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Yesterday evening, Chicago Police made an unusual arrest when they picked up Rex Flodstrom, 40, for surfing off of Oak Street in Lake Michigan.
Flodstrom, who is a resident of Chicago, was baffled when he returned to shore only to be placed in handcuffs and have his board confiscated.
"I was surfing and saw a couple of guys on the beach and thought that they were spectators…I figured they might be friends or just someone checking it out. Then I noticed a car and a couple others pull up," said Flodstrom in a video interview with a FOX affiliate station in Chicago. "When it was time to come in I didn't know it was going to be a big situation, but I walked onto a hostile beach. They immediately grabbed me, handcuffed me, took me to the station and the regular police stuff…I was thinking this was insane."
Until recently, surfing was completely banned in Chicago. The law was reportedly enacted after a deadly tragedy that involved three girls and an inflatable raft. As a result, the city banned all floatable devices, including surfboards.
But in 2009, backed by efforts from a group that would later become the Surfrider Foundation Chicago Chapter, the city lifted the ban on surfing in certain beaches. Presently, there are four breaks accessible to surfers in the winter months while two breaks are accessible in the summer.
According to Mitch McNeil, the vice chairman of the Chicago chapter of the Surfrider Foundation, the break that Flodstrom was surfing at, Oak Street, was considered off limits.
"Unfortunately, Oak Street was not on the list of legal beaches," said McNeil. "I'm actually not really familiar of many people surfing over there."
According to Flodstrom, the break only gets decent a few times a year.
"The wave doesn't really get very good often, maybe once or twice a year," he said. "But yesterday was one of those days it was breaking. I actually live really close to the break so it's really convenient for me to walk down there and go for a surf. I've surfed there a bunch of times and never had any problems with the cops, so I was pretty shocked to get arrested."
When asked if the session was worth the jail time, Flodstrom chuckled. "Yeah, it was actually pretty good…for a lake. But yeah, if I were able to surf my home spot and go take a hot shower, then it would've been a great session. But if I'd had known that I would be arrested and would have to spend four hours in a holding cell in a freezing wetsuit, then I probably wouldn't have paddled out."


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|Home > Shyann
♀ Shyann
What does Shyann mean?
Shyann [shyann]▼ as a name for girls is a Native American Indian name, and the meaning of Shyann is "unintelligible speakers". Shyann is an alternate form of Cheyenne (Native American Indian): from the French name "shaiyena".
VARIANTS Shyanne▼, Shayanne, Shayan, Chyanne, Cheyanne▼, Chayanne, Chayan
RELATIONS VIA CHEYENNE Cheyanna, Chiana, ChiannaCREATIVE FORMS
(female) Shaann, Sheann, ..
(male) Shyden, Shyni, .. MIDDLE NAME PAIRINGS
Shyann Hillary (S.H.), ..
How popular is Shyann?
Shyann is an uncommon given name for females. Shyann is also a unique last name for all people. (2000 U.S. CENSUS)
Shyann was first listed in 1991 and reached its apex position of #687 in the U.S. in 2001, but is not in the list at the moment. (TOP BABY NAMES, 2015)
Which version is better?with its source form and related girl names. Cheyanna, Cheyanne (#1419 FROM RECENT DATA), Cheyenne (#347), Chyanne and Shyanne (#1561) are the popular related forms of Shyann. Usage of these relations of Shyann was well-received among parents 2 decades ago (MEDIAN #723) and is now significantly diminished (#1554, ▼83%), with versions like Cheyenne becoming less stylish.
Similar Names
Shyann▼ is pronounced similarly to Sean, Shaine, Shan, Shan-, Shane, Shaun, Shayne, Shene and Shone. Other suggested similar names are Bryann, Dayann, Dyann, Joyann, Kayann, Rayann, Rhiann, Rhyan, Ryann▲, San, Sana, Sanna, Sanny, Seana, Seanna, Shaena, Shaina▼, Shana▼, Shanae▼, Shanah, Shanay, Shanea, Shanee, Shaney, Shani, Shania▼, Shanie, Shanna▼, Shannae, Shannah, Shannea, Shanon, Shauna▼, Shaunna, Shawna▼, Shawni, Shawnna, Shayana, Shayna▼, Sheena▼, Sheina, Shena, Shianna, Shiona, Shona, Shonna, Shuna, Shyanna, Shyvon, Sian, Siana, Sianna, Suanny, Sueann, Sueanna, Sueanne, Susann and Swanny. These names tend to be more commonly used than Shyann.

