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Fashion & Beauty
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Bridal Party
Real Weddings
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71 results
29 Glam Metallic Wedding Cakes
From gold and silver to bronze detailing, even the most traditional brides will find themselves obsessing over these metallic wedding cakes!
June 25, 2014
Planning & Budget
Wedding Color Scheme: Burgundy and Gold
Deep red and gold embolden the classics. These rich tones will imbue your wedding with a regal air.
August 22, 2013
Bridesmaids & Groomsmen
A Sparkly, Gold Sequin Bridesmaid Dress by Kirribilla
It doesn't get much more fun than this shiny, bow-adorned shift.
July 24, 2013
Planning & Budget
Wedding Color Scheme: Emerald and Gold
A rich jewel tone and a chic neutral create instant glamour.
July 11, 2013
Bridesmaids & Groomsmen
A Gold Polka Dot Bridesmaid Dress by Shop Lovely
You can't get more party-ready than this darling polka dot dress.
June 11, 2013
A Geometric Clutch for the Minimalist Bride
A chic, geometric clutch for city girls at heart!
April 11, 2013
12 Ideas for a Mint Green and Gold Wedding Color Palette
Keep your wedding light, crisp, and ever-so-refreshing with this exciting color scheme.
April 10, 2013
A Green and Gold Art Deco Wedding Cake
An Art Deco-themed wedding cake is perfect for a modern, glamorous wedding.
March 26, 2013
Real Weddings
A Top-Secret Midnight Wedding in Central Park
For their two-part wedding, a New York couple exchanged secret midnight vows in Central Park followed by a traditional wedding reception at an Upper East Side club the next day.
March 24, 2013
Real Weddings
Francesca and Tyler in Philadelphia, Pennsylvania
"It hit me that I love everything gold, and that would fit perfectly with the elegant wedding I wanted," the bride said of their September affair.
March 21, 2013
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Real Weddings
A Traditional Ballroom Wedding in Philadelphia, Pennsylvania
One military couple recites their wedding vows at the second-oldest church in the country—followed by a sword tunnel recessional.
March 20, 2013
Planning & Budget
Rustic, Whimsical Wedding Ideas for a Purple Color Palette
Create a festive, rustic vibe with a gem-toned gown, a couture cake, and whimsical accessories.
March 12, 2013
Planning & Budget
Wedding Color Scheme: Mint with Gold
For a fresh feel, team cool green with a luxe metallic.
March 12, 2013
Planning & Budget
Style Details for an Elegant, Eclectic Wedding
Want to go eclectic and elegant? Mix motifs, like silhouettes and toile, but stick to a single water-washed color palette.
March 12, 2013
Real Weddings
A Romantic Summer Wedding in Southern California
Ashley and John hold a warm, intimate wedding celebration with a classic gold, peach, and white color palette.
January 1, 2013
Real Weddings
A Classic, Intimate Outdoor Wedding
One couple hosts a warm, intimate wedding celebration in Southern California with a gold, peach, and white color palette.
December 26, 2012
A Romantic Wedding Palette in Blush and Gold
Get inspired for a wedding in a soft, rosy glow with these blush and gold wedding color scheme ideas.
November 23, 2012
Planning & Budget
Romantic Wedding Color Scheme: Blush with Gold
Go romantic in pale pink ruffles and hints of gold
November 11, 2012
Color Scheme for a Fall Wedding: Pink and Soft Gold
Refresh a rusty fall palette with cheery pops of pink and mellow gold.
September 21, 2012
Wedding Dresses
A High-Fashion Gold Wedding Dress from Elie Saab
This gilded confection turns up the volume on Saab's already ornate sensibility.
August 1, 2012
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Smart Forms
From concept to design and implementation, you're always in control.
Create any form you need in minutes. No programming required.
- Simple drag and drop online form builder
- Multiple form field types
- Custom styles
- Build conditional logic
- Easy data integration
- Define user access and permissions
- Built-in e-signatures from Adobe Sign or DocuSign
Smart Flow
Create and manage workflows for any business situation. Begin with a template or start from scratch and quickly save time and money across your organization.
- Simple drag and drop interface
- Integrated with forms
- Easily build logic and rules
- Define permissions and security at any point in the workflow
- Create custom notifications and alerts
- Publish workflows to any location even, your own sites
- Track workflow process through all stages
- Integrated e-signatures at any stage along the workflow process
Smart Data
TAP's workflows seamlessly integrate data from across your organization.
- Create or upload data tables in Excel
- Manage relationships between data fields
- Manage data in forms and workflows to centralize transactions
- Integrate across internal and external systems
- Build conditional logic
Smart Analytics
Audit trails that live forever. With TAP, every transaction is tracked and managed.
- Transparency across any business process
- Custom dashboards with drill-down capability
- Real time data updates
- Reports delivered to your inbox
- Multiple chart types, reporting interfaces, and custom views
- Data export for offline reviews
Smart Signatures
Seamlessly create secure transactions using TAP's integration with Adobe Sign and DocuSign.
- Add eSignatures to any workflow stage
- Initiate eSign actions and view signature status
- Manage multiple signers
- Sign documents anywhere, anytime

subset: commoncrawl


text:
Jim Douglas wrote:
> My site uses tigris and I had made a lot of change so I thought the
> reason it was not working was because it was somethig I had done. So I
> just rebuilt a webapp, it works for pelt, not for tigris on the new one.
> It might be a bug?
> Jim
The output you supplied says pelt, and you didn't mention tigris.
Glancing at the stylesheets for tigris, at appears the skin does not
support meta tags in xdocs. You could modify
FORREST_HOME/main/webapp/skins/tigris/xslt/html/document2html.xsl and
FORREST_HOME/main/webapp/skins/tigris/xslt/html/site2xhtml.xsl in place,
but it's less of a maintenance issue to do this at the project level.
For that, copy FORREST_HOME/main/webapp/skins/common and
FORREST_HOME/main/webapp/skins/tigris to
PROJECT_HOME/src/documentation/skins (if you haven't changed
Have a look at pelt's version of the two stylesheets above. You should
be able to copy the relevant lines from pelt to get the same
functionality in tigris. I'll try this now.


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- Address: Spirou Loui, Athens 151 23, Greece
- Hours: Check official site for event times. Tour reservations are available only for groups of 15 or more people
- Admission: Adults: €3
Olympic Stadium
Greece is where the Olympic Games began in the 11th century BC, as a festival dedicated to the god Zeus. The first modern Olympics was held in Athens in 1896 in the Panathinaiko Stadium, a 4th century BC stadium which was restored for the games. When Athens won the right to hold the 2004 games, people wondered if the chaotic and polluted city could make it work; they did. The result was a rebuilding program which re-invigorated the city and its transport system.
The Olympic Stadium of 2004 was originally built in the early 1980s for the European Olympic Championships and was remodeled by famous architect Santiago Calatrava for 2004. It seats around 70,000 and is now home to the major Athens football clubs and concerts. The stadium is called Spiros Louis Stadium after the winner of the 1896 marathon.
Practical Info
Bus X14 from Syntagma Square takes about half an hour to reach the stadium. The closest train station is Irini on metro line 1.
Tours & Tickets
City Sightseeing Athens Hop-On Hop-Off Tour
Experience the essential things to do in Athens aboard this City Sightseeing hop-on hop-off bus tour. You'll see all the historical and modern sights of Athens ... Read more
Location: Athens, Greece
Duration: 1.5 hours
Ticket is valid for 24 hours plus one day free from time of first use
Athens Half-Day Sightseeing Tour
Combine the sights of modern Athens with sites of historical importance on a 3.5-hour morning or afternoon tour by luxury coach. With an expert guide on hand ... Read more
Location: Athens, Greece
Duration: Varies
3.5 - 5 hours
Athens City Highlights Segway Tour
See the sights of modern and ancient Athens on a 2-hour Segway tour, led by a local guide! On your self-balancing electric Segway, glide through the city ... Read more
Location: Athens, Greece
Duration: 2 hours (approx.)
Private Tour: Athens City Highlights Including the Acropolis of Athens
Explore Athens with a private guide on a 4-hour tour, and discover the UNESCO-listed Acropolis of Athens, Temple of Zeus, Panathenian Stadium and more! After ... Read more
Location: Athens, Greece
Duration: 4 hours (approx.)


