, and its Malaysia business to SapuraKencana Petroleum Berhad for $898 million.
During 2014, it continued to market its China business. Due to the precipitous decline in oil prices, the company was unable to sell the China business at an acceptable price and determined it was in Newfield Exploration's best interest to retain the cash flow from the China business. Accordingly, it reclassified this business as continuing operations.
Company Background
In 2013 the company announced a major natural gas discovery on the Block SK 310 Production Sharing Contract (PSC) area, located 50 miles offshore Sarawak (Malaysia). Newfield Exploration, which operates Block SK 310 with a 30% interest, estimated that the discovery had gas reserves of 1.5 - 3 trillion cu. ft. That year the company also announced that it was evaluating strategic alternatives for the company's international businesses.
In 2012 it sold its remaining Gulf of Mexico assets (78 federal offshore lease blocks on 432,700 gross acres) to W&T Offshore for $228 million.
In 2011 Newfield Exploration bought oil and gas assets in Utah's Uinta Basin from Harvest Natural Resources for $215 million.
The company was incorporated in 1988.
4 Waterway Square Pl #100
The Woodlands, TX 77380-2764
Phone: 1 (281) 210-5100
Fax: 1 (281) 405-4242
November 15, 2017
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November 10, 2017
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Fifty years ago, John Steinbeck's now classic novel, The Grapes of Wrath, captured the epic story of an Oklahoma farm family driven west to California by dust storms, drought, and economic hardship. It was a story that generations of Americans have also come to know through Dorothea Lange's unforgettable photos of migrant families struggling to make a living in Depression-torn California. Now in James N. Gregory's pathbreaking American Exodus, there is at last an historical study that moves beyond the fiction and the photographs to uncover the full meaning of these events.
American Exodus takes us back to the Dust Bowl migration of the 1930s and the war boom influx of the 1940s to explore the experiences of the more than one million Oklahomans, Arkansans, Texans, and Missourians who sought opportunities in California. Gregory reaches into the migrants' lives to reveal not only their economic trials but also their impact on California's culture and society. He traces the development of an "Okie subculture" that over the years has grown into an essential element in California's cultural landscape.
The consequences, however, reach far beyond California. The Dust Bowl migration was part of a larger heartland diaspora that has sent millions of Southerners and rural Midwesterners to the nation's northern and western industrial perimeter. American Exodus is the first book to examine the cultural implications of that massive 20th-century population shift. In this rich account of the experiences and impact of these migrant heartlanders, Gregory fills an important gap in recent American social history.
A thorough study of the migration of Oklahomans, Arkansans, Texans, and Missourians to California in the years of the Dust Bowl and the Great Depression. Gregory dispels the popular Okie image built from The Grapes of Wrath , placing this unique exodus in economic perspective. He is particularly successful in tracing Okie impact on the San Joaquin Valley, where the Okie twang and culture have taken root to become the Californian. Gregory's prose is conversational, although his narrative lacks the compelling anecdotes that enrich history for the lay reader. This is, nevertheless, an important and necessary work on this period. Recommended.-- Timothy L. Zindel, Hastings Coll. of the Law, San Francisco


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17 Comments
He definitely is +1
Helldemonik Human from Florida, United States
Just because Boba Fett is the man and i have the Mandalorian symbol tattoo'ed on me in the same spot he does… this gets my vote!! Long live the Fett!! =DD
@Helldemonik I have mandalorian tattoo on my leg :)
Nice design, definetly +1, .......
word of advice : try making ur own custom brushes, it will add much more originality to ur artworx
hi, glad you like it, thanks for the advice :)
So good.
andreastark Human from New Zealand
LOVE this
Like! +1
thanks! :)
Awesome … you are right !!! Boba is the man !!!
nice!! +1
very nice job
thanks people! glad you like it :)
RLMarkossa Artist from Brazil
Cool style! +1


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Councils warn of funding black hole for flooding
The Local Government Association has challenged the environment department (DEFRA) to explain its funding assumptions in the draft Flood and Water Management Bill. It believes the government is significantly underestimating the real costs.
Sorry you do not have access to this article. Please contact Customer Support at
or call 020 8267 8120


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Baked Pineapple Cream Cheese Wontons Recipe
- 36 wonton wrappers
- coconut oil or olive oil for brushing wontons
Wonton Filling
- 8 oz. cream cheese, softened
- 2 green onions, chopped
- 1/4 cup sweetened coconut flakes, roughly chopped
- 1/4 teaspoon powdered ginger
- 1 teaspoon Sriracha/Asian hot chili sauce
- crushed pineapple from 8 oz. crushed pineapple can (reserve juice for sweet and sour sauce)
Easy Pineapple Sweet and Sour Sauce
- 1/4 cup kethup
- 1/4 cup white vinegar
- 1/4 cup sugar
- 2 garlic cloves, minced
- Pineapple juice form 8 oz pineapple can
- 1 tablespoon cornstarch
- sriracha to taste (optional)
- Preheat oven to 400 degrees.
- Add 1/2 cup water to a small bowl.
- In a large bowl, whisk together wonton filling ingredients until well combined. Place a heaping 1 teaspoon wonton filling in the center of each wonton wrapper. Wet your finger and brush along the edges of the wonton wrapper, then fold into a triangle, pressing edges together to seal well. Repeat for the rest of the wontons.
- Place finished wontons on a baking rack ontop of a baking sheet and lightly brush both sides of each wonton with olive oil or coconut oil. Bake for 8-12 minutes or until corners are browned and crispy.
- To make the Pineapple Sweet and Sour Sauce, whisk together ketchup, vinegar, sugar and garlic in a medium saucepan. Pour pineapple juice into 1/2 cup measuring cup then add water to equal full ½ cup. Whisk in cornstarch to the pineapple juice/water then add to saucepan and stir until well combined. Bring ingredients to a boil and simmer until thick – 1-2 minutes. Taste and add additional vinegar for more tang/sour or sugar for sweetness according to your preference. You can also add sriracha for a little heat.


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This week, things get technological as we discuss virtual reality. Among the questions we tackle: What is virtual reality? Why did Facebook buy Oculus? What is Oculus? What is Facebook? What ever happened to Virtual Boy, the Nintendo system from the mid-90s? Is it possible to use virtual reality to accurately simulate the sensation of kissing Juliette Lewis? Why is it so cold in cyberspace?
We also talk about curing people of stab wounds by draining their blood and freezing them, stealing broaches from parties, and sneaking in to R-rated movies as a young teen. In a new installment of Tim & Tom Solve Your Problems, we answer an email from a listener who thinks he's some sort of big-shot funny man.
This week's episode is brought to you by Audible. Get a free 30 day trial and an audiobook download of your choice by going to tcgte.com/audible.


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See All
Video Recipes
"Pachakam" means cooking in kerala and Pachakam.Com welcomes you to the magnificent world of easy and healthy Indian cooking with a probe into the fascinating Indian cooking recipes. Cooking is not just about making food but is an art of presenting your culinary skills to those who love food with a different flavor and Indian cooking, by no means is an exception.
