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Each month, direct to your email inbox, we'll send the best camping news, tips, recipes and more, to enhance the camping lifestyle that you love so much. Learn More
Experience the wilds of Oregon on this iconic highway.
Follow the Mississippi and explore the heart of the US on the Great River R...
Take a tour through South Dakota and Wyoming as you visit Devils Tower.
Plan the perfect trip from home or on the road with the official KOA app. Learn More
Open April 28 - October 15
Reserve: 800-562-5836
Info: 603-838-5525
2154 Route 302
Lisbon, NH 03585Get Directions
Exit 42 from I-93: Go west on US 302 5 miles. Exit 17 from I-91: Go east on US 302 18 miles. Use GPS system at your own risk! Please refer to a road map or call the campground.Get Google Directions
All Sites
Check-in: 11:00 am, Check-out: 11:00 am
Camper Rating 4.5 out of 5


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Vogue 2686
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Vogue Basic Design 2686; 1970s; Misses' Dress, Tunic and Pants. Dress, mid-knee, two inches below knee, evening length or tunic, has split neckline, with or without self or contrast shaped collar. Fitted self or contrast bodice, inset waistband and gathered skirt. With or without patch pockets, trim variations and purchased belt. Sleeveless, short or full length sleeves with self or contrast cuffs. Straight-legged pants have elasticized waistline.
Featured in Vogue Pattern Book April/May 1972
Links to reviews/blog posts Edit
Sources/Vendors Edit
- NostalgieVintage
- The Perfect Pattern sz 12 bust 34
- Holding Patterns ATX Bust 32.5 Uncut
Gallery Edit
[insert your photos of this pattern made up]
Wishlist Edit
[insert your username, and make sure your preferences allow for people to contact you via e-mail. Do not list your email address here!]

subset: commoncrawl


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NO PURCHASE NECESSARY. Void in Quebec and where prohibited. Open to legal residents of the 50 United States and the District of Columbia, Mexico, and Canada (excluding Quebec) who are at least 18 years old or the age of majority in their jurisdiction of residence at time of entry. Begins 9:00 a.m. MT 7/4/16; ends 11:59 p.m. MT 7/31/16. For complete Official Rules and eligibility, visit:www.tellurideskiresort.com/happythoughts/telluride-storytelling-contest. Sponsor: Telluride Ski Resort.
1. CONTEST PERIOD: The Your Telluride Contest (the "Contest") begins at 9:00 a.m. Mountain Time ("MT") on July 4, 2016 and ends at 11:59 p.m. MT on July 31, 2016 ("Contest Period").
2. ELIGIBILITY: No purchase necessary. This Contest is open only to legal residents of the fifty (50) United States and the District of Columbia, Mexico, and Canada (excluding Quebec) who are at least eighteen (18) years old or the age of majority in their jurisdiction of residence (whichever is older), as of the date of entry. Employees of Telluride Ski Resort ("Sponsor"), and any of their affiliates, parents or subsidiaries, respective parent, subsidiary, and affiliate companies and advertising and promotion agencies and members of their immediate families (spouses, parents, children, and siblings and their spouses), any of their affiliates, subsidiaries, advertising and promotion agencies and their immediate family members and/or those living in the same household of each are not eligible. Void in Quebec and where prohibited or restricted by law. Subject to all applicable laws, ordinances and regulations.
3. HOW TO ENTER: During the Contest Period, you may access the Contest by visiting www.tellurideskiresort.com/happythoughts/telluride-storytelling-contest ("website"). From the website, you must complete the online registration form including full name, email address, and photo (optional), and provide a story about your favorite memory in Telluride ("Story"). Limit one entry per person/household. Multiple Contest entries from any person/household will not be accepted. All eligible entries must be received by 11:59:59 p.m. ET on July 31, 2016, to be eligible. No information regarding entries, other than as otherwise set forth in these Official Rules, will be disclosed. Any attempt by any entrant to obtain more than the stated number of entries by using multiple/different email addresses, identities, registrations and logins, or any other methods will void such entries and that entrant may be disqualified. Use of any automated or computer system to participate is prohibited and will result in disqualification. Internet/data/usage charges may apply. Incomplete, corrupted, or untimely entries are void and will be disqualified. Sponsor and its agencies are not responsible for lost, late, incomplete, damaged, or misdirected entries; lost, interrupted, or unavailable network, server, or other connections; or miscommunications, website, computer or software malfunctions, telephone transmission problems, technical failures, garbled transmissions, damage to a user's computer equipment (software or hardware), or other errors or malfunctions of any kind, whether human, mechanical, electronic or otherwise. Proof of submission will not be deemed to be proof of receipt by Sponsor. In the event of a dispute as to the identity of an entrant, the authorized account holder of the email address used to enter will be deemed to be the entrant. The "authorized account holder" is the natural person assigned an email address by an Internet access provider, online service provider, Internet service provider, or other organization (which may include an employer) responsible for assigning email addresses for the domain associated with the submitted address. Potential winners may be required to show proof of being the authorized account holder.
Entries must be unique. All entries must comply with the "Entry Requirements" set forth below.
Entry Requirements:
• Entries must be in English.
• Entry may feature additional people in optional photo. If so, please make them aware that you are submitting their image in this Contest and that they agree to the submission of their image. If an additional person is a minor is his/her jurisdiction of primary residence, entrant must be parent or legal guardian of minor depicted. If optional photo features additional people, they (or entrant as parent or legal guardian) may be required to sign a Release Form, in Sponsor's sole discretion.
• Entry must be original. Entries must not be copied or otherwise plagiarized from any source.
• The entry must not have been submitted previously in a giveaway or promotion of any kind or previously exhibited or displayed publicly (i.e., disclosed beyond your immediate circle of friends and family or social media sites) through any means.
• The entry must not contain content that is known by you to be false, inaccurate or misleading.
• Any entry deemed inappropriate or unsuitable, in Sponsor's sole discretion, will be disqualified. Entries must not contain material that is inappropriate, indecent (including, but not limited to, nudity, or pornography), profane, obscene, hateful, tortious, defamatory, slanderous, libelous (including words or symbols that are widely considered offensive to individuals of a certain race, ethnicity, religion, sexual orientation, or socioeconomic group), violent, self-mutilating (e.g., relating to murder, the sales of weapons, cruelty, abuse, etc.), or illegal (e.g., underage drinking, substance abuse, computer hacking, etc.).
• The entry must not contain or depict material that promotes bigotry, racism, hatred or harm against any group or individual or promotes discrimination, including without limitation, discrimination based on race, sex, religion, nationality, disability, sexual orientation or age. The entry must not contain or depict material that is threatening to any person, place, business, group, or world peace or contain words or symbols that are widely considered offensive to individuals of a certain race, ethnicity, religion, sexual orientation, or socioeconomic group.
• The entry must not contain any content that infringes or may infringe third party rights, including, without limitation, any copyright, name, trademark, logo, trade dress, or other personal or proprietary right of any person living or deceased (including but not limited to rights of privacy or publicity or portrayal in a false light) or entity or make reference to any commercial/corporate advertising (including but not limited to corporate logos, brand names, charities, slogans, political, or religious statements), or be otherwise objectionable. Without limiting the generality of the foregoing, publicly displayed and publicly accessible Sponsor content, materials, or products are permitted to be displayed in entries submitted for this Contest.
• Any clothing shown in the photo should not contain any visible logos, drawings, cartoons, phrases, trademarks or other third-party content or materials (but showing publicly displayed or publicly accessible Sponsor content, material, and products as described above is permitted).
• The entry must not include any representation of celebrities, athletes, musicians, or any other third-party (public or private), include any anti-social, political or religious groups, any commercial solicitation or promotional materials or name, address, phone number, or URL address. Entries must not contain advertisements, personal solicitations or commercial solicitations.
• Photos may not be owned, taken or edited by a professional photographer.
• The entry must not contain viruses, Trojan horses, worms, bots, spyware or any other computer code that is intended to damage, interfere with, or surreptitiously intercept or expropriate any system, data or information.
• Entrants and all submitted entries must be in keeping with Sponsor's image as determined by Sponsor, in its sole discretion, or entry will be disqualified from the Contest. The entry must not disparage persons or organizations associated with Sponsor.
• Entries must not reference any of Sponsor's competitors.
Each entrant grants to Sponsor a worldwide, royalty-free, perpetual, non-exclusive right and license to copy, distribute, and display each submitted entry, in any media, and with right to use, copy, modify, edit, and create derivative works therefrom, and agrees to execute documents confirming such right and license at Sponsor's reasonable request. By entering, you understand that your entry will be screened by the Sponsor and may be posted online, to Sponsor's social media channels, in print or in other media in Sponsor's sole discretion, to be viewed by members of the general public. By entering, each entrant warrants and represents that his/her entry is original, has not been previously published or won any award, does not contain any material that would defame or otherwise violate or infringe upon the rights of any third party, including patents, copyrights, trademarks or rights of privacy or publicity, and will not violate any federal, provincial, state or local laws or ordinances. Sponsor reserves the right in its sole and unfettered discretion to disqualify any entry that it believes contains obscene, offensive or inappropriate content, that does not comply with these Official Rules or that is not consistent with the spirit or theme of the Contest. No information regarding entries, other than as otherwise set forth in these Official Rules will be disclosed.
4. WINNER DETERMINATION: All eligible entries (Stories only) will be judged by a panel of Sponsor representatives on or about August 2, 2016, based on the following criteria: Quality of Story– 40%; Relevance – 40%; and Creativity – 20%. The eligible entry with the highest score will be deemed the potential Grand Prize winner, subject to verification. The eligible entries with the next two (2) highest scores will be deemed the potential First Prize winner, and Second Prize winner respectively, subject to verification. In the event of a tie, tied entries for any prize level will be re-judged based 100-percent (100%) on Quality of Story. Decisions of the Sponsor and judges are final with respect to all matters relating to the Contest. By participating, entrants agree to the decisions of the Judges, which shall be final and binding in all respects. Under no circumstance will information regarding judging be shared with entrants.
5. WINNER NOTIFICATION: Potential winners will be notified and confirmed by email. Potential Grand Prize winner (and guest) may be sent via email, an affidavit of eligibility or Declaration of Eligibility, Liability & Publicity Release (where legal) and Assignment of Rights (Affidavit" or "Declaration") and will be required to complete, sign and return the Affidavit or Declaration via email/fax within three (3) days of being notified in order to claim his/her prize. In the event a guest is a minor, the winner must be guest's parent or legal guardian and must complete the Affidavit/Declaration on guest's behalf. Potential Frist Prize, and Second Prize winners will be required to confirm their mailing address/execute an assignment of rights prior to prize award. All winners may also be required to send the RAW images (7500px optimized ideally) of their submitted photos to email@example.com prior to winner confirmation. If a potential winner fails to return the required document (or fails to send the RAW images) within the required time period, or the prize notification is returned undeliverable, or in the event that a potential winner is disqualified for any reason, Sponsor will award the applicable prize to an alternate winner determined as outlined in section 4 from among all remaining eligible entries received throughout the Contest Period, time permitting. All prizes will be awarded provided a sufficient number of eligible entries are received throughout the Contest Period. Potential winners are subject to verification by Sponsor and/or Administrator, whose decisions are final and BINDING IN ALL MATTERS RELATED TO THE CONTEST. An entrant is not a winner of any prize unless and until entrant's eligibility has been verified and entrant has been notified that verification is complete. All federal, state, provincial and local laws and regulations apply. All federal, state, provincial, municipal and local taxes are the sole responsibility of winner.
6. PRIZES AND APPROXIMATE RETAIL VALUES ("ARV"): Grand Prize (1): A one (1) night stay at The Peaks Resort and Spa [one (1) room/double occupancy], and dinner for two (2) at Allreds (awarded as a $150 Gift card). The ARV of the Grand Prize is $500USD. Grand Prize must be used during Sponsor-specified dates or prize will be forfeited. All details of the stay are in Sponsor's sole discretion. First Prize (1): a USD$200 Telluride Ski Resort Gift card. Second Prize (1): a USD$100 Telluride Ski Resort Gift card. The ARV of all prizes is $800USD. Limit one (1) prize per person. An expiration date may apply to Gift cards. PRIZES ARE AWARDED "AS IS" WITH NO WARRANTY OR GUARANTEE, EITHER EXPRESS OR IMPLIED BY SPONSOR. Gift cards redeemable at Telluride Ski Resort retail locations, lift ticket offices, ski school, on mountain dining and more. See Gift card for specifics. Transportation to/from Telluride/winner's home not included with any prize. All prizes will be awarded by mail in 6-8 weeks from winner confirmation. All other expenses and costs, not expressly listed above, including, but not limited to, taxes, insurance, telephone charges, room service and laundry services, personal expenses, gratuities, entertainment, transfers, incidental charges, or any other items not specifically described in these Official Rules, any transportation not mentioned within such prize descriptions and all expenses for any of the foregoing are the sole responsibility of the winner. No substitution or transfer of prize permitted except as specifically stated in these Official Rules and at the sole discretion of the Sponsor.
7. GENERAL RULES: By participating in the Contest, entrants agree to be bound by these Official Rules and the decisions of the judges/Sponsor. The Sponsor, and their parent companies, subsidiaries and affiliates, advertising and promotion agencies, and each of their respective agents, officers, directors, employees, and assigns ("Released Parties") are not responsible for technical, hardware, software or telephone malfunctions of any kind, lost or unavailable network connections, or failed, incorrect, incomplete, inaccurate, garbled or delayed electronic communications caused by the user or by any of the equipment or programming associated with or utilized in the Contest or by any human error which may occur in the processing of the entries in the Contest or for any liability for damage to any computer system or device resulting from participation in, accessing or downloading information in connection with the Contest. The Sponsor reserves the right at its sole discretion to disqualify any individual that tampers or attempts to tamper with the entry process or the operation of the Contest; violates the Official Rules; or acts in an unsportsmanlike or disruptive manner, or with intent to annoy, abuse, threaten or harass any other person. Any attempt by any person to deliberately undermine the legitimate operation of the Contest may be a violation of criminal and civil law, and, should such an attempt be made, Sponsor reserves the right to seek damages from any such person to the fullest extent permitted by law. Sponsor's failure to enforce any term of these Official Rules shall not constitute a waiver of that provision. If, for any reason, the Contest is not capable of running as planned, including infection by computer virus, bugs, tampering, unauthorized intervention, fraud, technical failures, or any other causes beyond the control of the Sponsor which corrupt or affect the administration, security, fairness, integrity or proper conduct of the Contest, then the Sponsor reserves the right at its sole discretion to cancel the Contest and determine the winners from among all eligible entries received prior to cancellation, based on the same criteria listed in Rule #4 above.
8. RELEASE: You represent and warrant that: (i) all rights to the entry belong to and are original to you, or you have written consent to use, and the entry does not and shall not infringe on any copyright or any other third party right nor violate any applicable law or regulation, (ii) you have the right to grant any and all necessary rights and licenses provided herein, including without limitation, all necessary copyright and other related rights to the entry, free and clear of all claims and encumbrances without violating the rights of any person or entity, including any right to privacy or publicity, (iii) you hereby hold the Sponsor and Released Parties harmless from and against any third party claim arising from use of the entry and you waive any right to inspect or approve uses of the entry or to be compensated for any such uses. Participating in the Contest constitutes permission to the Sponsor and their agencies to use entrants' and winners' names, biographical information, pictures/portraits, likenesses, voices and/or entry, for purposes of advertising and trade without further compensation, unless prohibited by law. By participating in the Contest, the entrant agrees that Sponsor and Released Parties will have no liability whatsoever for, and will be held harmless by entrant for any liability for any bodily injury, loss or damages of any kind to persons, including death, and property, due in whole or in part, directly or indirectly, from entry creation, the acceptance, possession, use or misuse of the prize, if applicable or participation in the Contest or participation in any Contest related activity. You hereby represent and warrant that you have read these Official Rules and are fully familiar with its contents.
9. DISPUTES: Except where prohibited, entrant agrees that: (1) any and all disputes, claims and causes of action arising out of or connected with this Contest or any prize awarded shall be resolved individually, without resort to any form of class action, and exclusively by the United States District Court for the District of Colorado or the appropriate State Court located in Colorado in the U.S.; (2) any and all claims, judgments and awards shall be limited to actual out-of-pocket costs incurred, including costs associated with entering this Contest, but in no event attorneys' fees; and (3) under no circumstances will entrant be permitted to obtain awards for, and entrant hereby waives all rights to claim, indirect, punitive, incidental and consequential damages and any other damages, other than for actual out-of-pocket expenses, and any and all rights to have damages multiplied or otherwise increased. All issues and questions concerning the construction, validity, interpretation and enforceability of these Official Rules, or the rights and obligations of the entrant and Sponsor in connection with the Contest, shall be governed by, and construed in accordance with, the laws of the State of Colorado, without giving effect to any choice of law or conflict of law rules (whether of the State of Colorado or any other jurisdiction), which would cause the application of the laws of any jurisdiction other than the State of Colorado in the U.S.
10. PRIVACY: Information collected from participants is subject to the Sponsor's Privacy Policy, which can be found at http://www.tellurideskiresort.com/content/privacy-policy/. Participants should be aware that Sponsor may be collecting non-public, personally-identifiable information about them in connection with the operation of the Contest and that their personal information will be transferred securely to the United States.
11. WINNERS LIST: For the first names, last initials and cities/states/provinces of the winners, available after August 15, 2016, for a period of at least 30 days, send an email to email@example.com.
12. SPONSOR: The Sponsor of this Contest is Telluride Ski Resort, 565 Mountain Village Blvd, Telluride, CO 81435, USA.