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The Spoke Tee boasts a Factory Pilot graphic and woven label up front for an Oakley-approved athletic look. The sweat-wicking fabric blend of this lightweight t-shirt helps keep you dry and won't weigh you down.
Thank you for visiting Oakley Spoke Tee T-shirts on oakleysbikes.co.uk
We bring the products from many websites to one website for you to search, save and compare.


text:
Steps to reproduce problem:
1. Start SeaMonkey
2. From the Tools menu, select Switch Profile
3. Highlight the current profile, if it is not already selected
4. Click Manage Profiles, then click Delete Profile
Expected result: "Delete Profile" alert "... it is in use"
Actual results: Nothing happens.
Created attachment 441501 [details] [diff] [review]
Proposed patch
Neil anything holding up checkin?
Pushed changeset 058e1555a691 to comm-central.
Pushed changeset 78393f7ceacf to releases/comm-1.9.1


text:
Search Our Full 2000 Product Catalog!
This charismatic bangle distinguishes itself in hammered copper with brass Celtic trim.
Measues approx. 1.6 inch wide at its widest point.
Made by Grange Celtic Jewelry, Dublin, Ireland
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text:
Publisher's Description+
From K_SOSHO: UP!UP!DOWN! DOWN! LEFT! RIGHT! LEFT! RIGHT! B!A! Please input and overthrow the command for which it presses! Please strike a controller correctly quickly! Dominate ranking!! How to play only inputs the key of a controller according to the command with which the bottom flows through simplicity and a top and B flows through a top and the bottom with B! Sharpen kinetic vision, concentration, and instantaneous power well and aim at a high-speed-steel core!!
What's new in this version:
We changed program.
read more +


text:
Cutting fluid engineered for difficult machining applications
QualiChem has introduced Xtreme Cut 292 water-based metalworking fluid. It is designed for use with difficult alloys such as titanium, INCONEL® alloy, and stainless steel. Low drag-out rates help reduce coolant usage, and extended sump life helps reduce disposal costs.
The fluid eliminates foaming, staining, and residues. It is formulated with a low toxicity to improve safety for end users and the environment. According to the manufacturer, tests have shown that the fluid can replace straight oils for applications in which other water-dilutable products have failed.


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Poetry is whats begun to flow from me,
veiws and opinions expressed, pure,crystal clear
never second guessed,plain ,untainted,the true face of my feelings,
un painted,un moved,un changed
you can challange me with intellegence,shower me with hate
beat me with pipes, or threaten my life
but you cant stop me,im always gonna write.
let me use your mind as a canvas
with these words ill paint you a picture of madness
in this world people close their eyes to the lies and the sadness
they block out the screams and the violence
deaf dumb and blind is all they are,
driving by the needy in their brand new car
fumbling around in this world were meaningless
usless,wastes of skinn,but what if we step up?
mabey then our life would really begin.
© Copyright 2017 dudepiston. All rights reserved.
Status: Finished
Genre: Poetry
Poem / Poetry
Paste the link to picture in the entry below:
Paste the link to Youtube video in the following entry:
Cannot annotate a non-flat selection. Make sure your selection starts and ends within the same node.
An annotation cannot contain another annotation.
There was an error uploading your file.


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Date Nut Pie
|9 inch pie shell
|Boiling water
|1 Cup (16 tbs)
|Chopped dates
|16 Ounce (2 Packages, 8 Ounce Each)
|Dairy sour cream
|1 1⁄2 Cup (24 tbs)
|Packed brown sugar
|1 Cup (16 tbs)
|Coarsely chopped walnuts
|1 Cup (16 tbs)
|Grated orange peel
|1 Tablespoon
|Orange juice
|2 Tablespoon
|1⁄4 Teaspoon
|3⁄4 Teaspoon
Prepare pie shell.
Refrigerate until ready to fill.
Pour water over dates in a mediumbowl; let stand 10 minutes and drain.
In a large bowl with rotary beater, beat eggs until fluffy.
Blend in remaining ingredients, except dates.
The final step, stir in dates.
Pour into unbaked pie shell.
Bake at 375 degrees for 45-50 minutes or until filling is set in center when pie is gently shaken.
Recipe Summary
Rate It
Nutrition Rank
Nutrition Facts
Serving size
Calories 1195 Calories from Fat 478
% Daily Value*
Total Fat 54 g82.8%
Saturated Fat 17.6 g88.2%
Trans Fat 0 g
Cholesterol 150.6 mg50.2%
Sodium 484.9 mg20.2%
Total Carbohydrates 180 g59.9%
Dietary Fiber 12.5 g50%
Sugars 131.8 g
Protein 14 g27.8%
Vitamin A 13.2% Vitamin C 16.8%
Calcium 23.7% Iron 19.9%
*Based on a 2000 Calorie diet


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Abigail Washburn: China Meets Americana
Set List
- "A Fuller Wine"
- "Kangding Qingge/Old Timey Dance Party"
- "Great Big Wall in China"
Harnessing a passion for both old-time American folk music and ancient Chinese culture, Abigail Washburn & The Sparrow Quartet achieves an unlikely sound that absolutely works. The group's innovative first album flawlessly combines banjo and violin-driven melodies with Chinese lyrics and rhythms. Washburn and her band visit World Cafe host David Dye to share music from their self-titled debut.
This segment originally aired July 10, 2008.
Related NPR Stories
Abigail Washburn: Have Banjo, Will Travel Dec. 13, 2005
Abigail Washburn: Chinese Lyrics, American Roots Sept. 12, 2005


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Bruegger's Suddenly Closes Madison Avenue Location
It's been around since the 80's and is the only walkable Bruegger's location in the Albany area and it has closed its doors for good.
It's been around since the 80's and is the only walkable Bruegger's location in the Albany area and it has closed its doors for good.
RadioShack supposedly is in deep doo doo. An update to a past blog (because I care).
I never realized this, but according to the Times Union, there are a boatload of restaurants shutting their doors around these parts -
You thought you had financial problems after all your Christmas shopping, wait until you hear how bad it is for Eddie Montgomery.
There's been a lot of media coverage about Revel and their upcoming pre-packaged Chapter 11 Bankruptcy filing. Most of the coverage has been hyper negative.
Financial issues have forced the owners of Redwood Lanes in Colonie, to file for Chapter Seven bankruptcy this week.
Gary Busey was the bad guy on the original "Lethal Weapon" movie with Mel Gibson and Danny Glover. He also played rock legend Buddy Holly in "The Buddy Holly Story."
Friendly's has closed five more Albany area restaurants.
These guys are partying. I think they heard the news that their sponsor Dish Network just bought Blockbuster in a fire sale after Blockbuster entered bankruptcy protection. What does it mean?


text:
Location: Somewhere, Anywhere, United States
Member Since: December 2011
Open for read requests: Yes
Book / Action and Adventure
Book / Action and Adventure
Short Story / Humor
Well, time to write something reletivly awesome, I guess.
Name: Eh.... I'll just go as Sky. (Soon To Be Changed)
Age: Between 0-1000. Take Your Pick.
DOB: I'd rather not say.
Favorite Color(s): Green, Blue, White, Black
Pastime: Whatever App's on my iTouch, I guess. Oh and writing.
Favorite Song(s):
Yeah, basically anything. Except country and Justin Bieber. Sorry Country and Justin Bieber Lovers.
Favorite Other Stuff:
And that's all folks.
This is where you can leave a short message for the writer. All Quickees are public. To leave a private message, use the private.
If you want to write a quickee (a remark or a hint for example) on this writer's profile, please sign in.