Prawns and other ingredients are ground and fried in oil
Category :
Published On: 18 May 2011
English: Prawns
tamil: Eral
malayalam: Chemmeen
kannada: Sigadi
hindi: Jinga
Bengali: Chingri
Konkani: Sungtan
Marathi: Zinga
Tulu: Etti
for more details, click the name of the ingredient
English: Ginger
tamil: Inji
malayalam: Inchi
telugu: Allam / Allamu / Sonthi
kannada: Shunti / Alla / Ashi Shunti / Ardraka
hindi: Adrak / Adu / Soonth
Bengali: Ada
Gujarati: Aadu / Soonth
Konkani: Alley
Marathi: Aale
Oriya: Ada
Punjabi: Adrak
Tulu: Soonthi
Urudu: Adrak / Adhrak
English: Green Chillies
tamil: Pachchii Milagai
malayalam: Pachamulagu
telugu: Patchimirapa / Pachchi Mirapakayalu
kannada: Hasi Menasinakai
hindi: Hara Mircha / Hari Mirch
Bengali: Kancha Lanka / Maricha
Gujarati: Marcha
Konkani: Jeevisaang / Tanrni Mirsang / Tanrni Miriyasang
Marathi: Pachchai Milagai
Oriya: Lila Marcha
Punjabi: Mirchan
English: Coconut
tamil: Thengai
malayalam: Nalikeram / Thenga
telugu: Kobbari Kaaya
kannada: Thenginakai
hindi: Nariyal
Bengali: Narcole
Gujarati: Naliyer / Nariyal
Konkani: Naarlu
Marathi: Naral
Oriya: Nadia
Punjabi: Gola / Nariyal
Kashmiri: Narjeel
English: Cilantro / Coriander Leaves
tamil: Kothamalli Ilai / Malli Ilai
malayalam: Kothamalli Ila / Malli Ila
telugu: Kothimeera / Kothamalli Kooraku
kannada: Kottambari Soppu
hindi: Hara Dhania Ke Patte / Dhania Patha
Bengali: Dhonay Patha
Gujarati: Kothmir / Dhana
Konkani: Kottambari Pallo
Marathi: Kothimbir
Oriya: Dhania Patra
Punjabi: Hara Dhania
English: Salt
tamil: Uppu
malayalam: Uppu
telugu: Uppu
kannada: Uppu
hindi: Namak
Bengali: Laban / Noone
Gujarati: Meethu
Konkani: Meet
Marathi: Mith
English: oil
tamil: Ennai
malayalam: enna
telugu: camuru
kannada: taila
hindi: tela
Punjabi: moyen
For preparing tasty prawn vada, grind prawns, roasted groundnut, shallots, ginger, green chillies, coconut, pepper, coriander leaves and salt in a mixy.
Make balls out of the mixture and press it as for parippuvada.
Fry it in oil.
Tasty prawn vada is ready. Serve hot.
Specialities:1)Naadan recipe.
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Chicken bonda is a non- veg version of normal Aloo bonda.Whe...
Nizana Shammas is a hosewife who has lots of interest n cooking. She is an expert in providing various traditional recipes.
Renukadevi Kumanan is a well versed person in providing varities of South Indian recipes and also some modern recipes. She used to try varities of recipes from different cuisines.
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Olives, A lot of Cheese, Mushrooms and Basil.
Swiss cheese, mushrooms and ham.
Haha! That guard was always soooo freaken annoying. I loved the song, thank you for sharing.
I've never played Skyrim but I do get the joke. The "arrow to the knee" was an iconic moment for Skyrim. It inspired many memes and jokes. I'm sure many gamers love this jokey music video


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Satin Ladyboys
Ultimate Tgirl Productions/Exquisite Multimedia
D: Jonathan Sable
Wi, Jenny Star, Lilly, Emmy, Opo, Mona, Fa, Others. 100 Min.
Extras: Bonus Scenes, Still Gallery.
Director Jonathan Sable brings his gentle eye and love of lingerie and shoes to the ladyboy league. Alas, it's not as magical a combination as one might think.
It's not that the ladyboys in question aren't comely enough. It's just that some of them don't quite seem to know what to do with themselves or their fellow performers.
Mona and Fa are dressed as black and white lingerie opposites. Although each girl goes through her moves, including licking one another's shoe, there's just no heat or sense of attraction. Although Wi's partner seems moved by the kissing and slapping he administers to her, she remains largely unresponsive until his cock tickles her prostate.
Lilly and Emmy start with a panty inspection and end with a seminal exchange. Opo doesn't seem to care for the sensation of ejaculate on her face, but doesn't mind rubbing it on her shoe. Tiny Jenny makes half of a cute Asian cock sucking couple.
— Originally published in AVN magazine —


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Recent History
Chalkboard Rooster Decor
$19.99 $10.00
Leave a note, post the day's menu, or scribble a favorite quote--our handsome Chalkboard Rooster Decor gets the message! This clever tabletop rooster figure holds a stick of chalk near his wing, inviting you to make your mark on his chalkboard belly. He'll make a fun, functional addition to your kitchen or home decor, and makes a great gift, too!
- Rating
- 5
- Features
- Includes 1 piece of chalk
- Dimensions
- 11.26" x 11.57" x 3.27"


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Rugby player picks up oppenent to use as battering ram
George North carried off a move in a rugby match which has been referred to online as the 'Plymouth Backpack'.
George North carried off a move in a rugby match which has been referred to online as the 'Plymouth Backpack'.
Wales and New Zealand captains and coaches give their reactions to the Kiwis 36-0 victory.
Cardiff Blues' Sam Warburton looks back at the World Cup in New Zealand, where he captained Wales.
Australia may be coming off a 26-12 victory over New Zealand, but Jonathan Thurston believes England will be ready to take advantage of any mistakes they make in their 4 Nations match at Wembley.
New Zealand are hoping for a more consistent performance in their 4 Nations match with Wales at Wembley after losing 12-26 to Australia last week.
The official launch of the 17th Heineken Cup took place today at Dublin's Convention Centre. Leinster's Leo Cullen, Munster's Paul O'Connell, Connacht's John Muldoon and Ulster's captain, Johann Muller look forward to this year's tournament and tell us what makes the tournament so special.
Despite the heartbreak, Wales's First Minister Carwyn Jones said the country's team had done the nation proud.
Half-back Danny McGuire is elated he has finally been named in England's squad for the Four Nations, while lock Chris Heighington joins the squad, despite being born in Australia.
England rugby league coach Steve McNamara is excited to his squad back together again for the Four Nations, claiming they don't play together often enough.
Wales meet France in the World Cup semi-finals on Saturday.
Tuilagi, 20, took the plunge as a number of players returned from a day trip to Waiheke Island and he swam to a nearby pier, where was met by police.
Wales are aiming to maintain their momentum as they prepare for their World Cup semi-final with France.
The RFU will undertake a review of England's failed World Cup campaign before deciding whether Martin Johnson should continue as manager.
Ireland stand on the brink of Irish rugby history with a place in the last 4 of the Rugby World Cup at stake ahead of kick off against Wales.
The English rugby team prepare for quarter final clash with France.
Toby Flood comes into the side for Mike Tindall, who has been sidelined by a dead leg, as one of four changes from England's 16-12 victory over Scotland last weekend.
Neil Jenkins welcomed the return of Wales' World Cup injury casualties today as preparations continued for a quarter-final showdown with Six Nations rivals Ireland.
"This, famously, is the unspoilt... Travel Talk
At this time of year... GAA
This is... International Soccer
I'm standing on a... World/USA
John Downing on what was needed to keep Government on track Politics
The star of Ireland's World Cup tilt has always polarised opinions. But who is James McClean? International Soccer


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The much awaited 2016 model Ford Endeavour SUV to be Launched Soon in India with luxury options and features. Ford Endeavour 2016 is a special vehicle which is Engineered for Extraordinary. This will be available in diesel engine option.