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Definition of device
1 : something devised or contrived: such asa (1) : plan, procedure, technique a marketing device mnemonic devices (2) : a scheme to deceive : stratagem, trickb : something fanciful, elaborate, or intricate in designc : something (such as a figure of speech) in a literary work designed to achieve a particular artistic effect irony and other literary devices a plot deviced archaic : masque, spectaclee : a conventional stage practice or means (such as a stage whisper) used to achieve a particular dramatic effectf : a piece of equipment or a mechanism designed to serve a special purpose or perform a special function smartphones and other electronic devices a hidden recording device
2 : desire, inclination left to my own devices
3 heraldry : an emblematic design used especially as a heraldic bearing (see bearing 4)
Examples of device in a Sentence
The store sells TVs, VCRs, and other electronic devices.
agreeing to dismantle all nuclear devices
a useful mnemonic device for remembering the names of the planets
The company's method of tracking expenses is just a device to make it seem more profitable.
Origin and Etymology of device
Middle English devis, devise, from Anglo-French, division, plan, from deviser to divide, regulate, tell — more at devise
First Known Use: 14th century
Other Literature Terms
DEVICE Defined for English Language Learners
Definition of device for English Language Learners
: an object, machine, or piece of equipment that has been made for some special purpose
: a weapon that explodes
: something that is done in order to achieve a particular effect
DEVICE Defined for Kids
Medical Dictionary
Medical Definition of device
: a piece of equipment or a mechanism designed to serve a special purpose or perform a special function
Learn More about device
See words that rhyme with device Thesaurus: All synonyms and antonyms for device Spanish Central: Translation of device Nglish: Translation of device for Spanish speakers Britannica English: Translation of device for Arabic speakers
Seen and Heard
What made you want to look up device? Please tell us where you read or heard it (including the quote, if possible).