text:
We're sorry, this listing is off the market. Try these listings instead:
Bar - Cheers Branded - Dancing, Drinking and Fun #452859 posted Aug 31, 2016
- Florida, United States
- $75,000
For seven years, this bar went by the name of OZONE....seller re-branded it to CHEERS - 4000 sq ft - dance floor, DJ booth, large bar, pool tables, electronic darts and video games. Small kitchen for bar food. 4COP liquor license has to be purchased outside of the deal for $25,000 down and assume...
Successful 8 Year Old Sports Bar #391467 posted Oct 7, 2015
- Florida, United States
- Less than $100,000
Located in busy shopping center. Featuring full menu and large bar area and out door seating. 4500 sq ft in strip center. Has great customer following.
Sports Bar #461688 posted Jan 25, 2017
- Florida, United States
- $650,000
Grossly undervalued lease for this very high visibility location with lots of parking. 4COPSRX License. Absentee owners now understand that it needs hands on owner to run correctly. Build-out over $500,000, place looks great. Previous businesses with same type of venue have done well over $2M in gross...
Did you know that social networking is a great way to buy a business? Sign up now and we'll show you how.
Suggested Searches
Disclaimer: DealStream has not independently verified any of the information in this listing and makes no warranty as to its accuracy or completeness.


text:
India's workhorse launcher Polar Satellite Launch Vehicle (PSLV), one of the most reliable launch vehicles, has 38 consecutively successful flights so far. It has been in service for more than two decades and has launched various satellites including historic missions like Chandrayaan-1, Mars Orbiter Mission, Space Capsule Recovery Experiment and Indian Regional Navigation Satellite System (NavIC). With its three configurations, PSLV has proved its multi-payload, multi-mission, multi-orbit capability in a single launch and its geosynchronous launch capability.
Comprehensive timeline of ISRO's journey through decades.
- 1 of 183
- next ›


text:
Fate of California Teacher-Protection Rules Now in Hands of Judge
Lawyers presented their closing arguments in the fractious Vergara v. California teacher-protection lawsuit.
Lawyers presented their closing arguments in the fractious Vergara v. California teacher-protection lawsuit.
State chiefs have some tough questions for the teachers' unions and their recent shifts in position on the common core.
AFT will no longer take money from the Bill & Melinda Gates Foundation for its Innovation Fund, the union says.
Chris Cerf, departing from the role of New Jersey chief, criticizes the state union's 'misinformation' on teacher evaluation.
A national survey of some 20,000 teachers finds generally positive opinions about the common core.
Newark's Cami Anderson wants the Christie administration to waive the state's reverse-seniority layoff requirements.
Florida becomes the latest state to bow to a court's request that teacher value-added data be released to news outlets.
Like Portland, Ore., earlier this week, St. Paul, Minn. has reached a tentative deal with its teachers' union.
The NEA slams common-core implementation and makes recommendations for improving it.
Portland, Ore., appears to have averted a teachers' strike.


text:
Home > Yaoi > Yaoi Illustration Books > Natsuki Kojima Art Book - Lover's Paradise (Yaoi)
More Reviews
Current Promotion:
All Tezuka titles are up to 60% Off!
FREE SHIPPING over $60
(only within United States, excludes Alaska and Hawaii)
* Items that are discounted 70% off or more do not count toward your free shipping total.
Follow us and get more exclusive information!


text:
John Madill
Dan Smith of St. Joseph, Mich, has been decorating his yard for twenty-one years, including a haunted house in his garage visitors can tour. So he is not afraid of ghosts, even this one waving in the wind Saturday, Oct. 29, 2011. (AP Photo/The Herald-Palladium, John Madill)
Unlike those traditions that dismiss Halloween as a pagan custom, my local parish of St. Luke's celebrated a lively Halloween parade. Why, it might be asked, do so many Catholics in America welcome witches, zombies, monsters, ghosts and the like when this day before All Saints' Day clearly has pagan roots? The answer: we welcome witches, zombies, monsters and ghosts because they have a place in our Catholic theology.
It is a well documented fact that All Hallow's Eve is linked to Samhain, the Celtic religion's ancient New Year. Catholic missionaries long ago adopted a policy of co-optation of previous religious beliefs in spreading the Gospel. Some call this "syncretism," and Protestants early on considered such syncretism to have diluted the faith, resulting in a third religion that was neither authentic "paganism" nor authentic "Christianity." But we should not ignore how the Gospels cite the existence of Satan and possession by evil spirits. In other words, witches, zombies, monsters and ghosts are embedded in Christian belief. And, as demonstrated in the appropriation of Aztec belief in the "Day of the Dead" by Latin American Catholicism, we consider the dead to be "family." In the Patristic age, Origen (c. 185-232) wrote (erroneously) that Christ would save even the damned.
This is where the paranormal enters into Catholic America. There are observable phenomena like voices and self-moving objects that violate normal rules of physics. We Catholics believe that the causes of certain paranormal events are spirits: if they are the saints, we call them "miracles:" when we are unsure they can be ascribed to "restless spirits" to diabolical forces attacking people of virtue.
Before attaching the labels of "superstitious" and "gullible" to this aspect of Catholic belief, recall that the Church has been rigorous in applying science to the detection of the paranormal, precisely to avoid confusing the phony and fake with faithful and factual. At Lourdes, for instance, scientific rigor has been applied to the examination of claims for spiritual intromission with careful record keeping. Every person seeking a cure is examined by doctors and past medical records are requested. While most people exit from a washing in the shrine's water with little more than psychological calm about accepting their sufferings, there have been some 67 cases categorized as "unexplainable by science." These include phenomena like the sudden dissipation of tumors, the disappearance of cancerous cells, the regeneration of damaged organs of sight and hearing.
Attempting to discredit the role of faith, some claim that these effects are natural occurrences. Tumors sometimes dissipate outside of any religious setting, thus proving it is "only" a natural phenomenon. What such an opinion does not explain satisfactorily is why such phenomena take place so often after a religious act.
When it comes to things like levitation – that is, a person floating several feet in the air without support – rationalists simply deny such things are possible. This rationalist denial is old hat for Catholicism: Remember that the Lutheran Duke John Fredrick of Brunswick converted to Catholicism after seeing St. Joseph Cupertino, the Franciscan friar float in the air, something the saint did on more than 50 recorded events before assembled witnesses. You also don't have to be Catholic to levitate.
We need to consider the stigmata, i.e., the wounds of Christ appearing on a person's hands, feet and side in imitation of the Crucified Jesus as "paranormal." Padre Pio, the Italian priest, was probably the most recent and best documented case.
Often rationalists denying any spiritual order to human existence or the existence of God come up with fantastic explanations that do little more than claim "what happened didn't happen." Actually, it is more logical to acknowledge the realm of the spirit in explaining these observed events than it is to stretch the imagination with such near-paranoid claims.
I know that the kid dressed like a ghost asking for candy at my door is not espousing this theology of the paranormal; still I still like celebrating our tradition that even the wild and weird in the afterlife remembered at Halloween fit into the Catholic cosmos.


text: Just been issued the new haversack for the GSR, so thought I'd let you know what your in for. Please note I have only been issued the Haversack and not the actual GSR yet. At first notice this new haversack is a lot bigger than the one for the S10 (but then the GSR is a bigger respirator. As well as the main pouch there as 2 side pouch's that are attached with Molle straps (what reason these would be removed for I don't know) and both have 3 pockets for where your combo pens would go. They also have longer strips of Velcro than what is necessary to close the flap shut. Inside the main pouch on the back there are 6 poppers and an elastic strap- these are to hold the GSR's holder (issued with the mask) in place- from what the Ships Q told us it took him about 5 minuets to attach this holder in place and from sight it took up quite a lot of actual space in the bag. There are also 2 pockets inside for the stowage of canisters. The front of the pouch is fastened with a Velcro and 2 poppers are fitted on the lid flap and 3 on the main body. Under the flap in the main body is 2 zips that allow the pouch to be expanded allowing the mask to be fitted inside before zipping up to allow for a snug fit meaning that the mask won't rock about inside. As visible from the photos the bag can be carried with the shoulder strap (which can be unclipped completely) or could be attached to webbing, there is what also appears to be a leg strap at the bottom of the bag also- possibly to reduce the bag from lunching off the thigh when running. As stated this is the Army's version, apparently the Navy are to be issued a bigger haversack than this due to us carrying more kit in our haversacks. Any questions please ask and I'll be happy to answer them.