Ford Endeavour 2016 powered by a 3.2L TDCi Diesel engine. This can churns out 197 bhp power and 470 Nm torque on ride. Engine mated to 6-Speed Automatic Gearbox for smooth transmission. The SUV features 3000 kg Maximum Towing Capacity.
Ford Endeavour 2016 looks appealing and measures 4882 mm Overall Length x 1862 mm Overall Width x 1836 mm Overall Height. There is 2850 mm wheelbase, 225 mm Minimum Ground Clearance, 2357 kg Kerb Weight and 2900 kg Gross Vehicle Weight.
There is 7 Person seating capacity in Ford Endeavour 2016. You have finest braking and suspension option. Front brakes used in this SUV is a Disc type. Rear brake is drum type. You have Independent double wishbone suspension in front and Leaf springs suspension at rear.
Other options and features available are Alloy Wheels, Steering Mounted Controls, Air Conditioner, Keyless Entry, Power Steering, Rear Defogger, cruise Control, Rain Sensing Wipers, Power Windows, Collapsible Steering Column, Side Impact Beams, Airbags, Parking Sensors, Hill Start Assist Control etc.
You have Electronic Brake Distribution (EBD), Anti-lock Braking System (ABS), Electronic Stability Program (ESP), Engine Immobilizer, Anti-theft Alarm, Central Locking, Darkness Sensing Headlamps, SYNC2 infotainment system with an eight-inch touchscreen display, Leather Seats etc.


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We often think of celebrations as centering around special occasions, like Birthdays, Christmas, or other holidays. But there is no need to wait for those times. Everyday is a cause for celebration. The very fact that you are alive, the wondrous world around you, and the special people in your life are all reasons to rejoice.
That's what this audiobook is all about. Over 500 suggestions for living life to the fullest. A compendium of "glass half full", common sense, these witty and wise words from both the rich and famous, as well as the not-so-rich and the not-so-famous, will, I hope, inspire you to make every day a special day.
Pianist Artur Rubinstein once said,"To be alive, it's all a miracle". Yes indeed, it is all a miracle, and all a cause for celebration.
©2013 Viva Editions (P)2013 Viva Editions
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text: Human Rights Observatory WFP Chief: Throughout Africa, Hunger Grows From Familiar Roots A large swath of Southern Africa has been hit by a double whammy of epic floods followed by a miserly drought -- a phenomenon that has affected countless people in Malawi, Zimbabwe, and Mozambique. Meanwhile, the fledgling nation of South Sudan is in the throes of a major hunger crisis as conflict has pushed the country's population to the brink of famine. As different as these two scenarios appear, the head of the UN's World Food Program said both crises grow from the same roots. WFP...Read complete article© Voice of America - Friday, April 3rd 2015


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Rett Syndrome (RTT) is caused by mutations of MECP2, a methyl CpG binding protein thought to act as a global transcriptional repressor. Here we show, using an isogenic human embryonic stem cell model of RTT, that MECP2 mutant neurons display key molecular and cellular features of this disorder. Unbiased global gene expression analyses demonstrate that MECP2 functions as global gene activator in neurons but not in neural precursors. Decreased transcription in neurons was coupled with a significant reduction in nascent protein synthesis and lack of MECP2 was manifested as a severe defect in the activity of the AKT/mTOR pathway. Lack of MECP2 also leads to impaired mitochondrial function in mutant neurons. Activation of AKT/mTOR signaling by exogenous growth factors or by depleting PTEN boosted protein synthesis and ameliorated disease phenotypes in mutant neurons. Our findings indicate a vital function for MECP2 in maintaining active gene transcription in human neuronal cells.
Rett syndrome (RTT) is a monogenic X-linked neurodevelopmental disease that belongs to autism spectrum disorders (ASDs). It has been well established that mutations in the MECP2 gene account for the majority of RTT cases (Amir et al., 1999). We and others have generated mutant mice bearing loss-of-function alleles of Mecp2, and showed that they recapitulate many of the cellular and behavioral phenotypes of RTT patients (Chen et al., 2001; Guy et al., 2001). Recent work using these mouse models demonstrated that the disease pathology in MECP2 mutant mice could be reversed either via re-expression of the wild-type Mecp2 gene (Giacometti et al., 2007; Guy et al., 2007), or by exogenous growth factors (Chang et al., 2006; Tropea et al., 2009). These findings serve as important proof-of-principle evidence that RTT, and perhaps ASD in general, are treatable disorders. With the advent of induced pluripotent stem cell (iPSC) technology (Takahashi et al., 2007; Yu et al., 2007), it has become feasible to confirm conclusions from animal models in human cells by deriving patient-specific iPSCs for disease modeling and therapeutic investigation (Ananiev et al., 2011; Cheung et al., 2011; Marchetto et al., 2010). However, due to differences in genetic background and method of derivation, human embryonic stem cells (ESCs) and iPSCs display highly variable biological characteristics such as propensity to differentiate into specific lineages, complicating their use in disease modeling (Soldner and Jaenisch, 2012). This is of particular relevance to RTT, in which genetic background has been demonstrated to influence the severity of disease symptoms (Scala et al., 2007). To overcome this complication, isogenic experimental and control cells that differ exclusively at the disease-causing genetic alteration have been generated, allowing the study of disease-specific phenotypes under highly controlled conditions (Soldner et al, 2011).
It has been well established that MECP2 protein is abundantly present in neuronal cell types, and binds methylated-CpG sites throughout the neuronal genome (Skene et al., 2010). Such binding specificity and mode of distribution strongly suggested that MECP2 functions as a global transcriptional repressor (Nan et al., 1997). However, the role of MECP2 as a repressor received little support from in vivo studies as exhaustive gene expression analyses on pre-and post-symptomatic mutant mice provided little evidence of global transcriptional activation (Ben-Shachar et al., 2009; Chahrour et al., 2008; Jordan et al., 2007; Kriaucionis et al., 2006; Nuber et al., 2005; Tudor et al., 2002; Urdinguio et al., 2008).
In the present study, we used TALEN-mediated gene editing to generate human ESCs with a loss-of-function MECP2 allele. This strategy ensures that neuronal cells derived from the control and mutant ESCs differ only at the MECP2 gene. We found that although neural precursors (NPs) derived from mutant ESCs were largely normal as compared to their isogenic controls, an array of cellular and molecular abnormalities developed in differentiated MECP2 mutant neurons. To investigate the impact of MECP2 deletion on the neuronal transcriptome, we adopted a newly developed gene expression analysis method that took into consideration possible global shifts in transcriptional activities. We found a significant genome-wide transcriptional down-regulation in mutant neurons. This striking reduction of global transcription was echoed in significantly decreased protein synthesis levels. Pharmacological and genetic manipulations that boost protein synthesis ameliorated RTT-related disease phenotypes. These findings strongly support the notion that one of the key functions of MECP2 is to facilitate global transcription.
To generate a MECP2 loss-of-function allele, we designed TALENs to specifically target the third exon of the MECP2 gene, which encodes most of the methyl-CpG-binding domain (Figure 1A and S1A). A donor construct containing an in-frame eGFP-polyA sequence and a PGK-puro cassette flanked by two homology arms corresponding to the genomic sequence of the MECP2 gene was used for targeting (Figure 1A). This targeting strategy disrupts gene function and generates an endogenous reporter for MECP2 activity. We used a male (WIBR1) and a female ESC line (WIBR3) to generate MECP2 hemizygous mutant male and heterozygous mutant female clones (Figure 1B, S1B and S1C). The WIBR3 ESCs were maintained in the XaXi state, in which the targeted MECP2 allele resided on the active and the wild-type allele on the inactive X chromosome. For subsequent analyses, we used 1 pair of control and mutant WIBR1 ESCs (WIBR1-Con, WIBR1-Mut), and 2 sub-clones each of the control and mutant WIBR3 ESCs (WIBR3-Con1, WIBR3-Con2, WIBR3-Mut1, WIBR3-Mut2). In addition, similar to their isogenic wild-type controls, mutant ESCs maintained the expression of pluripotency marker expression (Oct4, Nanog and Sox2, Figure S1D) and formed teratomas when injected subcutaneously to NOD/SCID mice (Figure S1F–G).