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Days Inn - Moose Jaw
No prices found through our partners. Please contact the business directly or check some of our recommended alternatives.
How has this hotel rated in the past?
Photos of Days Inn - Moose Jaw
TripAdvisor Reviews Days Inn - Moose Jaw
Travel Blogs from Moose Jaw
Brooks to Moose Jaw
Another rainy, miserable looking day. The road trip to Moose Jaw took around 4 hours. The country was flat, but with the odd undulating hill.For much of the way it didn't look unlike the country north of Carrieton. There were lots of empty paddocks, with a few jam packed with cattle, which would suggest their use of cell grazing systems. There were a few lakes with water birds. ...
Made it to Moosejaw
... 91 and they think it might be in large part due to Jurassic world being released. Drumheller was a great stop for the kids and there was more we could have done but Nova Scotia is calling. With relatives set to arrive Sunday we are feeling the pull there. When we hit the road with a goal this morning our goal was hitting Swift Current. Because we had emerged from the museum an hour early we decided to make a stretch goal of Moose ...
Land of the Moose!
One thing I haven't touched on since we left BC, is the trailer. I would like to write only the positive things that happen daily, unfortunately that's just not real! So bear with me while I vent for a few minutes and then I'll get back on track with better stuff.
We have had issues with the trailer since the day we picked it up and it wasn't ready. Yup, brand ...
RV fixed and back on the road
... it we went on an underground tunnel tour in the city. We saw where Al Capone hid his bootleg whiskey, and himself, from the authorities. It was quite entertaining but the actors were hard to understand because of their exaggerated accents. We saw the world's largest moose while we were here. Moose Jaw is also home to the snowbird air ...
A Day for Visiting
A cloudy morning encouraged us to make a slow start to the day. Of course we also had to take time to visit the Cypress Hills interpretation centre before leaving! And that was time well spent! Don and I share an interest in the geology of regions we visit and the Cypress Hills displays did not disappoint.
Once we were back on the road, our first stop was at the Saskatchewan welcome centre for literature about the province for both this ...


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What are tonsil stones?
Tonsil stones are hard yellow or white formations that are located on or within the tonsils.
It's common for people with tonsil stones to not even realize they have them. Tonsil stones aren't always easily visible and they can range from rice- to pea-sized. Tonsil stones rarely cause larger health complications. However, sometimes they can grow into larger tonsilloliths which can cause your tonsils to swell.
Pictures of tonsil stones
What causes tonsil stones?
Your tonsils are made up of crevices, tunnels, and tonsil crypts. Different types of debris, like dead cells, mucus, saliva, and food can get trapped and build up in these pockets. Bacteria and fungi feed on the buildup and contribute a distinct odor. Over time, the debris calcifies to varying degrees of hardness. When this forms, it's known as a tonsil stone. Some people will have only one tonsil stone, while others will have many smaller formations.
Potential causes of tonsil stones include:
- bad dental hygiene
- having large tonsils
- chronic sinus issues
Symptoms of tonsil stones
Although it may be difficult to see tonsil stones, there are symptoms that may accompany them.
Symptoms of tonsil stones include:
- bad breath
- sore throat
- difficulty swallowing
- ear pain
- swollen tonsils
- white or yellow debris on the tonsil
Smaller tonsil stones may not result in any symptoms, but they're more prevalent than larger tonsil stones.
Preventing tonsil stones
Tonsil stones commonly occur on a regular basis. Fortunately, there are steps you can take to prevent them. These include:
- Practice good oral hygiene, including cleaning the bacteria off the back of your tongue when you brush your teeth.
- Stop smoking.
- Gargle salt water, which can prevent tonsil stone formation and eliminate the odor they cause.
- Drink the recommended daily requirement of water and stay hydrated.
- If your tonsils cause you regular discomfort, ask your doctor about treatment options.
Tonsil stone removal
Most tonsilloliths are harmless, but many people want to remove them because they can smell bad or cause discomfort. Treatments range from home remedies to medical procedures.
Gargling vigorously with salt water can ease throat discomfort and may help dislodge tonsil stones. Dissolve 1/4 to 1/2 teaspoon salt in 8 ounces warm water and gargle.
You may first discover that you have tonsil stones when you cough one up. Energetic coughing can help loosen stones.
Manual removal
Talk to your doctor before considering removing tonsil stones with tools such as a cotton swab or toothbrush. Your tonsils are delicate tissues so it's important to be gentle. Manually removing tonsil stones can be risky and lead to complications.
Laser tonsil cryptolysis
During this procedure, a laser is used to eliminate the crypts where tonsil stones lodge. It's often performed under local anesthesia. Discomfort and recovery time are usually minimal.
Coblation cryptolysis
In coblation cryptolysis, radio waves transform a salt solution into charged ions. These ions can cut through tissue. As with lasers, coblation cryptolysis reduces tonsil crypts but without the same burning sensation.
The surgical removal of tonsils may be achieved by use of a scalpel, laser, or coblation device. Performing this surgery for tonsil stones is controversial. Doctors who recommend tonsillectomy tend to use it for severe, chronic cases and after all other means have been exhausted.
In some cases, antibiotics can be used to treat tonsil stones. Antibiotics can be used to eliminate the bacteria that play a crucial role in the tonsil stones' development and growth.
The downside of antibiotics is that they won't treat the underlying cause that's resulting in the stones, and they come with their own potential side effects. They also shouldn't be used in the long term, meaning the tonsil stones will likely return.
Find a Doctor
Complications of tonsil stones
While complications stemming from tonsil stones are rare, they are possible. The biggest complication that may result from tonsil stones is damaged tonsils.
Damaging the tonsils is most likely to happen when you try to remove tonsil stones manually at home with a probe. The probe (cotton swab or tooth brush) is often pushed too far or used too aggressively.
Tonsil stones linked to tonsil infections may also require surgery, which can have complications including excessive bleeding or infection.
Tonsil stones are a common problem that may affect a large part of our population. Though they can bring a host of symptoms, tonsil stones rarely result in serious complications. While prevention methods and natural removal of the stones are possible, those who experience recurring tonsil stones in spite of taking precautions may benefit from a consultation with an ENT, who can discuss surgical options with you.
For those prone to tonsil stones, practicing good dental hygiene, staying hydrated, and gargling salt water could help prevent the formation of future stones, or at least keep their symptoms at bay.
Recovery period after tonsil removal
Recovery time will depend on how much of your tonsils are removed or resurfaced. Recovery time from a full tonsillectomy can take 10 days to two weeks.


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Save the products you like here
This product is out of stock. Customers interested in it also viewed these products
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Super DryT Sdwsyl128w Purple/Purple Analog Watch
Rs 7944
SizeFREE SIZE
Be the envy of all your friends as you show off your keen fashion sense by owning this purple analog watch from Superdry. Made from silicone, this watch features a round dial and has black stones at the centre set in a circular pattern. It also features a plastic strap and has a one year warranty. It is water resistant upto 10 m, so you can rest easy even on rainy days. This watch can be teamed with a shift dress and a pair of sneakers to complete your funky look.
- MovementQuartz
- Dial ShapeRound
- Dial ColorPurple
- Dial Diameter42 MM
- Dial Thickness (mm)12 MM
- Strap ColorPurple
- Product warranty3 Months Against The Manufacturing Defects
- Model NumberT SDWSYL128W


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It only takes a minute to get started. Fill out our simple sign up form and login to the website.
This step is voluntary but will greatly boost your chances of getting interest from other members on the site. Write a little about yourself, your pasttimes and upload a nice photo of yourself.
Utilise our website's advanced search to encounter members who meet your requirements. Or just look through listings and encounter people that attract you.
Located someone who interests you? Send a note to them or just a wink and find out if they're interested in you. With a little luck you'll be on your way to locating the love of your life.
It only takes a few clicks


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"Writers have no patience for bad stories."
A friend of mine told me that, and I've realized how true that is.
How many times have I gotten myself a book, settled down with it, and gotten half-way through before I realized, "This book sucks."
It used to be that I would force myself to continue with the book, and suffer through it, thinking, "It'll get better."
The only time, recently, that that happened to me was with The Clash of Kings. I was halfway through and thinking, "This is just so tiring for me. It's got to get better." In some places it did, so I read those parts.
So out the 50 or so books that I've read so far this year, only ONE gets better. I don't like those odds, so I decided this year that if a book sucks, I'm tossing it.
How do you tell if a book sucks?
1) If you're counting pages.
2) If you're arguing with the narrator.
3) If you realize the secondary characters are better than the main character and you skim the MC's point of view to get to the secondary character(s).
4) If there's such a complication that seems impossible for the MC or even secondary characters. (Simon Green almost...ALMOST did it to me, but I pressed on...and it got more impossible. But the writing style kept me going.)
5) When the book goes "Deus ex machina" on you. It means the author saves the protagonist...impossibly.
6) When you know, you just know, that the author is writing a Mary Sue.
Let me give you an example: Twice Burned, by Jeannie Frost.
Now, I loved the first book in her Dark Prince series. The first book I plowed through in two days, and stayed up late reading it. I was chomping at the bit for the second book, and got it a couple of months after it came out. I don't usually read the next book in the series right after (because I get burned out), but this time I did.
I was looking forward to the end of the chapters (1). I found I was doing (2) an awful lot. My Kindle highlights tons of parts that I was arguing with the narrator, calling her stupid, and insipid, and why-doesn't-she-accept-what-she's-got nasty words. I wanted to know more about Maximus than the idiot gymnast(!) who was narrating the story (3). Exactly at the half way mark, she had "died and gone into a coma" and Vlad's blood saved her (4/5). That's where I stopped reading. I have no idea if (6) came into play.
I'm sure you've seen this kind of thing happen in your own writing. Just remember to lead up to it. Please, for the love of Pete, don't kill your character all of a sudden and have her be reborn (unless, of course, she's going to be a vampire or zombie or something). If you're going to kill them, kill them dead, dead, dead.
Meanwhile, write your Mary Sue somewhere else. Like here. :)