text:
Call (888) 651-9785
Make sure to meet Rex, an impressive 16.5-foot (5-meter) saltwalter crocodile, who lives in a habitat that recreates the Kakadu Gorge of the Northern Territory. Weighing more than a small car, Rex is one of the world's largest crocodiles.Expect to take at least 1.5 hours at WILD LIFE Sydney in order to fully discover its nine different habitats, which are home to approximately 6,000 native Australian animals.
Attractions Pass upgrade:
Enjoy savings off the single-entry admission price by combining your WILD LIFE Sydney admission with an Attractions Pass that includes your choice of two, three or four attractions. Your pass is good for one month from date of first use. Visit as many attractions as you wish in one day, you have one month to complete use of the pass, which is valid for the following attractions: SEA LIFE Sydney Aquarium, Manly SEA LIFE Sanctuary and Sydney Tower Eye.
December 2014
Visiting Wild Life Sydney gives one the opportunity to see several animals native to Australia up close and in person in a short period of time. You can be in a "walkabout" area with kangaroos and wallabies and also stand a few feet away from koalas. There are a number informative talks during the day as well. Be sure to buy your tickets online in order to save significantly on the entrance fee.
August 2014
It was great with small kids
February 2014
really enjoyed
January 2014
Enjoyed it!
February 2013
Great place to see for such a short stay in Sydney
November 2012
Turned out to be school holidays while I was there! Skip the Line made my day quick and easy... Perfect for when you've just landed. And then of course, I also saved money! :0)
October 2010
August 2008
June 2016
It was nice to see all the endemic wildlife of australia.
October 2015
A good place for the family to go. The kids will enjoy the different species of animals in this zoo.
There are many Australian species to look at and the koalas and kangaroos are the highlights here.
Recommend you get a multiple attraction pass to save money if you want to explore other attractions.
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text:
Only Show: Kayaking & Canoeing | Other Water Sports | Parasailing & Paragliding | Scuba Diving | Snorkeling | Swim with Dolphins | White Water Rafting & Float Trips
Page: 1
Snorkel, Kayak and Dolphin Experience in the Big Island's Kealakekua Bay
Surround yourself with beautiful scenery, dolphins and the occasional humpback whale as you paddle a kayak in picturesque Kealakekua Bay! This narrated Big ... Read more
Location: Honalo, Hawaii
Duration: Varies
Ocean Kayak Tours
The Kona Dolphin Watch Kayak and Sea Cave Tour is a small-group kayaking tour along the Hawaiian coastal spinner dolphin course. The tour takes place in the ... Read more
Location: Kailua-Kona, Hawaii
Duration: 4 hours
Big Island Keauhou Bay Kayaking and Optional Snorkeling Cave Tour
Enjoy an exciting day of kayaking below Hawaii's soaring cliffs and around its sea caves! Experience the picturesque beauty of the Big Island on this ... Read more
Location: Kona, Hawaii
Duration: 3 hours 30 minutes
Guided Outrigger Canoe Tour in Kealakekua Bay
Try your kayak tour, Hawaiian style, with our traditional one-of-a-kind outrigger canoes. We offer Outrigger Canoe Tours to the famous Captain Cook Monument in ... Read more
Location: Kealakekua, Hawaii
Duration: 2 hours 30 minutes
Big Island Manta Ray Night Kayak and Snorkel Adventure
Experience the thrill of seeing manta rays up close! Kayak and snorkel through the Big Island's pristine waters to see Hawaii's playful manta rays at night. ... Read more
Location: Kona, Hawaii
Duration: 90 minutes
Hawaiian Outrigger Canoe and Snorkel Adventure
Experience the Big Island from the sea on an outrigger canoe and snorkeling adventure. Set out aboard a traditional float-supported canoe similar to the Wa'a ... Read more
Location: Kailua-Kona, Hawaii
Duration: 2 hours
Hawaiian Outrigger Canoe Night Snorkel for Manta Rays
Skip the big crowds on this manta ray–viewing excursion at night, a Hawaiian experience you shouldn't miss while on the Kona Coast. You'll take an outrigger ... Read more
Location: Kahaluu-Keauhou, Hawaii
Duration: 2 hours
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Welcome to Poppy Franchising
It takes a particular kind of person to operate a modern funeral care business. It goes without saying that you need to have exceptional interpersonal skills to deal with vulnerable people at a time of grief and stress.
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The nature of our business means that our customers place a great deal of trust in us to provide the final farewell befitting the dearly departed. With that trust goes a high degree of responsibility.
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Want an effortless way to maintain your look away from the comforts of home? The Japonesque Professional Touch Up Tube Set bundles five brushes essential for keeping makeup flawless throughout hectic days and nonstop nights. This travel-ready tool kit includes a foundation brush, a lip brush, two eye detailers and a blush/powder brush. All feature short handles for convenience and superior control. Sleek silver container is a perfect petite fit for bag, desk drawer or glove compartment.
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Aung San Suu Kyi, Burma's "woman of destiny" and one of the most admired voices for freedom in the world today, comes alive through this brilliant rendering of Burma's tumultuous history.
Award-winning journalist and former State Department speechwriter Rena Pederson brings to light fresh details about the charismatic Nobel Peace Prize winner Aung San Suu Kyi: the inspiration for Burma's (now Myanmar) first steps towards democracy. Suu Kyi's party will be a major contender in the 2015 elections, a revolutionary breakthrough after years of military dictatorship. Using exclusive interviews with Suu Kyi since her release from 15 years of house arrest, as well as recently disclosed diplomatic cables, Pederson uncovers new facets to Suu Kyi's extraordinary story.
The Burma Spring also reveals the extraordinary steps taken by First Lady Laura Bush to help Suu Kyi, as well as how former Secretary of State Hillary Clinton injected new momentum into Burma's democratic rebirth. Pederson provides a never-before-seen view of the harrowing hardships the people of Burma have endured and the fiery political atmosphere in which Suu Kyi has fought a life-and-death struggle for liberty in this fascinating part of the world.
©2015 Rena Pederson. Foreword © 2015 by Laura Bush (P)2015 Blackstone Audio, Inc.
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"Interesting modern history of Burma"
This book discusses the modern history of Burma - from the British occupation, the deal made with the Japanese in WWII, Aung San's father's rise to power, his death and how Aung San became the voice of the Burmese people. The good stuff is in the middle when it discusses the history. The beginning of the book makes Aung San into a saint and sounds like pure propaganda. She didn't have any inner conflict about this role? The book basically makes it sound like her shit doesn't stink. I didn't like the person reading the book. She spoke in a robotic staccato voice, with a fake soft British accent for Aung San. I put the book on 1.5 speed just to get the reader to move more quickly.
I learned a lot from this book and it is especially relevant to current times.
"inspirational and fairly informative"
This book focuses on the inspirational life of Aung San Suu Kyi and the often tragic circumstances of the Burmese people.
It is high on human interest, a bit less on information, and there are some very graphic descriptions of torture, rape, and murder. It captures the brutality of Burma.
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With aging, it appears the heart's ability to withstand injury declines markedly. Unfortunately, the incidence of ischemic disorders increases dramatically with age. Though the genesis of the ischemia-intolerant phenotype is incompletely understood (and likely multi-factorial), it may involve changes in intrinsic cardioprotective responses. In this respect we and others have interrogated the role of the adenosine receptor (AR) system in dictating ischemic tolerance and the impact of age on AR-mediated cardioprotection. It is intriguing to note ARs impact on many processes implicated in myocardial 'aging': adenosine counters Ca2+ influx and oxidant injury, modifies substrate metabolism to improve tolerance, is pro-angiogenic, inhibits myocardial fibrosis, and can limit apoptosis. Thus, dysregulation of the AR system could contribute to many features of aged hearts (including ischemic intolerance). The latter is borne out by observations that AR-mediated protective responses decline with intrinsic tolerance and that transgenic manipulation of the AR system restores intrinsic tolerance and protective responses in aged hearts. Mechanisms underlying failure in adenosinergic protection remain undefined. Here we review data on the effects of aging on cardiovascular AR transcription and expression, generation of signal (adenosine formation), and protective signaling coupled to ARs.
1. Introduction
Despite a decline in mortality rates over the last decade, ischemic heart disease remains a leading cause of death and disability in developed countries, and is the single greatest cause of death in individuals over 65 years of age. Coronary artery disease affects 50% of those older than 65, contributing to an increased incidence of angina, myocardial infarction, arrhythmia, congestive heart failure, and sudden death. The age of hearts employed in cardiac transplant is also increasing in an attempt to expand the donor pool [1], and surgical ischemia-reperfusion in the older population is increasing with expanded use of thrombolysis, recanalization, and revascularization. Unfortunately, advanced age (≥ 70 years) is a significant risk factor for operative mortality during cardiac surgery in coronary artery bypass, and age is an adverse prognostic factor in morbidity and mortality following a myocardial infarction. Estimates in the USA indicate up to 80% of deaths from coronary artery disease occur in those over the age of 65 [2]. The problem is growing–it is anticipated the elderly population may nearly double (to 25%) within 25–30 years. Morbidity and mortality attributed to cardiovascular disease will thus increase dramatically. It is thus something of a paradox that most research into the pathophysiology and therapy of cardiovascular disease has been undertaken in young adult tissue/models. The initial exciting potential of such potent stimuli as preconditioning must now be tempered by emerging evidence of limited utility in the "at-risk" aged population [3–5]. Aged myocardium likely requires specific management strategies [4], not evident from studies in young tissue.