subset: commoncrawl


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With the latest full-year financial results for Australia Post under new boss
Australia Post made a net profit of just $90 million in 2009-10 on revenue that fell $115 million to $4.9 billion. Its profit was dragged down by $150 million of restructuring costs necessary to continue the transformation of the business.
The 2009-10 results maintained the trend seen in recent years, 2008-09 delivering a net profit of $260 million and in 2006-07 a little over $400 million-plus. It is, by all accounts, a large and difficult transformation.
The challenge Mr Fahour and Australia Post's employees face, however, differs little to the magnitude of the transformation task the chief executive or employees of any other government postal service in the Organisation for Economic
Co-operation and Development zone faces.
At least Australia Post doesn't lose money on its core services. This year, the UK's Post Office asked the government regulator for a 7 per cent mandated price rise just to break even on the delivery of mail.
In the transformation of Australia Post, there is a significant amount of retail brand goodwill to build on. Australia Post is, in fact, our largest footfall retailer in the country. More shoppers visit the 3800 Australia Post outlets than any other retailer – and most of these outlets are open only five days a week.
Other retailers need to buy media to create footfall in order to sell products. Australia Post is in the enviable position of having a high volume of consistent footfall. It just needs to sell more products.
Manufacturers and retail marketing agencies have tried for years to harness the footfall in Australia Post stores with limited success, as no clear retail brand strategy has been apparent.
Australia Post's strong retail brand is supported by the 109-year legacy of having the widest geographical footprint, creating a truly trusted brand (in fact, Australia Post was the third most trusted brand in Australia last year, according to Grey and Sweeney Research's annual Eye on Australia report). Evidence of this is that there are far fewer column inches or chat rooms dedicated to undermining the Australia Post brand, in marked contrast to other ex-government-owned monopolies such as Telstra and Qantas.
Australia Post is, therefore, ideally placed to reposition its retail brand and relaunch itself in a new and relevant way as an end-to-end, bricks-and-mortar and online retailer of products and services.
With such a wide store network, and flexible physical and electronic logistics infrastructure, Australia Post has an embarrassment of products and services options for its brand. I was in an Australia Post outlet in regional NSW and observed an electronic cash transaction, small envelopes, mid-sized parcels and 12 kilograms of a dozen premium wines from Wine Selectors all passing though the one small outlet. There are very few store networks that can achieve this day in, day out.
Add to that an innately trusted brand and Australia Post could comfortably move deeper into financial services and online retailing of stationery and office equipment and reinforce its position as the trusted shipper of products behind the burgeoning micro-business and small-to-medium-size enterprise online retailing sector. There are literally tens of thousands of micro-businesses buying and selling products via websites, with Australia Post's network being the shipper of choice.
Australia Post is already looking at widening its online offering away from the traditional office technology, stationery and telco hardware space to embrace giftware and entertainment. An extension into financial services, even into full banking services, is also a distinct possibility and one that would fit comfortably under the Australia Post retail brand.
What is missing, however, is a clearly articulated retail brand strategy, one that is understood and bought into by Australia Post's employees, franchisees, suppliers and customers. The adoption and communication of this retail brand positioning – in print, online and crucially in-store – will be the turning point in the minds of all of Australia Post's shoppers and suppliers.
No other retail brand position can be built "shelf back" in Australia by harnessing the significant number of consumers who stand in its stores every day. A "shelf back" brand is built by exposure in-store, at the shelf, until it has such scale that it can be funded via traditional media such as television, print and outdoor. Jalna yoghurt and Vodka Cruiser are classic examples.
Over the coming months, expect to see a new and innovative approach taken to branding our Australia Post.
The Australian Financial Review


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A big smile can show friends you're happy to see them and enemies the number of tooth marks they could potentially have on their arms. Make friends in a flash with this Groupon.
Choose Between Two Options
- $49 for one in-office teeth-whitening treatment (a $99 value)
- $69 for three in-office teeth-whitening treatments (a $297 value)

During in-office treatments, dental technicians use a combination of LED lights and carbamide peroxide to brighten teeth and break up stains from coffee and tobacco. In-office treatments take 30 minutes to complete and lighten teeth between three to six shades.