text:
The BBC Panorama television programme, 'Poison in the Mouth', claimed new evidence showed that the metal used to fill back teeth, which is 50 per cent mercury, lodges in the brain and kidneys and can cause nerve damage.
But the allegations were refuted by the British Dental Association and the Department of Health.
Richard Ibetson, head of conservative dentistry at Eastman Dental Hospital in London, said: 'There is no doubt that amalgam does release small amounts of mercury. What is in dispute is the levels at which that might become a problem. I have seen no research that supports the idea that it is unsafe to fill teeth with amalgam. Without . . . hesitation I would have amalgam fillings.'
A Department of Health spokesman said the new evidence from Germany did not alter the position of the Committee on Toxicity, which advises the Government.
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The Link Between Androgen Receptor Splice Variants and Castration-Resistant Prostate Cancer
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DOI: 10.1007/s12672-014-0177-y
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- Sprenger, C.C.T. & Plymate, S.R. HORM CANC (2014) 5: 207. doi:10.1007/s12672-014-0177-y
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Resistance to the latest advanced prostate cancer therapies, including abiraterone and enzalutamide, is associated with increased expression of constitutively active androgen receptor splice variants (AR-Vs). The exact mechanism by which these therapies result in AR-Vs is unknown, but may include genomic rearrangement of the androgen receptor gene as well as alternative splicing of the AR pre-messenger RNA (mRNA). An additional complication that hinders further development of effective AR strategies is that the mechanisms by which the directed therapies are bypassed may vary. Finally, the question must be addressed as to whether the androgen receptor remains to be the driver of most castration resistant disease or whether truly AR-independent tumors arise after successful androgen ablation therapy. In this review, we will examine androgen receptor splice variants as an alternative mechanism by which prostate cancer becomes resistant to androgen receptor-directed therapy.
Androgen Receptor Structure and Function
The AR belongs to the class I nuclear steroid receptors that include the glucocorticoid receptor, estrogen receptors α and β, progesterone receptor, and mineralocorticoid receptors. Binding to their cognate ligands activates the receptors; activated receptors are then transported to the nucleus where they bind to DNA as homodimers to two hexameric half sites. The dimerization of the AR can occur through N-terminal/C-terminal (N-C) interactions, dimer to dimer (D-D) interactions, and ligand binding domain (LBD) interactions [19]. The classic AR–ligand-driven activation of the AR requires ligand-induced N-C interaction. Once steroid ligand binds to the receptor's LBD, a highly conserved AF-2 interface is formed in the C-terminus. The AF-2 interface is the mediator of transcriptional activity in most class 1 steroid receptors; however, the AR is different in that upon binding of ligand the AF-2 domain interacts with the LXXLF and WXXLF domains in the N-terminus to initiate transcription. These interactions confer AR co-regulator binding to the transactivation unit 1 (TAU-1) and transactivation unit-5 (TAU-5). Thus, the AR is unique in that mediation of its transcriptional activity occurs through the N-terminal domain rather than the C-terminal domain, as occurs in the other class 1 nuclear steroid receptors. Importantly, the N-C interaction of the AR is ligand-dependent and the dominant interaction of the AR-driving transcription is the AF-2 LXXLF interaction. In contrast, the WXXLF-AF2 interaction is a minor contributor to ligand-induced AR transcriptional activity and the interactions between AF-2 and the WXXLF motif have been thought to be more important in ligand stabilization of the AR. However, recent mutation and deletion studies of the AR have shown that in the absence of the LBD, AR continues to have ligand-independent transcriptional activity that is primarily driven through the WXXLF motif in the TAU-5 domain (for more information, see these reviews on AR domain interactions [19, 20]). The significance of this brief introduction to the AR-transcriptional structure is to point out that among the class 1 nuclear steroid receptors, the AR is unique in that it can generate ligand and C-terminal-independent transcription though its N-terminal and DNA binding domains.
AR Splice Variants
Splice Variant Structure and Function
Truncated AR variants
Truncated variants
Alternate names
Original references
AR-V1 (exons 1/2/3/CE1)
Cell lines, 22Rv1; tissues, PCa (higher in CRPC)
AR-V2 (exons 1/2/3/3/CE1)
Cell lines, 22Rv1
AR-V3 (exons 1/2/CE4a/3/CE1)
AR 1/2/2b (exons 1/2/CE4)
Cell lines, 22Rv1 and VCaP; xenografts, LuCaP 23.1 and 35
AR-V4 (exons 1/2/3/CE4a/3/CE1)
AR 1/2/3/2b, AR5
Cell lines, 22Rv1; tissues, benign prostate and PCa
AR-V5 (exons 1/2/3/CE5b)
Cell lines, 22Rv1
AR-V6 (exons 1/2/3/CE5c)
Cell lines, 22Rv1
AR-V7 (exons 1/2/3/CE3)
Cell lines, 22Rv1, VCaP, and LNCaP androgen-independent lines; xenografts, LuCaP series and VCaP; tissues, benign and PCa (up in CRPC)
AR-V8 (exons 1/2/3/CE6)
Xenografts, VCaP
AR-V9 (exons 1/2/3/CE5)
Xenografts, VCaP
AR-V10 (exons 1/2/3/CE7)
Xenografts, VCaP
AR-V11 (exons 1/2/3)
Xenografts, VCaP
Exon skipping AR variants
Exon splicing variants
Original references
ARv567es (exons 1/2/3/4/8)
Cell lines, VCaP and LNCaP androgen-independent lines; xenografts, LuCaP 86.2 and castration resistant LuCaP series; tissues, PCa (highest in CRPC and metastases)
AR-V12 (exons 1/2/3/4/8/9)
Tissues, CRPC
AR-V13 (exons 1/2/3/4/5/6/9)
Tissues, CRPC
AR-V14 (exons 1/2/3/4/5/6/7/9)
Tissues, CRPC
While AR variants lacking the LBD are transcriptionally active when placed in AR-negative cell lines, the expression of AR variants has generally been reported to occur in conjunction with ongoing expression of AR-FL. Interestingly, Sun et al. [22] have demonstrated that in the absence of ligand, the ARv567es variant forms a heterodimer with AR-FL causing it to be translocated to the nucleus and that, in the presence of ligand, ARv567es enhances the activity of AR-FL [22]. Similar data have been seen with AR-V7 and AR-FL [30]. These data suggest that while AR variants can activate an AR transcriptional program by themselves, they also can potentiate the activity of AR-FL under low-ligand conditions; such conditions may be present in tumors of castrate men. In support of this view, Minges et al. [31] suggested that an AR co-factor, MAGE-A11, allows AR-Vs to dimerize with AR-FL by binding to the AF1 and FXXLF motifs in the N-terminus. When cells containing the dimerized AR-Vs/AR-FL were placed in low levels of androgens, this dimerization enhanced transcriptional activity of the AR-FL [31]. In a similar regard, Watson et al. [21] demonstrated that in the presence of both truncated and full-length AR, targeting AR-FL with the anti-androgen enzalutamide suppressed AR activity and cell growth as efficiently as when only AR-FL was present, suggesting activity of the AR splice variants is mediated through the full-length AR [21].
While AR-Vs can enhance AR-FL transcription, others and we have also demonstrated that there are unique gene sets expressed by the AR variants compared to AR-FL (Supplemental Table 1) [16, 32]. These unique gene sets are associated with mitotic and anti-apoptotic pathways and, therefore, suggest that variant expression could enhance progression through the cell cycle in the face of therapies that normally cause apoptosis of cancer cells. Clinically such biological effects are suggested by the rapid progression and shorter time to death of men whose tumors express variants (see "Clinical Associations of AR Variants"). Whether there are specific variant-regulated differences in promoter and enhancer effects upon target genes compared to the AR-FL or differences due to resident time on chromatin and other epigenetic effects of the variants is not known. We have clearly shown that the time course of nuclear entry of variants versus AR-FL receptor is markedly different [22]. However, a complication of most of the expression studies reported with the variants is that they have either been done in the LNCaP human prostate cancer cell line, which contains mutated AR-FL and PTEN genes, or in cell lines that do not otherwise express AR. In this latter circumstance, we have found that cells that have lost or never had AR expression often have low levels of the co-regulators needed for AR transactivation; thus, common AR-regulated genes such as PSA or TMPRSS2 are poorly expressed in these cells after introduction of AR.
It is clear that multiple forms of AR variants exist in prostate cancer and that the function of most variants is unknown. However, it is of interest that the structure of the variants is relatively similar between human and mouse models of prostate cancer, suggesting that these variants are structurally related and selected to potentially bypass the androgen deprived environment.
Formation of AR Splice Variants
Currently, it is hypothesized that the formation of the AR splice variants can occur through two different mechanisms: genomic rearrangements and alternative splicing events. Dehm's group has used paired-end sequencing to examine the AR gene in 22Rv1 and several LuCaP human prostate cancer xenografts to demonstrate that in cell lines/xenografts which consistently express AR-Vs, there is an intragenic re-arrangement of the AR gene that may account for the presence of AR-V7 or ARv567es [33, 34]. Further, using a combination of FISH and deep sequencing, these studies propose that individual prostate cancer cells can express either AR-FL or AR-Vs but not both. These data suggest that initially AR-Vs may only exist in subsets of cancer cells, but following castration and inhibition of ligand-driven AR-FL, the AR-V clones emerge to drive the tumor.
Evidence also exists to support a second mechanism of AR-V generation, alternative splicing. Alternative splicing is a common mechanism for generating the variety of proteins expressed in cells [35, 36, 37]. In malignancies, differential splicing of pre-messenger RNA (mRNA) is a frequent mechanism used by the cell to generate protein variants that have oncogenic activity [35, 36, 37]. We have demonstrated that transcriptional-associated alternative splicing generates AR-V7 in the VCaP human prostate cancer cell line but not in the LNCaP human prostate cancer cell line [38]. Neither of these lines has been shown to have an intragenic rearrangement or inversion of the AR gene [34]. However, LNCaP does have a PTEN mutation and a mutation in the LBD of the AR that increases the promiscuity of ligands that can activate the AR [39, 40]. VCaP cells have a TMPRSS2-ERG fusion and a marked increase in the copy number of AR-FL [41, 42]. When the LBD of VCaP cells was blocked by a small interfering RNA (siRNA), enzalutamide, or growth in charcoal-stripped serum, AR-V7 and ARv567es were generated in as little as 4–12 h. In contrast, LNCaP cells failed to generate AR-Vs under these conditions [34, 41, 42]. ChIP assays performed on VCaP cells treated with enzalutamide demonstrated that proteins comprising the splicesome (U1A, U2AF, ASF/SF2, and p54nrb), along with Pol-II, were recruited to the 3′ and 5′ splice sites of the introns/exons needed to generate AR-V7. These data indicate that the splicing occurs with transcription elongation [30, 43]. Further, under androgen deprivation conditions, it was not an increase in message of these splicing factors that led to creation of AR-V7 but rather an association of the splice factors with different splice sites within the AR pre-mRNA. This study identified one intronic splicing enhancer (ISE) and one exonic splicing enhancer (ESE) near the 3′ splice site of AR exon 3B (also known as cryptic exon 3 (CE3)). Following treatment with enzalutamide, U2AF65/hnRNP I bound to the ISE, while ASF/SF2 bound to the ESE. Liu et al. [38] observed that siRNA knockdown of splice factors or mutation of the ISE and ESE sites decreased the generation of AR-V7. While LNCaP does not express AR-Vs under androgen deprivation conditions, LNCaP 95, a castration-resistant LNCaP sub-line , does express high levels of AR-Vs [38]. These cells are maintained long term in an androgen-depleted medium, suggesting that LNCaP cells can become castrate resistant once they express AR-Vs. The LNCaP 95 cell line has a single copy of the AR gene with no intragenic rearrangements, but this line does express high levels of the androgen-glucuronidating enzymes UGT2B-15 and UGT2B-17, which maintain low levels of intracellular androgen and thus favor formation of AR-Vs by a transcriptional splicing mechanism. Of further note, Hu et al. [16] have described an additional non-transcribed 3′ sequence, termed exon 9, in AR exon-skipping variants (AR-V12, V13, and V14) [44]. The presence of exon 9 provides the potential for additional splice sites in the AR that may be involved in formation of the different exon-skipping AR-Vs. Together, the splicing data provide further evidence that androgen deprivation generates AR splice variants.
The possibility of both alternative splicing and intragenic AR gene rearrangements as mechanisms for the formation of AR-Vs following androgen deprivation indicate that there are rapid transcriptional mechanisms for AR-V formation as well as longer-term somatic mechanisms for the selection of AR-V-positive tumor cells. Regardless of the mechanism responsible for the generation of the constitutively active AR-Vs, their increase in response to androgen deprivation therapy (ADT) is clear and whether through clonal selection or transcriptional associated splicing, ADT is the prime enhancing factor. However, whether constitutively active AR-Vs are responsible for progression to castrate-resistant prostate cancer (CRPC) through AR signaling or are epiphenomena of AR response when it loses its stabilizing ligand is not yet known. In the next portions of this review, we will review clinical and laboratory evidence for or against the AR-Vs as potential mediators of CRPC.
Clinical Associations of AR Variants
Others and we have recently described the appearance of posttranscriptional AR splice variants following castration [15, 21, 22, 24, 45, 46]. The consistency with which AR-V7 and ARv567es are found in tumors and metastases from castrate men suggests that production of these variants may occur in response to castration, and it is notable that the variants most prevalent in human tissues are those most consistently found following androgen deprivation in vitro [26, 29]. We have found that the generation of ARv567es is especially sensitive to suppression of intratumoral androgens, suggesting growth of these tumors is associated with generation of AR variants in the presence of castrate levels of androgen [15, 16, 22, 47].
Expression of the two constitutively active AR-Vs, AR-V7 and ARv567es, has been most commonly associated with castrate-resistant prostate cancer and its metastases. In our experience, their expression is unusual in benign prostate tissue or primary prostate cancer. Interestingly, Sun et al. [22] demonstrated the presence of both variants in prostate tissue from healthy men treated with anti-androgens as part of a male contraceptive study. Such a finding further indicates that androgen deprivation drives the formation of the AR-Vs [22]. Other studies have seen expression of AR-V7 mRNA in 80 % of benign prostate tissues from men with no evidence of cancer [32]. Likewise, AR-V7 protein has been detected in benign basal epithelial cells using a specific antibody to AR-V7; however, these data have not been reproducible using other available AR-V7 antibodies. If AR-V7 expression does arise from intragenic re-arrangements, then it would not be surprising to see low levels of AR-V7 mRNA and protein in normal prostate tissue; upon castration, the cells expressing AR-V7 would then have a growth advantage and tissue-wide levels of AR-V7 mRNA and protein would increase.
In a recent study, Zhang et al. [26] performed AR staining on tissue microarrays that contained prostate cancer tissue from 55 non-castrate men at the time of radical prostatectomy (RRP) and 144 metastases from 43 castrate men who died from prostate cancer. C- or N-terminal-specific AR antibodies were used. Staining intensity as well as localization, nuclear (N) or cytoplasmic (C), was determined for each antibody [26]. Because the AR-Vs lack the C-terminal portion of the AR, the AR C-terminal specific antibody will not detect variants. In addition, since the two most common AR-Vs are constitutively active, samples with AR-Vs would be expected to have more nuclear staining with the N-terminal AR antibody. In the primary tumors, the ratio of nuclear to cytoplasmic AR staining was not significantly different, whereas in the metastases significantly more nuclear staining occurred. Although variant-specific antibodies were not used, these data show that there was a significant alteration in the levels of C-terminal containing ARs in the metastases of men who are castrate and die from their disease. These data are consistent with a high prevalence of C-terminal AR loss and AR nuclear localization, as is seen with the AR variants, and is consistent with the presence of constitutively active AR activity in castrate resistant prostate cancer.