Human ESCs and iPSCs can generate NPs, which can be induced to differentiate into different neural and glial subtypes (Soldner et al., 2009). To generate a homogenous population of NPs from control and MECP2 mutant ESCs, we utilized a SMAD-inhibition-based neural differentiation protocol (Chambers et al., 2009; Zhou et al., 2010). Adherent culture of control and mutant ESCs were differentiated side-by-side into neural rosettes, and further expanded as NPs in the presence of bFGF. These isogenic pairs of NPs were then cultured in medium that promotes terminal neural differentiation and maturation (Figure 1C). Using antibodies specific to antigens of these lineages, we demonstrate the generation of NPs (Pax6+, Nestin+) and neurons (TuJ1+, MAP2+) from pluripotent ESCs (Nanog+) (Figure 1C). Furthermore, using antibodies against vGlut1 and GAD67, we found that both excitatory and inhibitory neurons were present in the neuronal cultures (Figure 1C).
MECP2 is expressed in ESCs and NPs, but significantly more abundantly in neurons, as shown by immuno-blotting (Figure 1D–E). To confirm that the targeting strategy disrupted the MECP2 locus, we isolated mRNA from control and mutant ESCs, NPs and neurons. Quantitative RT-PCR revealed the absence of MECP2 expression in WIBR1-Mut and WIBR3-Mut cells (Figure 1F). Immuno-blotting confirmed the absence of MECP2 protein (Figure 1G). Furthermore, wild-type MECP2 protein was not detectable by immuno-staining (Figure S1E and not shown). The lack of wild-type MECP2 mRNA and protein was consistent with the hemizygous status of WIBR1-Mut ESCs, and the one X active (XaXi) state of WIBR3-Mut ESCs demonstrating loss of function in WIBR1-Mut and WIBR3-Mut cells.
Control and mutant NPs displayed similar morphology (Figure S1H) and expressed comparable levels of markers indicative of the cortical lineage (Figure S1I). Upon withdrawal of bFGF, both control and mutant NPs readily generated Doublecortin-positive immature neurons (Figure S1J). During the course of neuronal differentiation, predominantly excitatory neurons were generated (Figure 1H, I). Expression of genes characteristic for different cortical layers such as Calretinin (subplate), Reelin (layer I), FoxP2 (V/VI), CTIP2 (II to VI) and Cux2 (II) were similar in control and mutant cells (Figure S1K–P). These finding suggest that MECP2 deletion did not alter the differentiation potential of NPs.
A prominent feature of RTT patients is microcephaly with the reduction in brain size correlating with the reduction in neuronal size (Akbarian, 2002; Chen et al., 2001). Consistent with these findings, soma and nuclei of mutant neurons expressing MAP2 or marked by a Synapsin-GFP virus (Kugler et al., 2003) displayed a significantly reduced size as compared to isogenic controls (Figure 2A–D). In contrast, mutant NPs displayed a similar soma and nuclear size as compared to controls (not shown). Because excitatory neurons comprise the majority of the mature neurons generated in our differentiation protocol (Figure 1I), the reduction of soma size mostly represents deficits in the excitatory neuron population. Recent studies suggest that cell-type specific deletion of MeCP2 in inhibitory neurons was sufficient to impair GABAergic function leading to severe behavior deficits (Chao et al., 2010). To investigate whether human inhibitory neurons require MECP2 for proper morphological development, we co-stained the neuronal culture with MAP2 and GAD67 and found a significant soma size reduction in mutant cells (Figure 2A and 2B). We also investigated whether MECP2 deletion affects neurite arborization of individual Synapsin-GFP labeled neurons. Sholl analysis revealed significantly reduced neurite complexity in MECP2 mutant neurons (Figure 2E and 2F). Utilizing a dual-chamber multi-electrode array culture system that allows for continuous monitoring the appearance of spontaneous activities, we plated control and mutant neurons side-by-side (Figure 2G), and found that action potential rates were significantly reduced in mutant neurons (Figure 2H to 2J). We conclude that MECP2 deletion impairs neuronal development and function.
We next compared isogenic mutant and control cells to assess the effect of MECP2 deletion on global gene expression. Conventional global transcriptional analyses normalizing individual gene expression to total RNA (MAS5 for Affymetrix) indicated that the majority of genes were unchanged (Figure 3A and 3B). When the distribution of expression changes of all genes was examined, a minimal median change in mutant NPs and 2-week-differentiated mutant neurons and a small increase in 4-week-differentiated mutant neurons were found (Figure 3C). The minor gene expression changes in MECP2 mutant neurons, especially those found in the male WIBR1-Mut neurons, were consistent with previous findings in Mecp2 hemizygous mutant mice (Kriaucionis et al., 2006; Nuber et al., 2005; Tudor et al., 2002; Urdinguio et al., 2008). We found that the female WIBR3-Mut neurons displayed a higher level of differential expression compared to their isogenic controls, with a similar distribution of up- and down-regulated genes at 2-weeks, and slightly more up-regulated genes at 4-weeks of differentiation (Figure 3B).
The validity of conventional gene expression analyses, which usually are based on the assumption that total RNA content per cell remains constant, has recently been questioned. It was discovered that c-Myc over-expression results in a significant increase in nuclear size and an amplified per-cell expression of more than 90% of all genes. However, when the expression data were normalized using the traditional analysis method, i.e. normalization to total input RNA, this genome-wide gene expression change was not detected (Lin et al., 2012; Loven et al., 2012). These observations are highly relevant to MECP2 mutant cells, which display a significantly reduced soma and nuclear size (Figure 2A to 2D).
To investigate whether the reduced soma and nuclear size of MECP2 mutant cells affected per cell RNA levels, we isolated total RNA from equal numbers of NPs and differentiating neurons. Figure 3D shows that mutant neurons at 2 and 4 weeks of differentiation have 27% and 47% less total RNA, respectively, as compared to their isogenic controls. A significant reduction of differently sized rRNAs was found in differentiating mutant neurons consistent with ribosomal RNA (rRNA) and transfer RNA (tRNA) constituting the majority of total RNA (Figure 3E). In contrast, NPs of either genotype had similar levels of total RNA and rRNA (Figure 3D and 3E).
To assess how normalization to input cell number affects the interpretation of global transcriptional analyses, we prepared RNA from an identical number of control and mutant cells and added synthetic RNA spike-in standards as surrogates for cell numbers (Loven et al., 2012). After normalizing gene expression to RNA spike-ins, an average of 50% of all genes were down-regulated more than 1.2-fold in mutant neurons at 2-weeks of differentiation (Figure 3F and 3G; 62.3% in WIBR1-Mut; 37.9% in WIBR3-Mut). At 4-weeks of differentiation, the percentage of down-regulated genes in MECP2 mutant neurons was 60% (Figure 3F and 3G; 54.1% in WIBR1-Mut; 64.6% in WIBR3-Mut). In contrast, only about 7% of all genes were up-regulated more than 1.2-fold at 2- and 4-weeks of differentiation (2.4% and 5.8% in WIBR1-Mut; 12.6% and 7.4% in WBIR3-Mut). At the NP stage, expression levels were more evenly distributed, with 14% down-regulated and 8% up-regulated 1.2-fold or more (13.5% down and 5.8% up in WIBR1-Mut; 15.4% up and 10.5% down in WIBR3-Mut).