No appointment is required to redeem this Groupon; walk-ins welcome Monday–Saturday, 10 a.m.–9 p.m., and on Sunday, 11 a.m.–6 p.m.

The Perfect Smile
The Perfect Smile engineers whiter smiles through the dual efforts of LED light and powerful chemicals. During in-office appointments technicians delicately apply carbamide peroxide along with the LED light to slightly discolored dentines, then activate the products with exposure to specialized lights. Each 30-minute session helps break up the discoloring effects of food, coffee, and tobacco products. Customers can also opt to stylize their smile at home with take-home bleaching kits.


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Is Adult Learning the route for you?
If you can answer yes to the questions below then our Adult Learning part time courses could be your next step!
- Are you 19 years or over?
- Are you looking for courses to support with employment opportunities or to enable you to continue with your professional development?
At Havant Sixth Form College we offer a selection of part time, classroom based and work based courses. Please refer to the Adult Course list and brochure for specific course information, details and dates.
Do I have to pay for the courses?
If you're an unemployed adult on benefits some of these courses are fully funded by the government and free of charge to you.
If you are aged between 19 and 23 years and do not have a full Level 2 or Level 3 qualification, these courses may also be fully funded and free to you.
Anyone who does not have a GCSE in Maths or English at grade A-C are fully funded to undertake a functional skills qualification free of charge.
If you are 24 years + and wish to take a Level 3 course or above, then there are loan options available.
How do I apply for a course?
It is easy to apply for a course, you can either:
- Complete the online application form and email it to firstname.lastname@example.com
- Contact us on 02392714040
- Complete a form at the back of our brochure and post it to:
Adult Learning Department
Havant Sixth Form College
New Road
- Pop into the main college and ask for the Adult Learning.