Although a number of studies in the literature have shown an association between AR-Vs and prostate cancer metastases, only two clinical studies have demonstrated an association between AR-V7 expression and subsequent progression to castrate-resistant prostate cancer (CRPC) [24, 32]. In the first study, tissue microarrays of primary tumors were stained for AR-FL or AR-V7. There was no association between AR-FL expression and subsequent progression to castrate resistant disease; however, AR-V7 expression in the primary tumor correlated with subsequent chemical recurrence [48]. In the second study, tumor tissue was collected from men who presented with pathologic fractures due to prostate cancer. Two thirds of these men had been castrated, and one-third presented with fracture as the initial manifestation of their disease. AR-V7 and ARv567es were assessed in the tumor tissue. Men who expressed any ARv567es or who were in the upper quartile for AR-V7 expression died on average 2 months after diagnosis (with a maximum survival of only 3.3 months), whereas those patients who did not express the variants lived an average of 8 months following diagnosis (with a maximum survival of 36 months). Furthermore, tumors from patients who expressed the variants had a more mitotic gene expression pattern [26]. These data do not indicate that the AR-Vs cause resistance to therapy but do suggest that variant expression is associated with a significantly rapid progression of the tumor. However, because each of these biomarker studies had relatively small patient numbers, at this point, no definite conclusions can be drawn as to whether AR-V7 expression will serve as a biomarker to define prostate cancers that will progress. Therefore, as better antibodies are developed to detect more of the AR-Vs, it will be important to examine the potential of AR-Vs to serve as biomarkers of low-grade tumors with progressive abilities. This is especially important as more patients enter active surveillance protocols.
Castration-Resistant Prostate Cancer and AR Variants
Several studies indicate that the AR-Vs are drivers of castration-resistant prostate cancer and function independently of the full-length AR [22]. If correct, then current and future therapy targeting the ligand-binding domain would be ineffective since these AR-Vs lack the LBD. Unfortunately, this latter suggestion is not universal as the function of constitutively active AR-Vs is a more complex relationship that includes not only dimerization with AR-FL but also the differential effect of ubiquination and proteosomal degradation on AR-Vs expression. Others and we have shown that even potent inhibitors of the LBD, such as enzalutamide, do not inhibit the AR activity of prostate cancer cells driven by AR-Vs [29, 34]. Each of these factors appears to be altered in the progression to CRPC such that the role of AR-Vs is of greater significance as the LBD is compromised. Of further importance, the splicing mechanisms, which include specific components of the spliceosome that generate the constitutively active AR-Vs, can be activated by inhibition of AR signaling and conversely suppressed by transactivation of the AR. These data indicate that the generation of the constitutively active AR-Vs are not simply random splicing events but are probably specific tumor survival events. Finally, there is the issue of whether the variants actually lead to expression of a unique set of AR-regulated genes, distinct from the AR-FL transcriptome [22, 32, 34]. Again, this is a controversial but important issue.
Nuclear Localization of AR Variants
In addition to the ability of the AR-Vs to translocate to the nucleus independent of ligand, we have also shown in the absence of ligand that AR-FL can dimerize with both AR-V7 and ARv567es. This dimerization can result in the nuclear localization of the heterodimer with subsequent binding to AREs [22, 30]. Sequential chromatin immunoprecipitation (Re-ChIP) analysis with an AR-V7 antibody followed by an AR-FL antibody was performed in 22Rv1 cells, which express endogenous AR-V7 [31]. Co-occupancy of AR-V7 and AR-FL was shown on the promoter of the PSA gene. This co-occupancy was unaffected by androgen or enzalutamide treatment. However, the promoter of ubiquitin-conjugating enzyme E2C (UBE2C) was only bound by AR-V7. ChIP assays demonstrated that AR-FL knockdown did not significantly affect this binding, consistent with UBE2C being an AR-Vs specific target [14, 15]. These studies demonstrate that the mechanism by which the constitutively active AR-Vs translocate to the nucleus in the absence of ligand is AR-V specific and depends, in part, on whether the particular variant sequence contains both components of the bipartite NLS. Additionally, regardless of mechanism, the ability of the variants to heterodimerize with AR-FL results in nuclear translocation and ARE binding in the absence of ligand and, importantly, in the presence of enzalutamide.
In addition to the mechanisms responsible for nuclear localization of the AR-Vs, most AR variants lack the putative nuclear export signal (NES) located in the LBD (aa 743–817) [54]. This suggests that once in the nucleus, chromatin binding by the variants will be significantly prolonged and signaling altered. Additionally, components of the NES are associated with AR polyubiquination and AR degradation [55]. Thus, there is a potential for decreased rates of degradation of AR-V protein compared to AR-FL. The stability/degradation of the AR-Vs, however, has not been well defined at this point.
AR Variant Transcriptome
Initial studies demonstrated that LNCaP cells in which either AR-V7 or ARv567es were constitutively expressed were castration resistant when grown subcutaneously in immunocompromised mice [21, 22, 24, 25]. Mostaghel et al. [15] reported that the effects of AR-Vs in the presence of AR-FL appear to be regulated by the levels of intratumoral androgens [15]. Using a series of LuCaP xenografts in which mice were treated with the CYP17 inhibitor abiraterone, the authors demonstrated that if intratumoral androgens could be detected by mass spectrometry (MS) in the recurrent tumors, then AR-Vs, while detectable, were not significantly upregulated compared to pre-treatment levels. Furthermore, tumor recurrence in this case was associated with an increase in AR-FL ligand-dependent genes, e.g., PSA and TMPRSS2. However, when abiraterone recurrence was associated with the absence of MS-measureable intratumoral DHT, then the levels of AR-Vs increased significantly and were associated with mitotic genes, e.g., UBE2C. Hu, et al. [16] further demonstrated in clinical samples that expression of AR-V7 protein was also correlated with expression of UBE2C [16]. In the same study, prostate cancer cells treated with either a siRNA to the LBD or enzalutamide had decreased AR-canonical gene expression but increased mitotic gene expression [16]. These studies suggest that in the absence of ligand, AR-Vs function independently of AR-FL and their actions cannot be blocked by anti-androgen inhibitors. These studies also suggest that AR-Vs may express their own transcriptome.
Therefore, we still have the quandary as to what the contribution of the AR constitutively active splice variants are when they exist in association with AR-FL. Another criticism that has been voiced to show that the AR-Vs are not relevant in the presence of AR-FL is that the level of expression of the variants in tissue and most cell lines is approximately 0.1–2.0 % of the AR-FL [21]. The low levels of variant may, in part, be due to a lower affinity of N-terminal AR antibodies to the variants. Development of variant-specific antibodies is underway and is necessary to more accurately determine AR variant levels. For example, when an AR-V7-specific antibody was used for IHC, AR-V7 protein was readily detected in human prostate cancer tissues [16]. Even if specific antibodies show lower levels of AR variant proteins compared to AR-FL, low levels do not necessarily indicate a lack of functional importance for the variants. Unlike AR-FL, the constitutively active variants translocate directly to the nucleus where they function as transcription factors; therefore, comparing their levels to the AR-FL level, which must exist in the cytosol in order to bind ligand, is not an equivalent comparison. Recently, Cao et al. [30] confirmed the data of Sun et al. [22] by demonstrating that in androgen deprivation conditions when AR-FL associates with either AR-V7 or ARv567es, the heterodimers are transported into the nucleus and bind to canonical ARE promoter elements, e.g., PSA and TMPRSS2 [22, 30]. Importantly, transportation and binding were not blocked by enzalutamide. Further, in the absence of AR-FL, the AR-Vs bound to enhancer and promoter elements on genes shown to be upregulated when AR-Vs are highly expressed (e.g., UBE2C) [16]. Since UBE2C does not have a consensus ARE binding site in its promoter or enhancer elements, this suggests that long-range chromatin looping may play a role in its transcription [56]. These data indicate that the AR-Vs may require the presence of AR-FL for their activity on AR-canonical gene expression but that they can also act independently of AR-FL to generate a distinct AR-V transcriptome.
Whether the AR-Vs have a unique transcriptome remains unclear. Hu, et al. [16] recently published that the AR-Vs have a unique mitotic transcriptome; some of the upregulated genes in this transcriptome (e.g. UBE2C) are upregulated in a CRPC transcriptome published by Cuzick et al. [16, 48, 57]. In contrast, Li et al. [34] found prostate cancer cells driven by the AR-Vs have a biphasic classic androgen transcriptome, albeit in the absence of ligand. These studies, however, used different prostate cancer cell lines and different methods of expressing the variants. The difference in transcriptomes then is not surprising and may point to cell-specific transcriptomes. Further studies using a variety of prostate cancer cell lines that endogenously express AR-Vs as well as human prostate cancer tissues are necessary. Studies using the new AR-Vs transgenic mice could also highlight whether or not AR-Vs have a unique transcriptome.
AR Variant Transgenics
Current studies using prostate cancer xenografts in mice have resulted in conflicting data regarding the importance of AR-Vs. Watson et al. [21] did not see a significant effect of AR-Vs on tumor progression or in treatment resistance [21]. On the other hand, others and we have seen an association between increased AR-Vs expression and treatment resistance and prostate cancer progression [22, 24]. All of these studies, however, have examined what happens in cells or xenografts after exposure to AR-Vs for a few days to a few weeks; in this short amount of time, it may be difficult to discern the effect of the variants. Recently, two studies have addressed what happens in vivo in transgenic mice engineered to express either ARv567es or AR-V7 (AR3). In both studies, AR variant complementary DNA (cDNA) was inserted into a vector containing a rat probasin promoter (ARR2), which resulted in AR variant expression specifically in the prostate epithelium. The background of the mice, however, differed in the two studies: ARv567es was placed in the C57/Bl6 background while AR-V7 (AR3) was placed in the FVB mouse. While the FVB mouse tends to result in more aggressive cancer progression in transgenics, in this case, AR variant expression in the different backgrounds resulted in similar phenotypic alterations [58, 59].
Liu et al. [59] created a transgenic ARv657es mouse model. Using PCR and a human specific N-terminal antibody (AR441), ARv567es was detected in all four lobes of the transgenic prostate, with the highest expression in the lateral and ventral lobes. No ARv567es was detected in wild-type littermates. At 16 weeks of age, hyperplasia was evident in the transgenic prostate, with adenocarcinoma developing by 1 year. In castrate transgenics, ARv567es mRNA was still detectable by PCR. Immunohistochemistry, using a human-specific AR antibody, demonstrated positive nuclear AR staining pointing to the constitutive activity of ARv567es. Importantly, castration increased the aggressiveness of the carcinomas in year-old mice, with invasive carcinomas detected in two thirds of mice and liver metastases detectable in one out of six mice. Immunohistochemistry on transgenic prostates revealed increased levels of proteins associated with epithelial to mesenchymal transition, including vimentin and Twist. cDNA arrays revealed upregulation of genes commonly found in AR-V-positive tissues, including UBE2C. Gene set enrichment analysis (GSEA) further revealed upregulation of five oncogenic signatures associated with different stages of prostate cancer progression (Kras, NF-κB, β-catenin/Wnt, Gli1, and Stk33). Together, these data suggest that ARv567es plays a role in development of CRPC.
Sun et al. [58] reported that by 4 weeks of age, prostate-specific expression of AR-V7 (AR3) led to alteration in prostate gland structure in addition to upregulation of factors associated with both prostate stem cells (e.g. Sca-1, TGF-β) and an epithelial to mesenchymal transition (e.g., Snail, Slug, Twist, N-cadherin, and vimentin). By 1 year, the mice had developed prostate intraepithelial neoplasia (PIN). In addition, the authors noted a significant decrease in miR-29, a micro RNA associated with tumor suppressive activity in the prostate. In vitro studies demonstrated that miR-29 binds to the 3′UTR of IGF-1 thereby decreasing its expression and likewise decreasing the levels of pAKT, a downstream target of the IGF-1 signaling pathway. Examination of miR-29, IGF-1, and pAKT levels in the transgenic prostates in turn demonstrated a correlation between decreased levels of miR-29 and increased levels of IGF-1 and pAKT. In contrast to the ARv567es study, Sun et al. [58] performed early castration studies on 4-week-old mice; 2 weeks later, testosterone was reintroduced to half of the mice. AR-V7 transgenic mice showed more rapid regeneration following testosterone supplementation than wild-type littermates. It would be of interest to see if castration at 1 year would lead to development of carcinoma in the AR-V7 mouse as it did in the ARv567es transgenic mouse.
Future studies crossing these models with other prostate cancer transgenic models will further elucidate the role of AR variants in prostate cancer progression, especially their role in lethal CRPC.
New Agents Targeting AR Variants
Since the C-terminus of the AR can be crystalized, we have seen the recent introduction of very effective AR-FL inhibitors such as enzalutamide and ARN-509. However, because the N-terminus is intrinsically disordered and has not been crystalized, agents with a similar degree of activity are not yet available [48]. Further, it is unlikely that agents will be able to selectively inhibit each of the AR-Vs. In place of AR-V-specific agents, naturally derived compounds such as EPI-001 or mahanine that inhibit both AR-FL and AR-Vs are under study as new prostate cancer therapies [55, 60, 61]. While these agents are not yet in clinical trials, in pre-clinical studies, they demonstrate the best hope of inhibiting the AR-Vs. As indicated, a number of agents are under development that potentially can inhibit AR-V activity. Since the variants may be an important mechanism for initial tumor survival in response to ADT [3, 38], treatments targeting AR-Vs should be considered at the time androgen ablation therapy is initiated, when AR-Vs are likely to arise, rather than delayed until after recurrence and additional mechanisms of resistance such as point mutations in the LBD of the AR or a neuroendocrine phenotype develop.
Constitutively active AR splice variants are commonly increased in recurrent prostate cancer following castration. In cell lines and xenografts, these variants can continue to drive tumor progression in the face of potent C-terminal AR inhibition agents, such as enzalutamide and abiraterone. However, when AR-Vs are co-expressed with AR-FL, significant inhibition of xenograft growth can still occur in response to enzalutamide. This effect is likely due to heterodimerization between AR-Vs and AR-FL as well as the continued presence of intratumoral androgens. The answer to the question as to whether or not AR-Vs are causal mediators of CRPC or biomarkers of aggressive disease clinically is still in question with the majority of the preclinical and transgenic mouse data favoring causality. However, until N-terminal inhibitors of the AR are available for clinical use, it is unlikely the question will be resolved experimentally. To further complicate the issue is the idea that while different AR-Vs may be constitutively active, there appears to be some variation in function. For example, mechanisms of nuclear transport differ between AR-V7 and ARv567es; these differences can affect how the cells respond to cancer therapies such as taxanes. Regardless of the outcome of these functional questions, though, the overwhelming evidence points to AR-Vs playing a role in the development of castration resistant prostate cancer.
Pacific Northwest Prostate Cancer SPORE (2 P50 CA 097186-12), PO1-CA85859, DOD-CDMRP W81XWH-13-2-0093, Veterans Affairs Research Service, and NIH P01 CA163227-01A1 (S. Plymate).