Aging-related ischemic intolerance has been documented in multiple species including humans [3–16]. Genesis of the intolerant phenotype is not understood, though is likely multi-factorial (a "single" molecular basis of intolerance seems improbable). Amongst other things, cytosolic Ca2+ handling may be impaired [7,9,17,18], energy and substrate metabolism altered [12], oxidant injury exaggerated [11,19,20], gene expression modified [11,17–20], membrane structure and function altered [21,22], mitochondrial function impaired [8,22–24], apoptosis potentially enhanced [25,26], capillary/arteriolar density reduced and myocardial fibrosis and hypertrophy enhanced [27]. These factors may all contribute to intolerance, and have attracted attention. One possibility, less extensively investigated, is that endogenous or intrinsic "cardioprotective" processes, such as the AR system, may be impaired.
2. Age-related failure of intrinsic cardioprotection–the adenosine receptor system
The heart possesses a range of retaliatory mechanisms designed to provide resistance to injurious stimuli. Of these, considerable evidence points to an important role for the adenosine receptor (AR) system [28–32]. The ARs were attributed with regulatory functions in the heart and vessels three-quarters of a century ago [33]. More recent data indicate that adenosine is an endogenous determinant of myocardial ischemic tolerance [34–40]. Adenosine acts through 4 G-protein coupled receptor (GPCR) subtypes–the A1, A2A, A2B and A3ARs [30,32]–each encoded by a distinct adenosine receptor gene (Ador). Adenosine also enhances tolerance to ischemia via metabolic substrate effects [32,40,41]. Adenosinergic cardioprotection in ischemic-reperfused hearts involves reductions in oncotic [41–45] and apoptotic death [46], and improved functional outcomes [28–32,37,43]. Whether ARs specifically protect against reversible injury is difficult to ascertain, although AR agonism enhances post-ischemic contractility in models with minimal irreversible injury [37,43,47–49]. Recent work supports differential effects of acute adenosine [41,50] vs. transient adenosinergic preconditioning [51], consistent with multiple pathways of protection. In terms of cellular targets, adenosine appears to directly protect cardiomyocytes or myocardial tissue (likely via A1 and A3ARs) [32,49,52], and additionally protects via limiting inflammation and injurious interactions between inflammatory cells and vascular and myocardial tissue [30,32,34,38,42,53]. Though anti-inflammatory and "extra-cardiac" responses are important in adenosinergic protection [30,53], and as noted below may be altered with aging, further detailed description of these processes is unfortunately beyond the scope of the current review.
The different cardioprotective effects of AR agonism have been verified in animal [28–32,53] and human tissue [52,54,55]. However, few studies have addressed the possibility that altered AR-mediated protection might underlie specific cardiovascular disorders, though there is evidence to support this. Hypertrophic hearts, for example, display abnormal adenosinergic signaling [56,57], and dysregulated adenosine formation [58]. In the context of aging, we and others have acquired data demonstrating significant age-related changes in AR signaling [59–63], and more recently failure in AR-mediated protection against cell death and contractile dysfunction [16,64,65]. Interestingly, ARs impact on many processes implicated in cardiovascular "aging", regulating Ca2+ influx and oxidant injury [29,30,32,49], substrate metabolism [37], angiogenesis [67], myocardial fibrosis [68], and apoptotic processes [46]. Given evidence of a role for ARs in intrinsic cardioprotection [34–40], mediation of preconditioning [69,70], and modifying the above-mentioned processes, alterations in AR signalling could contribute both to ischemic intolerance and emergence of other features of aged myocardium. Data reveals failure in AR protection parallels the decline in intrinsic resistance to ischemia in aging mice (Fig. 1).
Several studies support impaired adenosine responses in aged heart [59–62,64,71–73], though findings regarding AR expression/signaling vary [16,60,71]. Our recent data verifies failure in adenosinergic protection with even moderate aging in mouse [16], consistent with findings of Gao et al. [64] and Schulman et al. [65] in aged rat hearts. Age limits effects of ARs on both contractile outcome and oncotic death during ischemia-reperfusion [16,64,65], and reduces protection via both pre-ischemic AR agonism [65] and adenosine treatment throughout ischemia-reperfusion [16,64]. The molecular basis for the global failure in adenosinergic cardioprotection remains undefined. However, evidence points to failed activation of signaling distal to mitochondrial ATP-sensitive K+ (mito KATP) channels [16]. Failure in AR-mediated cardioprotection may occur at the level of ARs themselves (expression and coupling), generation of protective "signal" (adenosine formation), and/or at sites within signaling cascades triggered by ARs. Potential sites are depicted diagrammatically in Fig. 2.
3. Intrinsic cardioprotection via adenosine receptors: effects of aging
Endogenous adenosine may protect via one or all of the four characterized AR sub-types–A1, A2A, A2B, and A3ARs [28–32]. All are considered to be expressed within cardiovascular cells. Studies in different species verify endogenous adenosine contributes to intrinsic ischemic tolerance [34–40], and support cardioprotective roles for A1ARs in vitro and in vivo [35,37,39], and for A2ARs in vivo [34]. Anti-ischemic effects of A1ARs appear direct (at cardiomyocytes), since similar protection is observed in isolated hearts, cardiomyocytes, and in vivo [28,32,35,37,49,52,54]. Protective A2AR effects involve modulation of vascular function, platelet adhesion and neutrophil activation [34,35,42,53,74], and are absent in cardiomyocytes [75] and in vitro models lacking blood [37,45,76]. Nonetheless, cardiomyocyte Adora2a mRNA expression [77], and functional A2AAR responses in cardiomyocytes [77–79] implicate a functional myocardial A2AAR (of obscure function). There is currently no direct evidence for acute A2BAR mediated cardioprotection, partially due to lack of selective A2BAR agonists/antagonists.
In contrast to A1 and A2ARs, there is little evidence that intrinsically activated A3ARs mediate protection–A3AR antagonists have no effect on ischemic outcomes in myocytes [80] or hearts [81]. A3AR overexpression enhances tolerance [82], implying an intrinsic function in cardioprotection. However, markedly elevated A3AR expression will exaggerate sensitivity to endogenous adenosine and thus the role of the receptor in wild-types. As shown by Hill et al. [83], the A3AR is over an order of magnitude less sensitive to adenosine than A1ARs. Thus, A1ARs will be intrinsically activated to a greater extent than A3ARs during ischemia.
Given a demonstrable role of A1AR and A2ARs in determining ischemic tolerance, changes in expression/functionality could contribute to evolution of ischemic intolerance. In preliminary transcriptional analysis of moderately aged (16–18 month) mice under ischemic and normoxic conditions [84], we detect down-regulation of genes encoding heat-shock and stress-inducible proteins, contractile proteins, transcription factors and signal transducers. Similar age associated changes have been observed in cardiomyocytes [85]. Many genes identified have putative roles in ischemic tolerance, and in AR-mediated protection. Indeed, in a recent micro-array study, 15–20% of aging-related transcriptional changes were involved in GPCR signaling [73], and included changes in Adora1 mRNA.
In terms of A1ARs, work in mouse hearts verifies no change in normoxic expression [16], in agreement with earlier findings of Cai et al. [60] for rat, and consistent with a lack of effect of aging on Adora1 mRNA levels in mice [16,87]. The latter study [87] also detected ischemic repression of Adora1 in aged (but not young) hearts. If translated into repressed A1AR expression, this may contribute to poor outcome at later time points in aged vs. young tissue. Despite no change in baseline A1AR expression in rat [60] and mouse [16], age-related changes in Adora1 mRNA are observed, though findings vary. Arosio et al. [88] and Dobson et al. [73] observed elevations in Adora1 whereas Jenner et al. [89] reported a 5-fold reduction in Adora1 with age. Irrespective of effects of age on mRNA, it appears that changes do not translate into altered A1AR expression [16,60].
While there is little evidence for alterations in cardiac A1AR density, the study of Cai et al. [60] revealed reduced coupling between A1ARs and G-proteins, leading to reduced A1AR responsiveness. Other work confirms the importance of changes in receptor–effector coupling, rather than A1AR expression, in dictating cardiac AR sensitivity [90]. Consistent with impaired A1AR activation of downstream effectors, we show A1AR overexpression overcomes age-related failure in adenosinergic protection and restores ischemic tolerance to levels in young tissue [16].