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Everbody has a story as to why Kodak failed. Here's mine:
It was the autumn of 1999 or 2000, I forget which year. CREO had just released Prinergy to great acclaim but had not yet become the dominant prepress workflow of the industry. But it was the hot new workflow and everybody wanted their output devices to hook up to it. Including Kodak, which had a proofer called the XP4 that made high-quality proofs, was expensive as heck and gobbled up super-expensive consumables. This was about five years before Epson took over the color proofing market for offset.
Prinergy. Kodak XP4. CREO. Kodak.
While not yet one company (Kodak would buy CREO in 2004), the two companies were business partners in the world of prepress, with CREO selling their computer-to-plate machines partnered with Kodak printing plates. A very good partnership for both. So what could wrong with Prinergy to XP4.
Well, somebody somewhere decided that Kodak should write the connectivity software for connecting Prinergy to the XP4. And it sucked. It sucked so bad that customers who bought Prinergy wouldn't pay for the system because it wouldn't print to the XP4. And that's where I came in, as I was the 3rd party output technician for the Prinergy development team.
Fortunately, there were two ways to drive an XP4 at the time. The first way was usually the lousy internally developed Kodak software. And when I say "lousy" don't think that what I thought of it. I never touched the software. It was the customers who thought up colorful names for it. The second way was to put a Harlequin RIP in front of it. So I set up a workflow of separated DCS (Desktop Color Separation) files from Prinegy to XP4 and it worked like a charm. Well, it was a bit slow but the most important was that it worked with spot colors while the internal Kodak application did not. And if you are in prepress, you sorta understand that spot are *kinda* important.
Anyhow, it worked, the customers signed off on the system, CREO got paid and just as important, the customers started gobbling up Kodak consumables. So guess the reaction from Kodak?
Well the XP4 team went ballistic that the customers threw out their software and it was me, me, me that caused this fiasco. I get phone calls from the Kodak product manager, and then phone calls from HIS boss about how I peed in the soup vis-a-vis the XP4. They threatened to go right upstairs to Amos (then CREO CEO) and report about how I totally screwed them.
Now eventually they finally released version 2 of that software and they finally got it working but by then I had been kicked upstairs to management myself and we had merged with Scitex. In the prepress world, for a few bright shining years, CREO prepress was bigger than Kodak prepress so we didn't have to take ANY crap from them. Too bad it didn't last.
Now in my 10+ years of product development, I have met a LOT of arrogant developers/engineer types. It's almost an oocupational hazard, which is really funny because the very best tend to come as humble guys. But those Kodak guys really made the top 3 list of biggest jerkoff-development teams I ever met. I mean, I was just doing my job so a parade down the main street of Rochester wasn't necessary but seriously, your stupid software didn't work and I was the one who screwed up?
That's my Kodak story. I sure there are thousands of stories like it.
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What A-list actor who's been teasing the press about his sexuality was spotted around town with a blonde transsexual?
37 Comments on "Mr. X Blind Item #8"
It's "so" not "totes". You have offended every "so" out there. FFS.
Easy. Franco.
@riven just for you to make you feal better on friday.. sugarhuggs to you boo!!
i can't do the talk,like the talk on the tv
and i can't do a love song, like the way it's meant to be
i can't do everything, but i'll do anything for you
i can't do anything except be in love with you
Because I'm a White Sox fan?
Have a good afternoon!
I hope you won't think me presumptuous if I say that I'm sending you good wishes.
Damn, I'm good!!! Adderall is famous for causing migraines, usually due to lack of sleep and strains it can cause, most notably teeth grinding. Be careful though, you should NOT take Rx migraine meds with Adderall.
Lady & Liddy thanks for the suggestions. I think it's probably the Aderall, I asked to change my dosage and dropped from 3 a day to 2. I've been having migraines for about a week now and the time frame matches, I just didn't even think of that. But I have been a hell of a lot less anxious since the change so I can deal with migraines until my body adjusts. I will definitely try some of those tips, starting with food!
@SYF internet group hug!! You always make me laugh (which is why I remembered you, I like you lol) so I'm happy to be wrong but yeah totes feelings sheepish for forgetting that it's a long-running joke. I face-palmed when I realized how bitchy I sounded AND that it was a joke that actually supports people like me against people like Enty. Yay Friday am I right?
why are you always mocking me??
eff off tbh
Franco is like camel/ beyonce. They like playing games and love the attention. Gay, straight, trandsgender- we dont really care. Enjoy ur life and stop trying to soak up soooo much attention.
Lady-fellow migraine suffer here. Look at foods u eat, they can be huge triggers. Any citrus fruit, melon, of all things, bananas all trigger headaches. As does weather. Eat regularly-if i skip lunch or dinner, im gonna have a migraine the next day. Put heat on your neck. Have 5 or 6 little pretzels, some caffinated soda and couple tylenol. Feel better soon:)
Thanks so much for writing this Riven!! Really! (-:
I learned something from you, again. (-:
You are soooooo right sugartits!!!
I get migraines too. I would first look into whatever meds you take. All sorts of drugs can cause headaches as a side effect, and other drugs like certain birth controls all the way to Adderall actually can be dangerous when interacting with migraine meds.
Stay hydrated and cool.
Unless they're from Transylvania
LOL thanks for the assist LadyH. I might have to break down and take a Tylonnol 3 at work. (God even trying to spell that word is making my brain die)
Yay!!! Peace restored. If anything: Mr X, NO ONE uses the term transsexual anymore. Except HSK. Get with it. At least Enty knows to refer to gender and not sex, despite his proclivity to add the "ed" to it. So…Mr X is not Enty then lol
Franco of course.
@SYF I sincerely apologize for taking it the wrong way, I've seen you do it so many times I stopped thinking you were mocking Enty. That was my error and I appreciate the clarification. I never speak up about it so of course the one time I do I'm totally wrong.
I understand where you are coming from Riven, I just hate to see anyone hurt by anything on here. You are entitled to feel however you feel about it. Take the day to your awesome self and feel better! HeisenHugs <3
It's Franco, there was a media blitz yesterday, even in the NYTimes that Gawker took up, that Franco has a male "roommate."
@riven. LadyH is super right. I promise I was not taking a stab at a person, I was only referring to vocabulary.
I would not want to offend you or any of the other nice people here.
It's transgender.
Oh James.
Genuine question: Lots of celebs have had affairs with transgendered people, in the past (Eddie Murphy) and now (Hank Baskett). If someone identifies as a woman, I consider them a woman. Is it a celeb kink, or do they also consider them women?
Cubsfan gonna get ya, FSP.
Play nice ya'all..
So back to the blinds..what ya say??
Or whatever reveals are left..and note enty-
Reveals beyond January would be appreciated….maybe March, April…..last week even better!!
Riven! Come back! I think SYF just made a silly jab at Enty's outdated vocab skillz. Don't be sadsies 🙁
@sugartitties. Lol!!
Btw – it's "transgenderED".
That guy in the story is a transsexual?
Didn't know Suki was a tranny though