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Need help ordering? Call us at 1-888-2GO-HIKE Store Locations
The super concentrated Sea to Summit Trek & Travel Wilderness Wash goes a long, long way and is not only gentle on fabrics and skin, but is also effective on dishes and laundry stains. It's biodegradable, phosphate and fragrance free.
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Results 1 to 1 of 1
2012 Audi A3 renderings and details
We already had a general idea of the next generation A3 thanks to the sedan concept from Geneva. AutoExpress brings us renderings of the hatchback which, no surprise, looks just like the sedan. There will be four body styles of the new A3; a five door hatch, 3 door hatch, sedan, and one that has not been announced (cab perhaps?). Audi is also going to offer an all electric A3 along with a hybrid version. That is great and all but we we are looking forward to is the RS3 sedan. Bring it Audi, bring it on.


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Warriors halfback Shaun Johnson praised his team's forwards for laying the foundation for Sunday's 42-0 demolition of the Gold Coast Titans in their final home game of the regular season at Mt Smart Stadium.
Johnson was a leading contributor to the Warriors resurgent performance, after last Sunday's humiliating season-worst 46-12 home defeat to the Sydney Roosters left their season on life support.
The 23-year-old playmaker combined well with halves partner Thomas Leuluai, playing a hand in four tries and using his speed to burn through the line and around the cover defence for a brilliant individual second-half effort, before adding the extras from the sideline to cap an immaculate seven-from-seven goal-kicking display.
Despite his 18-point haul, Johnson believes his team's change in fortune was down to the forward pack's determination to address some areas which had hindered their game-plan in recent weeks.
"We're very pleased that we got out here tonight and delivered as a team," Johnson said.
"I know first-hand the forwards were really disappointed with the platform they laid last week so they came out tonight and did a collective job. It wasn't just one or two of them it was all of them contributing to giving us that front-foot ball and me and Tommy, Sammy [Tomkins] and Nathan [Friend] were able to jump off the back of it. They all ripped in. It was fun to play off the back of."
The submissive nature of last week's loss and the repercussions it had for their finals hopes left the players in no doubts as to what was required to turn things around.
"I don't think too much needed to be said. We're all competitors and we're all men and to get beaten like we did last week in front of our fans, that hurt," Johnson explained.
"It's hard because we've known over this period what we need to do and what it looks like [competition ladder] for us. Just collectively as a group we really did it. There were no individuals out there."
The win keeps alive their hopes of hosting an elimination final and they will be assured of a playoff spot if they can get past the fourth-placed Penrith Panthers in a difficult last-round away clash on Sunday.
With the Warriors sitting in ninth spot locked together on 28-points behind the Cowboys and Broncos, Johnson acknowledged how important yesterday's defensive effort is to their points differential and final standings.
"We're aware of the situation we're in and any points you pick up at this time are going to be crucial. Defence has been something that we've built our season on and that's slipped away over the past couple of weeks. To bounce back like that showed that we as a team put an importance on it."
Being held scoreless in the final 30 minutes by a stubborn Titans outfit, whilst also refusing to concede any points themselves, would hold the Warriors in good stead.
"We got in that arm-wrestle and that's what you want to do at this time of year. We've obviously got a big game coming up next week which is going to be along those lines so we've got to be ready for it. It's an exciting challenge for us. We got over them a couple weeks back so we know what works for us and we know what it looks like so we've just got to get into it."