A similar global down-regulation was seen when a higher threshold (1.5-fold) was used, which shows that mutant neurons on average had ~10 times the number of down-regulated genes compared to up-regulated ones. By examining the distribution of expression changes of all genes, we saw a median 25% percent reduction in 2-week differentiated mutant neurons, and 37% reduction in 4-week differentiated mutant neurons (Figure 3H, 32.2% and 29.6% in WIBR1-Mut; 17.1% and 43.7% in WIBR3-Mut) whereas average gene expression in mutant NPs was not significantly changed. Gene ontology analysis revealed that genes involved in the biological processes of transcription and translation were enriched amongst the most significantly down-regulated genes (Figure 3I). Through this series of analyses, we found that female mutant WIBR3 cells displayed more differential gene expression changes than male WIBR1 mutant cells when compared to the isogenic controls (Figure 3F to 3H), possibly reflecting the inherent stability differences between cultured male and female pluripotent stem cells (Anguera et al., 2012; Mekhoubad et al., 2012; Zvetkova et al., 2005). Indeed, WIBR3-derived female NPs and neurons had increased expression levels of X-linked genes as compared to WIBR1-derived male cells (Figure S2A–B). Importantly, these unbiased global gene expression analyses revealed a consistent genome-wide transcriptional reduction in both WIBR1 and WIBR3 mutant neurons.
To further quantify expression changes, we divided all genes based on their expression levels (in control neurons) into 4 equal groups. Figure 3J and 3K show that higher expression was correlated with a more dramatic extent of down-regulation in 4-week-old mutant neurons. The most highly expressed genes (top 25%) showed a median 70% reduction in expression, whereas the lowest expressed genes (bottom 25%) showed only a median 4% reduction. A similar trend was seen in 2-week-old neurons (Figure S2C–D), but not in NPs (Figure S2E–F). In addition to analyzing the expression of all genes, we examined genes that were significantly up-or down-regulated in 4-week-old mutant neurons of both WIBR1 and WIBR3 genetic background (85 and 7265 commonly up and down-regulated genes). Figure 3L (and Figure S2G) shows that genes that were down-regulated in the absence of MECP2 were expressed at a substantially higher level, as compared to genes that were up-regulated. Notably, when the expression level of genes that were significantly up-or down-regulated in mutant NPs was examined, no such correlation was seen (Figure 3M). The selective group of up-regulated genes in 4-week-old mutant neurons, albeit numerically few, was less active in wild-type neurons and may represent instances where MECP2 binding exerted repressive effects. Indeed, some of the up-regulated genes (CALCR, Nanog, UGT2B10) were predominantly expressed outside of the nervous system, and may be mis-expressed due to the lack of MECP2-mediated repression (Figure S2H–J). Our results demonstrate that active genes were more susceptible to down-regulation upon MECP2 deletion strongly indicating a transcriptional activator function for MECP2.
We compared the specificity of transcriptional reduction of genes involved in nervous system development (Figure S3A, human.brain-map.org) and in synapse formation (Pirooznia et al., 2012). Figures 4A shows that both groups of genes were collectively down-regulated in MECP2 mutant neurons. In contrast, the expression levels of a group of genes known to be specifically expressed in astrocytes and oligodendrocytes were largely unaffected in mutant cells (Figure 4A) (Cahoy et al., 2008).
Recent reports have suggested a role for MECP2 in regulating the expression of immediate early genes, a distinct group of genes found to be critically dependent on transcriptional regulation (Kron et al., 2012; Su et al., 2012; Tullai et al., 2007; Yasui et al., 2007). When comparing the expression of a group of immediate early genes known to be activated by neuronal activity (Bateup et al., 2013), these genes were expressed at relatively high levels in control neurons (Figure S3B) and collectively down-regulated in mutant neurons (Figure 4B). Quantitative RT-PCR further confirmed the down-regulation of some of these key immediate early genes, such as Arc, Fos, NPAS4 and BDNF (Figure 4C). This coincides with mutant neurons displaying reduced network activities (Figure 2H-2G) thereby correlates transcription reduction with physiological impairment. To further investigate whether MECP2 plays a direct role in regulating immediate early gene expression, we treated control and mutant neurons with tetrodotoxin, followed by de-polarization with KCl. Quantitative RT-PCR revealed significant increases in the Arc, Fos, NPAS4 and BDNF expression in control neurons, while mutant neurons failed to display such induction (Figure 4D).
A recent study in mice showed that MECP2 binds to both 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC), with the latter enriched within active genes (Mellen et al., 2012). This observation is consistent with our finding that binding of MECP2 facilitates active transcription, and predicts that genes with higher 5hmC/5mC ratios would be more likely to be down-regulated in the absence of MECP2. We extracted the ranking of 5hmC/5mC ratios from wild-type mouse neurons, and correlated the expression of these genes in 4-week-old human neurons. Figure 4E–4F shows that genes with higher 5hmC/5mC ratios were more highly expressed in control human neurons (top panels), and were more likely down-regulated in MECP2 human mutant neurons (lower panels). In contrast, gene expression changes seen in MECP2 mutant NPs were not correlated to the 5hmC/5mC ratio (Figure 4G–4H) suggesting that this mode of MECP2-mediated differential gene expression is specific for differentiated neurons. Our findings suggest that MECP2 exerts bimodal regulation of gene expression, dictated by its binding to 5hmC or 5mC.
A prominent group of genes affected in MECP2 mutant neurons were ribosomal proteins (Figure 5A) which were collectively down-regulated at 4-weeks of differentiation (Figure S4A–B). Combining with the reduced level of rRNAs (Figure 3D), these findings predicted impaired capacity for translation. To evaluate nascent protein synthesis, we measured 35S-Cys/Met incorporation during a 30-minute period. Figure 5B shows that, while mutant NPs had similar levels of incorporation as their isogenic controls, 3-week-differentiated mutant neurons displayed significantly reduced incorporation (Figure 5C) suggesting impaired protein synthesis.
We have previously reported that MECP2 mutant mice could be partially rescued either by over-expression of BDNF, or by systemic delivery of IGF1 (Chang et al., 2006; Tropea et al., 2009), consistent with a reduced BDNF mRNA and protein level in brains of Mecp2 mutant mice (Chang et al., 2006). Indeed, MECP2 mutant neurons had both lower basal as well as KCl-induced levels of BDNF mRNA (Figure 4C–4D). Also, MECP2 mutant neurons secreted reduced levels of BDNF protein as measured by ELISA (Figure 5D). TrkB and IGF1R, the high affinity receptors for BDNF and IGF1, were abundant in human neurons and were expressed at similar levels in control and mutant neurons as evaluated by quantitative RT-PCR (Figure S4C). We further examined the activities of key intra-cellular signaling pathways downstream of these receptors focusing on the AKT/mTOR pathway because of its known central function in regulating translation (Zoncu et al., 2011). Mutant neurons displayed severely diminished levels of phospho-AKT and phospho-S6 as seen by immuno-staining (Figure 5E–5H).