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SRAM Brake Disc Centerline X two-piece 180 mm | 6-Bolt
Article details
SRAM brake Centerline X two-part 180 mm | 6-hole
New optimized design with large friction surface for more braking power and less brake fade. The newly designed aluminum spider with 7-point linkage of the friction ring also ensures better heat dissipation and low weight.
The noise has been reduced by reducing the vibration of the disc during braking again.
Technical specifications:
Material: Steel | Aluminum, titanium (screws)
Thickness friction ring: 1.8 mm
Disc diameter: 180 mm
Disc mount: 6-hole
Color: silver, black
Weight: 125g (manufacturer)
Delivery:. 1x brake disc including 6 Torx mounting screws made of titanium.
|Product weight:


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U.S. Senate Republican Leader Mitch McConnell released the following statement today regarding the President's call for a tax hike on small businesses and families in the middle of a slowing economy:
"It's not an accident that the President didn't explain how his plan to raise taxes on small businesses will create jobs--he can't say that with a straight face, it simply isn't true. In fact, according to the Joint Committee on Taxation, nearly a million small businesses would feel this tax hike right away, and up to a quarter of the entire American workforce depends on these employers for a paycheck. And since the President himself has previously acknowledged that this kind of tax hike is a drag on the economy, today's proposal is clearly based on a political calculus, not an economic one. But in the Obama economy, we need policies that are designed to create jobs--not designed to protect his. No one should see an income tax hike next year--not families, not small businesses and other job creators. We should extend all the tax rates while we make progress on fundamental tax reform. And we should be focused on the pro-growth jobs legislation that the House has passed, while ensuring that Washington does no additional harm to an all-too-fragile economy."
Source: http://www.mcconnell.senate.gov/public/index.cfm?p=PressReleases&ContentRecord_id=1e87b33e-9f76-4d5c-bc0e-9ca488057808&ContentType_id=c19bc7a5-2bb9-4a73-b2ab-3c1b5191a72b&Group_id=0fd6ddca-6a05-4b26-8710-a0b7b59a8f1f


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Love the Look! Kim Kardashian Lands at Nice Airport Wearing Cute Cat Eye Shades (PHOTOS)
Kim Kardashian's airport style is envied!Even
After her style-savvy week in Cannes, France, the Keeping Up with the Kardashians star, 31, was spotted touching down at Nice, France's airport on Friday, May 25, looking flawless per usual. Though the fashionista was head-to-toe glam, it was her super-chic sunglasses that caught our eye.
Kim's oversized cat eye sunglasses gave her outfit the edge and sleekness that it needed. Pairing the shades with a printed overcoat and black clothing, the reality star looked like just that, a star!
We're obsessed with these shades, but what do you think?
Click the pics and play fashion critic in the comments!