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Community mailing list archives
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Re: OPEN ERP OPEN OFFICE REPORT DESIGNERby
Luke Branch
Hi Peter,
are you using Odoo (version 8.0), or OpenERP (Version 7 or lower)?
If you're using version 8, and happen to have installed it on Ubuntu 14.04 then I don't think you'll be able to get the report designer to work.
The reason being that a package (pyuno) used in OpenOffice is written for Python (version 3+) in the default packaged version in Ubuntu 14.04, and is unfortunately not compatible with Odoo (running in Python 2.7+).
I found this out the hard way and wasted a fair bit of time on it, it is possible, however it requires rebuilding the OpenOffice package from another version of Ubuntu/Debian and required some scripting and Linux knowledge that is over my head at this point in time. With that being said however there are some alternatives.
Aeroo reports allows for creation of reports in XLS, ODS, DOC, ODF, PDF, and CSV formats
with some basic python, and a basic knowledge of the model being used in the report you're creating. It requires a bit of a learning curve, however it's my preferred reporting engine for Odoo.
You can find a script here for installation of Odoo + Aeroo reports here:
A few other popular reporting engines that work with Odoo are Jasper Reports and Pentaho, although I have no personal experience with those two yet.
If you need any help getting started with Aeroo I'd recommend hitting the Odoo and Alistek help forums, or ask on this mailing list.
Is be happy to send you a few sample reports (eg. quotation, invoice, etc) as examples to get you started if you like.
On 8 Sep, 2015, at 9:30 pm, Peter Mudoko <firstname.lastname@example.com> wrote:
Hi guys i am new to odoo, and have been practicing report design in open office, but when i click on open ERP Report designer everything seems ok even connecting to server modifying reports, but on modifying reports, when i click open report error comes ..The report could not be downloaded ..url seems to be unsupported, my open office version is 4.1.1 i have even tried 3.2 but impossible what am i missingKIND REGARDS
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OPEN ERP OPEN OFFICE REPORT DESIGNERbymudoko
Re: OPEN ERP OPEN OFFICE REPORT DESIGNERbymudoko
Re: OPEN ERP OPEN OFFICE REPORT DESIGNERbyLuke Branch
Re: OPEN ERP OPEN OFFICE REPORT DESIGNERbySerpent Consulting Services Pvt. Ltd., Jay Vora


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Shopping addiction, which is also known as compulsive shopping disorder or oniomania, is a socially and financially damaging psychological condition. Treatment for patients who seek help for their spending addiction from Priory can include the identification of any deeper psychological problems that may be affecting a person and subsequently treating with therapy and medicines.
The Priory can help with identification of shopping addiction and compulsive spending symptoms.
These can include financial problems as a result of spending beyond your means, with this spending hidden from friends and family, feelings of guilt associated with purchases and strain on relationships with loved ones.
Compulsive shopping is linked to many established psychiatric conditions. Amongst others, these include:
As with other addictive behaviours, the causes of compulsive shopping can be treated successfully and should therefore be treated as an addiction like any other.
Therefore, the impact of shopping addiction on the sufferer's quality of life should not be underestimated. The availability of access to the internet, and the greater trust in internet security for money transfer means that many more people who are in search of a bargain can end up in debt. Online stores such as eBay and Amazon are a huge temptation due to their vast product ranges, encouraging us into purchases that we didn't know we needed which can lead to a spending addiction.
The Priory has treatment centres located across the UK where you can seek help for shopping addiction.
Our experts can expertly assess your current shopping habits in the context of a global assessment of mental health. We can accurately identify any underlying psychological problems, and offer shopping addiction treatment them with a combination of psychology, therapy and medication if required. The most important step is seeking initial shopping addiction help.
The type and length of shopping addiction treatment is dependent on the individual's circumstances and the severity of the condition. Some people are treated as outpatients, which means they come to the Priory for hourly sessions with their consultant, psychologist or therapist. Others require a more structured treatment approach which can include staying as an inpatient at one of the Priory hospitals for the duration of their treatment where they take part in the psychological group programme as well as regular sessions with their consultant. Take a look at all the specific therapy treatment services we offer for shopping addiction.
We understand embarking upon shopping addiction help can be an emotionally turbulent time for you. With this in mind, the Priory offers a free initial assessment with an experienced therapist at all of our addiction treatment hospitals and clinics to help you discuss your addiction in confidence.
For further details on how Priory can provide you with further assistance regarding Shopping Addiction (Oniomania) Treatment & Help at the Priory, please call 0800 840 3219. For professionals looking to make a referral, please
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We treat Shopping Addiction (Oniomania) Treatment & Help at the Priory at the following facilities
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The Priory is pleased to offer you a free confidential assessment for all addictions; alcohol, drugs, sex, gambling, internet and more.
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Discover a place that CNN ranked as a top ten world destination for 2012.
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WHAT: The CRC meeting. The CRC is committed to receiving input from the public regarding issues or topics relating to the Orange County Charter and the County government's constitution.
WHEN: Thursday, July 9, 2015 4 p.m.
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201 S. Rosalind Ave.
Orlando, FL 32801
Anissa Mercado, CRC Administrative Assistant
407-836-5430 or email: firstname.lastname@example.com
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About Orange County Government: Orange County Government strives to serve its citizens and guests with integrity, honesty, fairness and professionalism. Located in Central Florida, Orange County includes 13 municipalities and is home to world famous theme parks, the nation's second largest convention center, and a thriving life science research park. Seven elected members make up the Board of County Commissioners including the Mayor who is elected countywide. For more information please visit www.OCFL.net or go to the Orange County Facebook and Twitter pages.