We next investigated whether treatment with BDNF or IGF1 could activate the AKT and S6 pathway and affect the in vitro mutant phenotype. Three-week treatment with BDNF or IGF1 significantly rescued the soma size and dendritic complexity deficits seen in MECP2 mutant neurons (Figure 5I–5J). Although BDNF and IGF1 treatment did not significantly affect the total RNA content per cell (not shown), nascent protein synthesis as evaluated by 35S-Cys/Met incorporation levels was elevated in treated mutant neurons (Figure 5K). Furthermore, BDNF and IGF1 treatment significantly increased the percentage of MAP2+ mutant neurons that co-stained for phospho-AKT and phospho-S6 (Figure 5L–5M). Thus, these results strongly support the notion that reduced levels of new protein synthesis in MECP2 mutant neurons was accompanied with impaired activities of the AKT/mTOR pathways and that treatment with exogenous growth factors promoted protein synthesis via enhancing AKT/mTOR signaling activities.
To further investigate the effects of promoting protein synthesis on the mutant phenotypes, we used a genetic approach to activate the AKT/mTOR pathway. PTEN is a known negative regulator of PI3K, an upstream component of the AKT/mTOR pathway (Sansal and Sellers, 2004). Ablation of PTEN has been shown to lead to constitutive activation of the AKT/mTOR pathway in a variety of tissues, including the brain (Kwon et al., 2006). We transduced control and mutant NPs with lentiviruses encoding a PTEN shRNA that has been proven to knock down PTEN efficiently (Luikart et al., 2011). Immuno-blotting confirmed significant reductions in PTEN protein, and corresponding increases in the levels of phospho-AKT and phospho-S6 proteins upon transduction (Figure 6A–6C). This lentivirus construct contains an mCherry reporter, which allows the identification of individual PTEN knockdown cells. Figures 6D to 6F show that PTEN knockdown significantly increased soma size and neurite arborization as compared to vector treated cells. This was accompanied by an increase in nascent protein synthesis as measured by 35S-Cys/Met incorporation (Figure 6G). These results demonstrate that genetic activation of the AKT/mTOR pathway in mutant neurons promoted protein synthesis and was sufficient to ameliorate the disease-related cellular impairments.
The expression of all genes predicted to encode mitochondrial proteins (Pagliarini et al., 2008) was significantly down-regulated in mutant neurons (Figure 7A). This is consistent with mitochondrial protein genes as a group being highly expressed (Figure S5A). A survey of all genes encoding mitochondrial ribosomal proteins revealed that similar to cytoplasmic ribosomal protein genes (Figure S4), the majority of these genes were also down-regulated (Figure S5B–C). Consistent with this observation, expression of the UQCRC1 gene, which was previously suggested to be up-regulated in MECP2 mutant mice (Kriaucionis et al., 2006), was in fact down-regulated in MECP2 mutant neurons (Figure S5D). To investigate the physiological consequences of these transcriptional changes, we measured cellular oxygen consumption. Despite having normal mitochondrial mass per cell as measure by mitochondria-selective dye uptake, mutant neurons displayed a 40% reduction in their basal oxygen consumption, and a similar reduction in the maximal respiration rate observed upon FCCP addition (Figure 7B–C). These results strongly suggest that the capacity of the mitochondrial electron transport chain is reduced in mutant neurons. Given that mitochondrial mass was similar between control and mutant neurons, this capacity could be limited by the availability of substrate due to an overall decrease in glucose metabolism. To explore this possibility further we measured rates of glucose consumption and lactate production in these cells (Figure 7D–E). No differences in glucose consumption or lactate production were observed in these cells. These data are consistent with the decrease in respiration being explained by down-regulation of mitochondrial gene expression resulting in fewer electron transport chain units.
Our study shows that compared to their isogenic controls, human neurons that lack MECP2 have smaller nuclei and soma, as well as less complex dendritic arborization. This decrease in cell size was coupled with a previously un-appreciated reduction in total RNA on a per cell level. In agreement with a recent report of decreased RNA synthesis in MECP2 mutant mouse neurons (Yazdani et al., 2012), our findings demonstrate that MECP2 mutant human neurons, but not NPs, have reduced total RNA and rRNA. More importantly, unbiased global transcription analyses revealed a striking genome-wide down-regulation in mutant human neurons. These findings highlight a drastic decline in the integrity of the neuronal transcriptional program in the absence of MECP2. Furthermore, although the downward shift in gene expression is widespread, the transcriptional activity of genes directly correlated with their probability to be down-regulated upon MECP2 deletion. In addition, genes known to have higher ratios of 5hmC compared to 5mC were more likely down-regulated in an MECP2-dependent manner in neurons but not NPs. This preferential down-regulation of active genes strongly supports a crucial role for MECP2 in facilitating active transcription in human neurons.
One of the key conclusions from our work is that MECP2 can act as a global activator of gene expression in neurons, a conclusion that contrasts with the widely accepted notion of MECP2 acting as a transcriptional repressor (Ebert et al., 2013; Lyst et al., 2013). Our results are based on gene expression analyses using the addition of synthetic RNA spike-in standards, which allowed unbiased gene expression analysis in equal numbers of cells. In contrast, traditional gene expression measurements are based on the assumption that control and experimental cells have a similar amount of total RNA and thus are normalized to input RNA. This assumption leads to erroneous conclusions if, as in RTT neurons, the amount of total RNA differs between experimental and control cells. The present and previous results (Lin et al., 2012; Loven et al., 2012) emphasize the necessity of a "per-cell" perspective for interpreting genome-wide gene expression data, particularly when the experimental manipulation could result in perturbations of global transcription.
It was surprising that control and mutant cells derived from the female WIBR3 ESCs displayed higher levels of gene expression changes than the male WIBR1-derived cells. While we have no mechanistic explanation for this finding, global differences in DNA methylation between male and female mouse ESCs have been reported previously (Zvetkova et al., 2005), and female human ESCs and iPSCs also display variable gene expression (Anguera et al., 2012; Mekhoubad et al., 2012). The lack of MECP2 mRNA and protein expression in female WIBR3-mut cells demonstrates that the MECP2 locus on the inactive X-chromosome remained silent and the global transcriptional down-regulation and the preferential vulnerability of active genes were independently identified in mutant male and female cells. Thus, our findings ascertain an unambiguous role for MECP2 in facilitating active transcription on a genome-wide scale.
Furthermore, we demonstrated that mutant neurons display several novel disease-related physiological changes as compared to their isogenic controls. Using multi-electrode arrays, we followed the course of neuronal maturation and identified a significant reduction in spontaneous network electric activity in mutant neurons. Prompted by the finding that many mitochondrial protein genes were down-regulated in the absence of MECP2, we investigated respiration in whole neuronal population, and identified significantly impaired metabolic function in mutant neurons. This echoes earlier observations that RTT shares hallmarks of mitochondrial encephalopathies, and was thought to be a mitochondrial disorder characterized by dysregulation of lactate metabolism (Cornford et al., 1994). These findings provide novel insights into the manifestation of disease symptoms for RTT and potential future avenues of therapeutic intervention.
Exogenous growth factors such as BDNF and IGF1 are effective in mitigating disease-related symptoms in MECP2 mutant mice (Chang et al., 2006; Kline et al., 2010; Tropea et al., 2009) and in patient iPSC-derived neurons (Marchetto et al., 2010). The underlying mechanism for these reversals remains to be identified. Using isogenic human cells we demonstrated that MECP2 mutant neurons have significantly lower protein synthesis activity. Furthermore, our study identified a severe defect in the activity of the AKT/mTOR signaling cascade, a crucial pathway known to directly modulate protein synthesis and is induced by BDNF and IGF1 (Ricciardi et al., 2011). Genetic activation of the AKT/mTOR pathway by PTEN ablation ameliorated the protein synthesis and the neural morphological defects in MECP2 mutant neurons, offering further evidence that protein synthesis impairment is central to RTT pathology. Thus, our results provide mechanistic insights into impairments seen in MECP2 mutant neurons and suggest the unifying hypothesis that a defect in the global control of transcription and translation is a fundamental cause of RTT-related symptoms.