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Winter 2017
Coping With Workplace Stress Taking steps to strengthen your resilience, plus seeking treatment if necessary, will help you handle cranky customers, toxic co-workers, andRead more...
By Matthew Solan
When it comes to losing weight, let The Beatles be your guide: "gonna try with a little help from my friends." For many of us, a buddy system may be the winning formula for dropping pounds and keeping them off.
A pile of studies backs this up. For example, researchers from the University of Pittsburgh School of Medicine found that people who joined a weight-loss program with three friends or family members lost more weight than people who entered the program solo—and were nearly three times as likely to maintain their weight loss after 10 months.
Whether you prefer an organized group program, finding a community online, enlisting in a Biggest Loser-type competition, or simply recruiting a friend or family member to cheer you on, bolstering your efforts with strong support can be the difference between weight lost and wasted time.
"Buddy systems work largely because they provide better accountability and turn [losing weight] into a social event," says Arya Sharma, MD, PhD, scientific director of the Canadian Obesity Network. "Many of the group programs also provide the opportunity to exchange ideas and provide support you otherwise would not have access to."
Here's a look at some of your options:
Group-based weight loss programs such as Weight Watchers, Take Off Pounds Sensibly (TOPS), and Overeaters Anonymous provide a peer support system that helps you stick with a diet plan, avoid and manage setbacks, and stay focused on your goal.
In fact, a study published in the October 9, 2012 issue of the journal Obesity found that participants in a peer-led group were even more successful than those in a group that received behavioral weight-loss treatment from a health professional.
After 48 weeks, peer group participants lost an average of 13.2 pounds, compared to 11.9 pounds for the professionally-led group. In addition, more than twice as many members of the peer-led group lost 10 percent or more of their starting weight—a benchmark for seeing health benefits.
The takeaway here is that some element beyond straightforward education appears to play a role in successful weight management.
Michelle, who was diagnosed with bipolar in 1998, credits Weight Watchers with helping her achieve her goal of losing 30 pounds before a high school reunion.
She gained a lot of practical information at the meetings, such as strategies for not overeating at a buffet and why fiber-rich foods help you feel more full. She learned to view managing her weight in terms of changing her lifestyle rather than just "dieting."
Just as important, though, was the camaraderie.
"We were all in the same boat," says Michelle, 51, who lives in Ontario. "We got to share our success, our setbacks, and our battles. Knowing you are not alone can help you stay focused and more in charge."
Sometimes support from friends and family members can make all the difference. That was true for Rena, a 61-year-old Toronto resident.
She'd made two attempts to control her weight by joining a weight-loss group, but with no success. It was only when her son, Josh, became involved that she found the extra motivation she needed.
She started to gain serious weight during the "breakdown" that led to her bipolar diagnosis in 2005.
"I was so depressed I just ate like crazy," she says. Even after medication smoothed out her moods, she says, "I was still eating because I just didn't care what I looked like and I was used to stuffing my face in front of the TV."
Add in medication-related weight gain and within three years, she hit 250 pounds. Her son became alarmed.
"He said, 'Mom you are going to die,' and that was it," Rena says. "After that I was determined."
Rena returned to Weight Watchers—but this time, Josh was in her corner. When she was recognized in meetings for reaching various milestones in her weight-loss journey, he came along to help celebrate. He helped at home by hiding treats to reduce temptation. He joined her on a 5K walk.
It took Rena four and a half long years to reach her goal of losing 105 pounds. Along the way, Josh offered crucial words of support to keep her on track. At one point, she recalls, "Josh encouraged me when I was plateauing by asking, 'Mom when are you going to the gym?'"
Rena is now maintaining her target weight of 145 pounds and enjoying the feel of size 8 pants.
"I needed that personal help," she says. "When you are fighting the weight you have to deal with so much negativity…. I needed someone in my corner, and for me, my son was my best weight-loss friend."
Two years into her marathon effort, Rena's son also took an extraordinary step to keep her moving forward. Although he was a university student at the time, he pledged to give her $20 for every week she was able to shed at least one pound.
"He was determined to help me reach my goal," says Rena, noting that the offer of a cash reward "was a real incentive."
Money certainly can be a powerful motivator. A recent Mayo Clinic study found that people who were paid $20 for meeting a monthly weight loss goal dropped 9 pounds on average, while a group not offered incentives lost an average 2.3 pounds.
According to Kevin Volpp, MD, PhD, director of the Center for Health Incentives and Behavioral Economics at the University of Pennsylvania, immediate gratification (the cash) has way more leverage than potential future benefits (like lowering your blood pressure).
"The incentives help to make the benefits of healthy behavior that drive weight loss more salient in the present," Volpp says.
Volpp is also senior author of a study published this April in the Annals of Internal Medicine that looked at how financial incentives worked for solo vs. team weight loss efforts. When the cash payout was pegged to a team effort, participants lost an average of around seven pounds more than individuals who chose to go it alone.