Despite no direct studies of aging-related changes in A2A or A2BAR expression, it is interesting to focus on these sub-types for a moment, as there is unequivocal data indicating aging limits cardiovascular A2AR sensitivity [59,63]. If such changes extend to A2ARs implicated in reducing infarct size and post-ischemic inflammatory responses in vivo [34,35,53,74], this form of cardioprotection may also decline with age. There is indirect evidence age impairs A2AR expression, since A2AAR transcription is significantly reduced in rat myocardium [88,89]. On the other hand, A2BAR transcription appears induced in rat [88] and mouse [87]. There are also no direct studies of effects of aging on cardiovascular expression of A3ARs, though recent work indicates Adora3 mRNA is repressed with age in murine myocardium [87]. It would be of interest to examine effects of age on ischemic tolerance in models of cardiac A3AR overexpression [82].
At a post-translational level, impaired GPCR responsiveness in senescent cells (of non-cardiac origin) has been attributed to up-regulation of caveolin expression [91], and manipulation of caveolin expression restores cellular responsiveness to GPCR stimuli [91,92]. Lasley et al. have observed translocation of A1ARs from caveolae upon agonist stimulation [93], a form of compartmentalization that may explain lack of direct effects of A1AR agonism under certain conditions. Given these latter findings [93], and effects of age on caveolins [91], it is possible that age-related reductions in AR-mediated protection against ischemic injury [16,64,65] may be related to altered caveolin expression and receptor interactions.
4. Generation of the protective "trigger"–adenosine formation
Ischemic intolerance could result from impaired endogenous activation of ARs. During ischemia/hypoxia, [adenosine] increases by an order of magnitude or more [32,39,69,94,95], triggering AR responses including cardioprotection. Myocardial adenosine formation occurs primarily via intra- and extracellular dephosphorylation of 5′-AMP via 5′-nucleotidases [32]. Adenosine is derived from cardiomyocytes, endothelial cells, and fibroblasts. However, endothelial-derived adenosine accounts for only 15–25% of basal release [96,97], and even less during ischemia/hypoxia [98]. Though problematic to measure relevant interstitial concentrations, a variety of methods (including microdialysis) suggest these are sufficient to activate cardiovascular receptors [39,69,94,95,99]. This is validated by actions of AR antagonists [34–36,39,69].
Few studies have assessed effects of aging and senescence on interstitial adenosine levels and handling. Early work by Ramani et al. [100] provided preliminary support that reduced adenosine contributes to ischemic intolerance. However, they assessed total tissue adenosine, which substantially overestimates physiologically relevant "free" levels due to existence of tissue adenosine in bound forms (e.g. with s-adenosylhomocysteine; coupled to contractile proteins). Other studies verify age-related impairment of maintenance of adenine nucleotides in ischemic hearts [12], which enhances 5′-AMP and is predicted to increase adenosine accumulation. This is indeed what is observed in aged rat hearts during normoxia, ischemia, and adrenergic agonism [59,72]. Elevated extracellular adenosine in aged rat hearts does not appear to stem from altered 5′-nucleotidase or adenosine kinase activities [72]. However, since these activities were assessed in tissue homogenates it remains feasible that in vivo activities may differ as a result of alterations in the intracellular milieu. The enzymes are subject to control by Mg2+, H+ and inorganic phosphate (Pi), and data supports enhanced ischemic acidosis and Pi accumulation, and impaired recovery of Pi and Mg2+ in aged hearts [12]. Importantly, elevations in adenosine in aged rat hearts cannot explain profound reductions in ischaemic tolerance in this species. However, in contrast to rat tissues, recent work documents comparable normoxic adenosine in young and aged mouse hearts, and a decline in post-ischemic adenosine with aging [101]. Thus, changes in endogenous agonism may contribute to impaired ischemic tolerance in mice.
Changes in extracellular adenosine with age in some species hint at another potential explanation for ischemic intolerance with age. Bolling et al. [102] first presented the notion of adenosine protecting the heart as "substrate" (for nucleotide pool repletion) vs. "signal" (via AR activity). Manipulation of nucleotide repletion and adenosine handling enhances ischemic tolerance in mature hearts [40,41,48,102], and protection with adenosine is reduced by adenosine kinase inhibition, confirming a role for phosphorylation [41]. In preliminary studies we have shown that treatment with adenosine deaminase or kinase inhibitors fails to modify ischemic tolerance in aged hearts [103]. Thus, the "substrate" role of adenosine may be modified with aging. Recent work demonstrates specific shifts in purine catabolism in aged hearts, which may predispose to ischemic intolerance [101]. Accumulation of salvageable adenosine is reduced while accumulation of poorly salvaged hypoxanthine and xanthine is enhanced. These changes may limit myocardial capacity to replete adenine nucleotides post-ischemia.
5. Cardioprotective signaling coupled to AR agonism
In addition to changes in AR expression, age may impair the signaling cascades coupled to ARs. It is interesting that other protective stimuli (e.g. ischemic preconditioning) may retain their ability to activate downstream protective proteins in aged myocardium, despite substantially impaired outcome [104]. Effects of A1AR overexpression indicate that protective signaling can be harnessed in aged tissue if AR expression is sufficiently enhanced [16], verifying existence of exploitable protective processes. Before considering repression of AR-triggered signaling, it is worth noting that not all studies document repressed AR signaling with age, and that different signaling coupled to the same AR sub-type may be differentially altered. For example, while A1AR-mediated cardioprotection is absent [16,64,65], A1AR-mediated bradycardia and anti-adrenergic effects may be enhanced with aging [30,62,73]. Preservation (or amplification) of contractile or electrophysiological responses to A1ARs, coupled with failure of A1AR mediated cardioprotection [16,64,65], clearly demonstrates different signaling paths are selectively modulated during aging.
Numerous investigations document impaired function of GPCRs with age, and these generalized effects have been reviewed [91]. There is also evidence of impaired cardioprotection via other GPCRs [66]. A recent study by Dobson et al. [73] found that 15–20% of transcriptional changes in aged myocardium relate to GPCR signaling, lending weight to the notion of generally impaired GPCR signaling. With respect to AR-mediated cardioprotection, signaling appears to involve G-protein mediated activation of phospholipases, PKC, mitochondrial (and possibly sarcolemmal) KATP channels, and potentially MAPK and PI3-kinase pathways [29–32]. Our own prior data, demonstrating conservation of protective responses to direct mito KATP channel activation, indicate the lesion in adenosinergic protection lies proximal to these channels [16]. However, given the possibility that mito KATP channels may present both a signaling intermediate and potential end-effector, since there remain discrepancies in effects of PKC inhibition placing the kinase distal and proximal to mito KATP channels [41,44,51,105,106], and since there is evidence that aging may impair protection via mito KATP activation [65], it is worth considering effects of aging at all levels of signaling. It is also worth mentioning that "parallel" paths may contribute to AR-mediated protection [107,108], providing signaling redundancy. This, of course, raises the question of how aging abrogates AR-mediated protection [16,64,65], and favors a sufficiently distal lesion to impact on multiple convergent paths (e.g. MAPK, PKC, PI3-kinase), and/or a lesion in the initial steps in AR signaling (e.g. G-protein function and phospholipase activity).
5.1. Phospholipase activation
The A1 and A3ARs couple to pertussis-sensitive Gi and Go family proteins. Liang et al. demonstrate (in chick myocytes) that A1AR and A3AR mediated protection involves Gi-dependent activation of PLC activity (a short-lived response) and RhoA-dependent activation of phospholipase D (PLD; a more long-lived response), respectively [109]. The A2A and A2BARs activate adenylyl cyclase via Gs protein, and A2BARs also trigger PLC activity via Gq protein [110]. Though not specifically addressed in cardiomyocytes, there is evidence that aging and/or cellular senescence impair PLC and IP3 activation [111,112], together with PLD activation [112,113]. Impaired activity of PLC and particularly PLD may not only involve altered upstream activation but also reduced expression [112]. No study has directly addressed the relevance of reduced phospholipase signaling to changes in anti-ischemic actions of adenosine.
5.2. PKC activity
Activation of PKC is considered crucial in adenosinergic protection, and is often thought to occur upstream of mito KATP channels [114]. This is consistent with failure of PKC inhibition to modulate protection via mito KATP channel activation [44], and abrogation of PKC-mediated protection with a mito KATP channel blocker [115]. On the other hand, PKC inhibition has been shown to eliminate protection via mito KATP channel openers [41,51,105,106], placing PKC downstream. To reconcile such differences, PKC could act up- and downstream of mito KATP channels (e.g. modulating mito KATP function and subsequently being modified by mito KATP channel-dependent signaling, including ROS generation) (Fig. 2).
The impact of age on PKC signaling has received some attention. Tani et al. [116,117] observe impaired PKC activation/translocation and altered PKC-δ expression with age. Data of Przyklenk et al. [118] indicate protective PKC signaling paths differ substantially in aged vs. young tissues, with a requisite role of PKC-ε in young but not aged tissues. If PKC does play a central role in AR-mediated protection [29,31,32], and is a point of convergence in signaling, these changes in activation/ translocation could certainly contribute to failure in AR-mediated cardioprotection with age.
5.3. KATP channels