The critical dependence on MECP2 in maintaining gene expression appears to be a phenomenon unique to differentiated neurons and was not seen in NPs. The critical role of MECP2 in neurons is supported by previous studies in mice showing that ablation of MECP2 specifically in post-mitotic neurons was sufficient to produce RTT symptoms (Chao et al., 2010; Chen et al., 2001). Thus, the mechanism by which re-expression of MECP2 reverses RTT-phenotypes may reside in its ability to reinstate proper gene expression regulation thus reversing the downstream transcriptional and translational impairments. Consistent with the notion that the RTT phenotype is reversible, BDNF, IGF1 addition and PTEN knockdown rescued the disease-related phenotype in mutant neurons suggesting that boosting protein synthesis by activation of the AKT/mTOR pathway may represent a potential therapeutic strategy for RTT.
TALENs-mediated gene targeting was performed as previously described (Hockemeyer et al., 2011). The DNA binding sites of the TALENs used for targeting the exon 3 of MECP2 are gcagccatcagcccaccact and ctctgctttgcctgcct.
HESC lines WIBR1, WIBR3 were previously described and cultured as previously described (Lengner et al., 2010). To induce neural differentiation, increasing amounts of N2 media (25, 50, 75, 100%) were added to mTeSR medium every other day whilst maintaining 2.5uM dorsomorphin. NPs were passaged at day 20–24 using accutase and cultured in N2 media with 20ng/ml bFGF. NPs were further differentiated in differentiation medium without bFGF. For morphological and electrophysiological analyses, cells were lifted using accutase and replated onto coverglass or culture dish.
Total RNA extraction and RNA electrophoresis was performed as previously described (Lin et al., 2012). RNA spike-in controls was added to total RNA extracted from equal numbers of cells, as previously described and following manufacturer's recommendations (Loven et al., 2012). RNA was reverse transcribed using Superscript III reverse transcriptase (Invitrogen) with random hexamer primers. Transcript abundance was determined by quantitative PCR using SYBR Green PCR mix (Applied Biosystems). Raw Ct values were normalized to GAPDH or ERCC spike-in standards.
Total protein extraction and immuno-blotting was performed as previously described (Li et al., 2008). Metabolic labeling of newly synthesis protein (Thoreen et al., 2012) was performed by labeling with 165uCi of EasyTag EXPRESS 35S protein labeling mix (Life Technologies) for 30min. The concentration of secreted BDNF protein in culture medium was measured using a BDNF ELISA Kit (Promega) (Li et al., 2012).
The authors thank Ping Xu, Raaji Alagappan, Tenzin Lungjangwa, Dongdong Fu, Daniel B. Dadon, Kibibi Ganz and Ruth Flannery for technical support; Drs. Bryan Luikart and David Sabatini for PTEN shRNA lentivirus constructs and access to Seahorse XF24; Dr. Carson Thoreen for advice on the protein synthesis assay; Drs. Peter Rahl, Bingbing Yuan and Jeong-Ah Kwon for assistance with microarray; and members of the Jaenisch lab for helpful discussions. Y.L. was a Simons Postdoctoral Fellow. Y.L. was supported in part by a NARSAD Young Investigator Grant from the Brain & Behavior Research Foundation, and the IRSF. A.W.C. was supported by a Croucher scholarship. J.L. was supported by a Swedish Research Council Postdoctoral Fellowship (VR-B0086301). D.O. and R.Y. were supported by NIH grant R01-HG002668. M.V.H and C.A.L. acknowledge support from P30-CA14051, the Koch Institute and Curt Marble Cancer Research Fund. R.J. was supported by NIH grants HD 045022, R37-CA084198, SFARI and the ELA foundation.
Accession numbers
The microarray data are available in the Gene Expression Omnibus (GEO) database under the accession number GSE50584.
Supplemental Information
Supplemental Information includes Supplemental Experimental Procedures and five figures.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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A man has been arrested after a woman was allegedly raped near a college campus.
The incident is said to have happened in Aurora Avenue, Clydebank, West Dunbartonshire, at about 9.50pm on Saturday.
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Police Scotland confirmed a 22-year-old man has been arrested in connection with the incident.
He is expected to appear at Dumbarton Sheriff Court today.


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On 21-01-13 20:54, Graham Inggs wrote: > If you want. Do you want to start a new thread there? Just continue. > I still have the source code for every Debian package that depends on > libmotif-dev and lesstif2-dev on my PC, so I ran 'grep -i > XmPrintPopupPDM -l -r *' for each of the six missing symbols you listed > previously and did not find a single match. > Good news is we can't break anything in Debian if we hack PrintS.c, bad > news is we don't have any applications with which to test. Fully ack. > Ok, let's try 3 and see where that takes us. I'm not keen on 2 because > there are still proprietary applications being used that need libXm.so.3 > and libXm.so.4. Yes, but it is still easy for system administrators to add the symlinks themselves, if they feel comfortable with it. > I've just come across this: > http://bugs.motifzone.net/long_list.cgi?buglist=1545 > https://bugzilla.redhat.com/show_bug.cgi?id=229409 > > It seems Red Hat deprecated Xprint in 2007, it may be that the > "official" Motif libraries are built without Xprint support. Yes, I understand. Debian also removed xprint from the repository. But the glue layer libxp is still there to PREVENT problems. This means that you don't have printing support anyway, but that things don't just break. > Maybe we have to drop the XmPrint functions in order to be binary > compatible? Nope, ADDITIONAL symbols is never a problem. Please read the policy chapter 8 [1] for some background if you didn't already, especially 8.6.2. [1] http://www.debian.org/doc/debian-policy/ch-sharedlibs.html > What do you think of releasing another openmotif 2.3.3 package including > the three patches from Ubuntu? > http://changelogs.ubuntu.com/changelogs/pool/multiverse/o/openmotif/openmotif_2.3.3-6ubuntu1/changelog No need. I think we will be uploading shortly, and then these changes will be gone anyway. Unless you fear that it might still take a long time. I don't think these patches warrant a release-freeze [2]. As it is, we are still waiting for an unblock of 2.3.3-7 anyway ... uhm, oops, I still have to file that one I see. [2] http://release.debian.org/wheezy/freeze_policy.html > If you are in agreement, is there anything I can do to assist? So unless you can convince me otherwise, I don't think we should do this. > In particular, I'd like the libmotif3 and display manager entries. I do > not know why Ubuntu needs the bin-utils-gold patch, and Debian doesn't > (Debian doesn't need it in 2.3.4 because this patch is against a demo). Unfortunately, "liking" is not on the list of freeze exceptions. I think Debian would also need the bin-utils-gold patch if it were using the gold linker. I believe Ubuntu actively tests for that. Actually, I hope Logan Rosen checked my patch in 2.3.3-6 as I think it is flawed. That is why I uploaded 2.3.3-7. Paul
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Updated – 15 November 2017
In response to the information you provided on your reseller application form we have determined that you are a 'Trade' customer. This means that:
1. You will get advantageous pricing.
2. You will be responsible for determining 'fitness-for-purpose' on behalf of the end user and deciding whether any advice we offer in this regard is accurate and applicable.