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Hanumant Singh, who won 14 caps for India as a batsman in the 1960s, censured Mike Atherton's side for "the manner of their appealing" during the drawn Test against Zimbabwe in Bulawayo at the end of 1996.
Now he is to oversee a three-match series, starting here on Thursday, which shows all the signs of turning into a tense, possibly tetchy, affair.
England and Sri Lanka have a track record when it comes to falling out on the field.
Their one-day meeting in Adelaide two winters ago was riddled with acrimony with Darren Gough and Alec Stewart among those drawn into verbal confrontations after their opponents had walked off in response to the noballing of Muttiah Muralitharan.
Two of the three warm-up games on this tour have already ended with play-ers being reported for verbal abuse while the other was most memorable for long, loud and generally unsuccessful appealing by both sides.
England maintained their discipline, almost without blemish, during the pre-Christmas tour of Pakistan.
Captain Nasser Hussain set just the right example by accepting several poor umpiring decisions against him with barely a flicker of emotion. They will need to demonstrate the same self-control here.
But, quite rightly, Hussain and Co have shown already they will not be walked over. Gough was reported by the opposition coach for "verbally threaten-ing" two members of the Sri Lankan Colts XI during the opening match of this tour. England said their fast bowler was reacting to derogatory comments and stressed he would not be reprimanded, but "reminded all the players of their responsibilities."
Now, perhaps to show they can play the same game, the tourists have lodged an official complaint against former Test paceman Ruchira Perera following his weekend verbal altercation with Craig White in Matara.
If passions are running high now, the Test series could be especially sparky.
"I've seen none of my boys go over the top yet," said Hussain. "The batsmen have walked off and the bowlers have carried on bowling.
"Our boys have played it just about right and, come Thursday, when all the cameras are on us we shall continue to play it in that manner."
Sri Lanka have named five spinners in their squad - and at least three are expected to play. Fielders will be crowded around the bat and appeals are likely to come thick and fast. Yet the umpires are two of the least experienced on the International Cricket Council panel - Sri Lanka's Peter Manuel and India's AV Jayaprakash.
The home selectors sound confident that Muralitharan will have recovered from a groin injury in time to play.
Sri Lanka's heavy emphasis on spin suggests it is even more important that left-armer Ashley Giles makes Thursday's starting line-up. Giles sent down 19 overs during yesterday's draw with a President's XI and appeared untroubled by his recent Achilles tendon problem.
- More about:
- India
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The Pocahontas Tea For One Set features the well-known princess in teapot form with a matching tea cup. The teapot is made out of ceramic and comes with a tea strainer that sits inside.
The Pocahontas Tea For One Set is perfect for making a relaxing cup of tea just for yourself. The Native American design featuring blues and reds is adorable and would look too cute in any kitchen. The set is available at Urban Outfitters.
State-of-the-Art Tea Pots
Terrorist Tea Pot
Heart-Shaped Tea Sets
Blossoming Beverage Sets
Macabre Tea Pots
The Pocahontas Tea for One Set is as Cute as a Button
Feb 12, 2011By: Chalaine Mantha -
References: urbanoutfitters
References: urbanoutfitters


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March 31, 2014
Speed limits in Idaho could soon move higher but trucks will still have to travel slower.
Legislation signed into law by Gov. Butch Otter allows an increase of up to 80 mph along interstate routes and 70 mph along state highways, but trucks would continue to be limited up to 10 mph slower.
The law leaves the final decision for any increase up to the Idaho Transportation Department, once it has competed studies to see if the routes could handle the higher speeds.
Supporters of increasing the speed limit say that many motorists are already driving around the higher speed limits and states that have made a similar hike have not seen an increase in truck crashes. Opponents, such as the Owner-Operator Independent Drivers Association, say different speed limits increase the chances of crashes.
While the new law doesn't take effect until July 1, Idaho's Transportation Department is expected to begin studies about hiking the speed limit this spring, with higher speed limits possibly appearing as soon as this summer, according to published reports.
If the higher speed limits are approved, Idaho would join Texas and Utah, which currently allow a top speed limit of 80 mph along select routes, while legislation in Wyoming was recently signed into law allowing the same increase, provided they are approved by the Wyoming DOT.
We offer e-newsletters that deliver targeted news and information for the entire fleet industry.
Scott Sutarik from Geotab will answer your questions and challenges
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On the Spot: U.S. Xpress Max-imum Tech Competition [Video]
Focus On... Volvo's VNR Regional Haul Tractor [Video]
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East Manufacturing Offers New Lightweight Tipper Trailer
Momentum's Tailgate System Designed for Refuse Trucks
Kit Designed to Clean Spills Around Large Trucks
Penray Kit Restores Headlight Covers


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1982 National Survey of Family Growth, Cycle III
Exposure Interval File
This data was extracted to create a file compatible with an analysis of contraceptive failure, using data from Cycle III of the National Survey of Family Growth (separately documented as DAAPPP Data Set No. 26). The selection of eligible intervals was accomplished in three stages. First, each respondent was examined to determine eligibility for inclusion in the study. Second, among eligible women, each pregnancy interval was examined and ineligible intervals discarded. Finally, intervals of use and non-use of contraceptives occurring within eligible pregnancy intervals were examined and eligible intervals were selected. In all, the 7,969 respondents to the NSFG contributed 11,253 separate, continuous intervals of exposure. Continuous intervals separated by changes in marital status and/or by periods of no intercourse were coded as multiple intervals, yielding 12,962 intervals available for analysis. For each of these 12,962 intervals, 33 interval-related characteristics are available from this data file.
Note for users of DAAPPP Data Sets #01-B1
DAAPPP data sets 01 through B1 are comprised of a User's Guide, SPSS syntax files (*.SPS or *.SPX) and raw data files only. Most of these datasets contain SPSS syntax files that use Job Control Language (JCL) from 1980s versions of SPSS-X. Because the syntax is old, the syntax files require editing to conform to the current syntax standards used by SPSS/Windows or SPSS/Unix. If you require technical assistance in using or editing these syntax files, please contact Sociometrics' Data Support Group at 800.846.3475 or firstname.lastname@example.com.


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The Carolina Panthers have found a new head coach.
The team hired San Diego Chargers defensive coordinator Ron Rivera to replace John Fox on Tuesday.
Rivera, who had interviewed for several other head-coaching opportunities in recent years, said he was excited to get a chance to run his own club.
And while acknowledging there's a lot of room to build on the Panthers' roster, Rivera said he's excited about the team's chances for a turnaround.
"I really like the set of circumstances I'm coming to," he said.
ESPN reported Rivera agreed to a four-year contract worth $11.2 million.
Rivera, 49, is taking over a team that went 2-14 last season. He will be just the second Latino head coach in NFL history (Tom Flores).
Rivera said he will run a 4-3 base defense with the Panthers, but said he wants the unit to be able to adapt to 3-4 looks in the right situations.
"Defensively we want to be an attacking and aggressive style of defense," he said.
He hasn't chosen an offensive coordinator, but said he wants his offense to be balanced in how it can combat other teams.
"I'm talking about having the balance that when you have to throw it, you will throw it," Rivera said, "when you have to run it,you run it. But you do it because you choose to."
Rivera led a Chargers defense that ranked first overall in the 2010. He was formerly a defensive coordinator for the Chicago Bears, the team he played for as a linebacker when they won Super Bowl XX.
Panthers owner Jerry Richardson said Rivera's experience as a former player helped him decide to hire him.
"He brings an approach and resume that we believe lends itself to success," Richardson said.
"There seemed to be a pretty quick bonding with us."
Rivera will work with GM Marty Hurney on a team that owns the first overall pick in April's NFL draft.
"He's a great coach to play for," Bears S Chris Harris told CarolinaGrowl.com. "I played under him for two years and I loved playing for him.
"He treats all his players like men while demanding respect without having to be an in-your-face kind of guy. I think he will do a great job there. I'm rooting for him and hope he can turn that program around."
-- Sean Leahy
Nate Davis is a reporter, blogger and editor who's been at USA TODAY since 2000. He has covered the NFL since 2005. No, he did not play quarterback for Ball State. Davis' succession of our esteemed colleague Sean Leahy at The Huddle is considered a Brady-for-Bledsoe swap by most "insiders."More about Nate


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-----Oorspronkelijk bericht-----
Van: Robin Parer <firstname.lastname@example.com>
Aan: firstname.lastname@example.com <email@example.com>
Datum: zaterdag 28 november 1998 18:41
Onderwerp: Re: Tuberous Rooted Geraniums
>The tuberous rooted geraniums, G. tuberosum, G. malviflorum, G.
>macrostylum, G. libani, and others, have not been grown in a wide
>enough variety of locales for us to say definitely what they will
>tolerate. ........ Common sense says they will not be hardy where the
>ground freezes, but is that actually true? I have no idea.
Hello Robin,
In the southern part of Holland, I grow G.malviflorum for more then eight
years. I always leave them in the ground. In summer they are dormant, the
first leaves appear in March en flowers sometimes in April.
When G.procurrens disappears from frost (-12 degrees C), G.malviflorum still
survives the winter, even when the ground is frozen. Even when they stay in
plastic pots of 15 cm, outdoors in winter, they still appear in
February/March. It gives me the idea that G.malviflorum is frost hardy.
Best wishes,