Stimulation of mito KATP channel opening is required, under most conditions studied, for expression of the anti-ischemic actions of AR. The A1AR can activate both sarcolemmal [119] and mitochondrial ATP sensitive K+ channels [32,41,44,51], the A3AR also activates mito KATP channels [120,121], and acute and preconditioning responses to AR agonism appear mito KATP channel mediated [41,44,49,51,120,121]. However, there remains support for a role for sarcolemmal KATP channels [122,123], despite the shift in focus to mitochondrial channels. Failure in KATP activation could certainly limit AR-mediated protection, however mixed data exist regarding ability of mito KATP channel activation to protect aged tissue. In mice a mito KATP activator retains its ability to protect against ischemic injury despite lack of AR-mediated protection [16]. This suggests failure distal to ARs yet proximal to mito KATP channels. In contrast, Schulman et al. [65] observed failure in both AR and diazoxide-mediated preconditioning in aged rat hearts, implying failure in signaling distal to the mito KATP channel. Differing observations could reflect different signaling with acute protection vs. preconditioning [41,51], and may be species-related. Complicating interpretation, there is evidence that effects of the commonly employed KATP opener diazoxide and inhibitor 5-hydroxydecanoic acid may be unrelated to mito KATP channel modulation [124,125]. If these agents indirectly target ROS generation and mitochondrial function, as suggested by Hanley and colleagues [124], or act via sarcolemmal KATP channels, as suggested by Suzuki et al. [125], then it may be these sites as opposed to mito KATP channels themselves, that are altered with aging. Indeed, strong evidence indicates protection attributed to mito KATP channels requires sarcolemmal KATP activity [122,125–127]. Direct reductions in sarcolemmal KATP channel expression and functionality do occur with aging (reviewed in Ref. [128]), and may thus lead to ischemic intolerance and failed AR cardioprotection, in agreement with intolerant phenotypes evident with reduced KATP channel expression [126,127].
5.4. MAPK Signaling
The mitogen-activated protein kinase (MAPK) family has been implicated in cardioprotective responses to adenosine [108,129]. Fredholm et al. show all ARs couple to MAPKs in non-cardiac cells [130], and preliminary studies support a role for p38 MAPK in A1AR mediated cardioprotection [131]. As noted by Gabai and Sherman [132], MAPK signaling may favor either cell death or survival depending on the balance of differing elements and pathways. Thus, subtle changes in MAPK signals with age may have profound effects on cellular outcome from ischemia and on effects of protective stimuli. Aging substantially reduces MAPK (JNK and ERK) activity/levels in rat myocardium [133,134]. Findings in the few studies of aged human hearts are equivocal, with studies generally undertaken in diseased groups of only moderate age (e.g. Refs. [135–137]). Changes appear to involve impaired activity in the absence of changes in protein content, and may reflect impaired levels of upstream receptor activation and/or changes in caveolin function [91,92]. Studies of effects of aging on transcriptional responses to oxidative stress reveal impairment of early response genes dependent on MAPK signaling and stress-response genes (e.g. Gadd45, JunB) [86].
5.5. PI3-kinase
Agonism of ARs can activate myocardial PI3-kinase via transactivation of tyrosine kinase [138]. A key target of PI3-kinase is Akt, which promotes cell survival and is implicated in cardioprotection [139]. There is evidence of repressed PI3-kinase expression in aged cardiac tissue [140], as in other tissues [141]. Immunohistochemical data verifies a decline in PI3-kinase expression and activity [142]. Additionally, Akt is repressed in aged cardiac tissue [142]. Such observations suggest the PI3-kinase/Akt pathway may well be of limited activity in aged myocardium, contributing to impaired intrinsic tolerance and adenosinergic protection. It should be noted, however, that preliminary data do not support essential roles for PI3-kinase/Akt signaling in A1AR mediated protection against cardiomyocyte death [46], or in adenosine mediated preconditioning [143]. Thus, the relevance of repressed PI3-kinase/Akt signaling to impaired AR-mediated protection remains to be defined.
5.6. Nitric oxide signaling
There is evidence supporting adenosinergic protection via modulation of nitric oxide (NO) bioavailability. Adenosine-mediated preconditioning may trigger changes in NO synthase (NOS) activity [144], and acute A1AR-mediated cardiac responses appear to be at least partially NO-dependent [145]. In mice, age-related changes in NO bioavailability parallel changes in adenosine-mediated protection [64]. However, there is also evidence that NO generation and iNOS activity are enhanced in aged mouse hearts [146]. Data for rats are equivocal. Recent work reveals impaired mitochondrial NOS activity in aging myocardium [147], while Ishihata et al. [148] observed no differences in basal NO release, though stimulated release was markedly reduced. Zieman et al. [149] detected increases in eNOS activity in aged rat heart whereas Chou et al. [150] report decreased eNOS activity with age. Precise changes in NO bioavailability with age, and their role in ischemic intolerance, remain to be more clearly defined. Nonetheless, impaired mitochondrial NO generation [147] and parallel changes in NO generation and cardioprotection [64] give credence to the possibility that alterations in NO signaling may contribute to impaired cardioprotection.
5.7. Anti-oxidant defense
There is evidence that A1AR agonism protects through improving anti-oxidant defense [31,32]. Adenosine receptor activation reduces mitochondrial radical formation [49] and oxidant injury [151,152], and increases cellular anti-oxidant capacity [153]. Moreover, cardioprotection via mito KATP channel-dependent pathways may involve inhibition of reactive oxygen species (ROS) generation [154]. Given the central role of oxidant damage in both reversible and irreversible injuries, these effects may contribute to the resistant phenotype observed with adenosine receptor activation. Aging is associated with increased oxidant generation and impaired anti-oxidant defences [11,155,156]. The documented elevations in radical generation and repression of endogenous anti-oxidant systems with age would be consistent with impairment of the beneficial effects of the AR system on radical generation [49] and anti-oxidant defences [153].
6. Relevance of failed adenosinergic cardioprotection
As already noted, the substantial evidence for intrinsic protection via ARs, coupled with parallel reductions in AR-mediated cardioprotection and intrinsic ischemic tolerance (Fig. 2), supports the idea that changes in adenosinergic protection may contribute to the ischemia-intolerant aged phenotype. This is further supported by the observation that enhanced A1AR expression renders aged myocardium comparable to young myocardium in terms of ischemic tolerance [16]. Changes in the AR system may additionally impact on post-ischemic events, with evidence that adenosine may regulate remodeling. Findings of Dubey et al. [68] indicate A2BARs normally inhibit cardiac fibroblast growth, and this group proposes A2BARs play a key role in regulating cardiac remodeling associated with fibroblast proliferation. This has yet to be more directly tested, although the normal role of A2BARs in regulating collagen synthesis and fibroblast growth is supported by other recent studies [157]. Since aging is associated with repression of A2BAR responses in vascular tissue [63], it is possible a decline in fibroblast A2BAR responses could enhance mitogenic/ fibrotic activity in aged tissue. Aging does impact on remodeling in experimental models and is associated with more advanced basal myocardial fibrosis [158,159].
Finally, age-related reductions in AR-mediated cardioprotection may be highly relevant to modest outcomes in recent clinical trials of adenosinergic therapies. Several placebo-controlled clinical trials have been conducted, including Acute Myocardial Infarction Study of Adenosine Trial (AMISTAD) I and II, Attenuation by Adenosine of Cardiac Complications (ATTACC), and ADMIRE (AmP579 Delivery for Myocardial Infarction REduction). In AMISTAD, infarct size was reduced and LV systolic function improved by adenosine, primarily in patients with anterior MI localization [160]. Morbidity and mortality were unaffected. In ATTACC, LV systolic function was unaffected, and there was a trend towards improved survival in patients again with anterior MI localization [161]. In ADMIRE, final infarct size was unaffected by the A1/A2 agonist studied (AMP579), though again there was a trend towards greater myocardial salvage in patients with anterior MI [162]. The disparity between these modest effects and more profound protection in animal models [28–32,34,35,42–44,53] may relate to the age of the patients. In ADMIRE the age range was 31 to 85, with similarly broad ranges and advanced ages in AMISTAD and ATTACC. Based on animal data (Fig. 1), failure in adenosinergic protection may occur well prior to senescence (by middle age), explaining lack of efficacy of adenosine-based therapies in clinical trials.
7. Conclusions
The adenosine receptor system and adenosine metabolism play important roles in determining cardiac outcome from ischemic insult. Despite advances in knowledge regarding the role of adenosine and ARs in protecting young tissues, it is now clear these responses are substantially impaired (or eliminated) with aging. These changes themselves may be important in the genesis of the ischemia-intolerant phenotype with aging. Origins of this dysfunction remain to be identified, but are likely to be multi-factorial (Fig. 2). Evidence does implicate failure in signaling as opposed to AR expression and adenosine handling itself. Clarification of changes in cardioprotective signaling may not only provide insight into the genesis of ischemic intolerance, but ultimately permit manipulation of myocardial tolerance and post-ischemic outcome in older subjects at greatest risk of ischemic events.
Dr. Headrick is the recipient of a Career Research Fellowship from the National Heart Foundation of Australia.