3. Consumer Protection law will not apply to your purchases from us.
4. You will be responsible for providing first line technical support to your end users.
5. As a result of continuing development the specification or design of goods may vary.
6. Goods are not sold on a trial basis except by prior written contract.
Online services & Orders:
We prefer orders to be placed via the website as telephone orders leave no trail. All web orders are stored electronically, so specific instructions relating to your order can be mentioned this in the comments section of the web order. Mistakes can happen if orders are made over the phone (we are only human!), and are much less likely on electronic orders.
Antenna cable connectors - these are available for resellers in packs of 10, if ordered individually they will be charged at retail price.
If you would like a full price list you can download this from the online reseller area as a CSV file.
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The provision of a reseller account does not imply that we are providing credit facilities; payment is required before goods are despatched.
- Surcharges for Credit and Debit card usage: The way that merchant fees for credit and debit card processing are calculated has changed. In particular the fee for most debit card transactions is now charged at a percentage rate rather than the former flat rate (18p). Here at Solwise we always try to separate the cost of payment processing from the prices of our products, listing a surcharge on each invoice where applicable. This means that we can keep our prices as low as possible whilst providing the widest range of payment methods for our customers. Also, prices are not inflated for everyone to fund the few who collect Air-Miles or reward points. The current surcharge rates for all card types are shown below.
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The surchage charged by Paypal is currently 2.4%
As we operate fairly low margins we feel it is fair to charge people for the payment method that they choose, the alternative would be to increase our prices across the board and then everyone would pay. With our shopping trolley system you are able to choose Bank transfer as an alternative to cards and if your bank operate the faster payment system we should see payments in our bank almost immediately, this way there is no charge either.
You may also have noticed we have introduced 3d secured processing on cards via our online shopping system, this is an excellent system for protecting your card details and we would encourage all customers to place their orders online.
We will accept most major credit/debit cards, cheques, postal orders, Paypal and Bank Transfers.
Solwise Ltd reserves the right to change prices. All goods are subject to availability. If we do not supply the goods we will refund any money already paid. We will not be liable for compensation or damages if we do not supply the goods. Goods are charged to the credit/debit card on despatch if telephone, fax or email orders or at time of order via the 3d secure system for weborders.
The price for the goods will be stipulated at the time when you place your order. We are entitled to make adjustments to the price to take account of any increase in our supplier's price or if due to an error or omission the price published for the goods on our website is incorrect. We will inform you of the correct price and give you the option to cancel your order.
All goods supplied remain the property of Solwise Ltd until payment has been received in full.
Stock permitting we try to despatch your order the same day (Monday - Friday), subject to receiving web orders by 3:00pm (telephone, email & fax orders by 2:30pm). Cable making orders are processed in our system as a two day service.
Next Working Day Carrier service is arranged through DPD Local (Interlink) and ParcelForce. Some items are sent Parcel Force, Royal Mail special delivery or DPD Local (Interlink) using a 2 day service due to location i.e. Scottish Highlands & Islands, parts of Cornwall, Isle of Man, Isle of Wight & Northern Ireland. We select the most appropriate carrier depending on size, weight, destination and value. Many small items will go by first class post. Most items require a signature on delivery. The DPD Local (Interlink) website is www.dpdlocal.co.uk - from there you will be able to find your local depot and track parcels, tracking numbers are detailed in the Solwise online trade area, and in your invoice email, with a link to the carriers tracking site.
DPD Local (Interlink) Deliveries - If the addressee is not available on the first day of attempted delivery then DPD Local will leave a card. They will then try again the next day. If there is not response on the second day they will hold the item at their depot for 7 days. If you get in touch with DPD Local they will do a third delivery. If no one gets in touch within the 7 day holding period the item will be returned to Solwise. Once returned to us we can resend the item to you at the standard delivery charge or credit back to your account less the original delivery charge and less any router configuration charge.
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Transit Damage –If you specify a carriage type with insurance which varies from our usual choice then our liability will be limited to the carriers compensation policy, for example First Class post insurance value is approximately £19.00.
Overseas orders – we can arrange a carrier for you. Our standard carriers are TNT and DPD/ParceLine with ParcelForce as a back-up for countries not covered by TNT or DPD/ParceLine. If you have an account with a Carrier we are happy to get orders ready for your carrier, though you must instruct them to collect.
Ideally we would like a telephone number for the delivery address in order that Carriers can contact direct if directions are required. If a telephone number is not provided we will provide your main landline number to our carrier.
We require an email address for all orders to inform you that goods have been dispatched. This will enable you notify us of any non-deliveries within our 3 working days, of the expected delivery date, deadline.
Any shortages or damage to your order must be reported to us within 7 days of despatch.
All goods are covered by a 12 month return to base warranty unless otherwise stated. It is entirely up to you as the reseller to determine if an item is fit for the purpose that your customer requires. Our liability under this warranty is limited to the value of the goods and does not extend to any consequential loss, however incurred. The return to base warranty includes return shipping back to a UK address only. Warranty replacement items will have a 3 month warranty or the balance of the warranty on the original item, whichever is the longer. We reserve the right to substitute warranty items with a product of similar or better specification. The warranty period starts from the date of your invoice however we will endeavour to do our best to resolve any issues after the warranty has expired to the best of our ability.
Technical Support
Technical Support can be called on 01482 644938. Technical support opening hours are 9.15 am - 5pm Monday to Friday. We expect resellers to act as first line technical support for their customers.
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If you cancel an order and wish to return the goods you must confirm, in writing, to us within 7 working days from the day after that on which the goods are received. You must ensure that reasonable care is taken of the goods and their original packaging, manuals CDs, accessories etc and that they are returned to us by some form of insured, signed for carrier at your expense. On receipt of the returned items, they will be checked and tested to determine that reasonable care has been taken and then we shall credit your credit/debit card with the total amount of the original order less the carriage and the credit card surcharge. Your right to cancel is not extended to goods made to your specifications such as custom made cables. If returning items please ensure that they are packed in a secure box or bag (ie do not just tape up the presentation box and put delivery labels on it!). We reserve the right to apply a restocking charge for items returned in an un-saleable condition. Note this applies to packaging, manuals, CDs and accessories etc as well as the listed product.
You will need to complete our RMA/Returns form for items coming back to us regardless of whether they are faulty or just not required.
Solwise Fulfilment service
Solwise 'No Paperwork' option
When you select the 'no Solwise paperwork' option for your order we will not include the Solwise delivery note with your package. You can upload your own delivery note, in PDF format, when making a web-order or forward a copy to email@example.com. Delivery notes included with web-orders are automatically printed with our despatch notes, if you email the delivery note we will endeavour to unite this with your package manually. Either way, our paperwork will be retained.
How hidden is Solwise from your customer?
Our intention is that the end customer will assume that the package has been shipped by you, but for various reasons, it is not possible for us to hide completely. We need to provide a return address on the outside of all parcels. Usually this is on the carrier label. Where possible we have removed our name, but the address will remain. Tracked services, e.g. DPD Local, Parcelforce, TNT etc. may reveal our identity if the customer enters the tracking number on the carriers website.
If you are providing a despatch document you should consider modifying the layout so that a return address is visible underneath the delivery name and address when the document has been folded to fit into a plain A7 'documents-enclosed' window-label. If you choose this option we would strongly advise that you use OUR address but your own business name. This is the best option for the rare occasion when deliveries go wrong and saves you having to handle returned items yourself.
If it is vital that your customer does not know who we are then we recommend that you have the product shipped to yourself for further handling. As discussed above there are a number of ways that an end user can find out who shipped a parcel and despite our best efforts, there may be others that are not covered here
These terms and conditions are subject to change from time to time are subject to English Law and may be applied in whole or part.