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Ao Sang Thien Tambon Pae Muang District Rayong, Ko Samed 21160, Thailand
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Check-in: 14:00
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Located on Ao Thian, Viking Holiday Resort's atmosphere is quiet service, friendly and suitable for leisure travel, because the sea journey to Koh Samed is comfortable with from Bangkok. Facilities - Massage, Restaurant - Thai - Europe Bar, Other activities such as fishing boating Traveling around Koh Samed, Motorcycle for rent. Bay candlelight Koh Samed (Ao Thian), a topography is painted by rocky beach in which some nice spots for skin diving are available. This beach is very quiet and free from group tours with bungalows and resorts available around the beach area.
Ao Sang Thien Tambon Pae Muang District Rayong Ko Samed 21160, Thailand


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The rising demand for crude-by-rail shipments from energy companies in North America is helping Canadian Pacific grow its business, said CP spokesman Ed Greenberg. "We're expecting the growth to continue throughout this year," Greenberg said. "Beyond 2013, our railway has a line of sight that is two to three times present volume going forward. So, it is a very positive story for our company."
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|"Vladimir Beliaev (JIRA)" <j...@apache.org>
|[jira] Created: (HARMONY-4585) [buildtest][eut] EUT3.3 integration to regular testing for winx86
|Wed, 01 Aug 2007 09:23:53 GMT
[buildtest][eut] EUT3.3 integration to regular testing for winx86 ----------------------------------------------------------------- Key: HARMONY-4585 URL: https://issues.apache.org/jira/browse/HARMONY-4585 Project: Harmony Issue Type: New Feature Components: build - test - ci Environment: Windows / x86 Reporter: Vladimir Beliaev The current passrate of EUT3.3 on Harmony iis pretty hight (~92%), and there are regression already (in comparison to M2) - HARMONY-4579... So it worth adding EUT3.3 to regular testing. Windows / x86 to be supported for now There are set of tasks to be done here: 1. write tests/eut scripts for EUT3.3. The scripts for EUT3.2 can be reused, the main difference is in parsing EUT3.3 results... 2. create Expected Failure List file for EUT3.3 winx86. 3. create adaptors & parameters for EUT3.3 I'll create sub-tasks JIRA for noted actions... Thanks Vladimir Beliaev -- This message is automatically generated by JIRA. - You can reply to this email to add a comment to the issue online.
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text: WONDERFUL NEWS! Four of my photographs and four of Ursula's paintingss have been accepted into the Cunningham Dax Collection, as part of the Bushfire Project ( creative responses to the Victorian Bushfires ). The Dax Centre promotes mental health and wellbeing by fostering a greater understanding of the mind, mental illness and trauma through art and creativity. The collection will enable the Dax Centre to preserve these experiences for perpetuity....More →


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1 review of Walt's Red Rose Cafe, first by you?
April 9, 2010
great place
I had the best hot chocolate every here! The portions were the perfect size and the prices were reasonable.
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