Competition among the team members played a role, the authors concluded. However, the power of team spirit can be especially effective. That was the case with Stan, 59, of Chicago.
At the urging of his daughter, Stan signed up for a weight-loss challenge on HealthyWage.com. He says more than 75 teams raced to lose the most weight in three months. The prize for first place: $10,000.
Stan says that compared to his previous weight-loss attempts, the lure of a big payoff "made the desire of losing weight stronger. I could lose weight and win money. And if I didn't win, I would still win because I lost extra weight."
According to Tricia Leahey, PhD, assistant professor of psychiatry and human behavior at Brown University, there's more at work with team competitions than just dollar signs.
Her research into weight loss contests suggests that the payoff potential and social support feed each other to create more powerful motivation and commitment.
"If your teammates or partner lose weight they create a positive social influence, and thus you tend to lose more weight. And if you are motivated to lose weight because of a cash award you may influence others to do the same," says Leahey. "It can create this ongoing circle where they both rely on and motivate each other to reach their health goals."
Stan's team, a group of family and friends, had weekly meetings where they shared advice on how to counter obstacles. They took a team photo every week to document their progress and committed to exercise together with regular three-mile walks.
There was no specific eating regimen to follow. The only firm rule was that no team member could lose more that 16 percent of his or her body weight. That was to keep anyone from embracing dangerous crash diets.
Stan chose what he called "Atkins light," shunning his beloved bread for more lean protein.
In the end, he dropped 55 pounds from his 290-plus frame. His team finished third with 237 total pounds lost, collecting $3,000. Stan spent his winnings on a new wardrobe, plus something special for his supportive wife.
Stan says the notion of being accountable to his teammates helped deflect temptation.
"When I was faced between eating yogurt or a doughnut, I would ask myself, 'Is that doughnut worth $10,000?'" he says. "I didn't want to let the team down and ruin our chance for winning.
"It changed my behavior and that is something I didn't have when I tried to lose weight by myself."
Matthew Solan is a freelance writer based in St. Petersburg, Florida.
Virtual support
Joining an online weight-loss community may be the way to go. You can get the support you need without paying a cent or leaving the house. Plus, many sites provide tools to track what you eat and how much you exercise—and research shows that self-monitoring is a vital component of behavioral change.
Even though it lacks the personal touch, connecting through cyberspace appears to be effective. A study in the January 15, 2013 issue of the Journal of Medical Internet Research found that people who were more frequent participants in a free online weight program—whether entering their weight weekly or posting at least once on the message board—dropped more pounds.
Creating an online community through Twitter also has potential. Research from the University of South Carolina, published in the January 2013 issue of Translational Behavioral Medicine, looked at a group of overweight and obese individuals who were asked to tweet about their weight-loss efforts. Those who were more engaged in sending the brief messages ("Went to the gym today. Felt great!") and responding to others' tweets lost more pounds than peers who were less involved. Here are a few places to start:
WeightLossBuddy.com: Message boards, chat rooms, blogs, tracking tools and the chance to find a "buddy" to cheer you through your weight-loss efforts.
SparkPeople.com: One of the largest online weight-loss communities, this site offers tracking tools and social forums plus daily emails with a recipe and exercise of the day.
R/loseit: The posts on this subsection of the Reddit social network (reddit.com/r/loseit) can provide inspiration and practical tips.
Meetup.com: A means to actual get-togethers with people in your area who are interested in weight loss and fitness—including participants in the Dr. Oz Buddy Up for Weight Loss network (meetup.com/DoctorOz). Generally, you'll get more hits in larger cities.
Bet you can do it
For some people, competition can be a powerful spur for behavioral change. For people with bipolar, however, there are red flags to consider.
If impulsive spending is an issue in your life, run the idea of a weight-loss contest by a trusted advisor first. Also, consider whether your budget can bear the expense if you don't earn your money back.
On a related note: If disappointment at not meeting your goal could become a trigger, then maybe this isn't the best weight-loss route for you. Ditto if you're likely to get too caught up in the chase.
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Christina Sunrise
Shelly Meets Unicandle Unicorn - Poem by Christina Sunrise
Shelly saw a flame shining bright, the waves of the ocean reflected it's light.
Shelly knew it was UniCandle unicorn, she heard of the legend of his magical flaming horn. UniCandle unicorn knew Shelly lives in Lake Worth town,
so he brought her a sparkly birthday crown.
Shelly welcomed UniCandle unicorn then Shelly jumped on his saddled back,
UniCandle's wings opened up to fly to Kavasutra Bar really fast.
UniCandle unicorn had to be back to Krendoll island soon,
UniCandle unicorn asked Shelly to join him at Kavasutra for a fun afternoon.
Then UniCandle unicorn bought Shelly a special birthday treat,
a delicious chocolate coconut banana pie which is really sweet!
Now UniCandle unicorn had to fly back to Krendoll island again,
but he would stop back to see Shelly who is his new found friend.
Written By Suzae Chevalier on January 13,2011
www.christinasunrise.com www.christinapoems.com
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Salon Static of Las Vegas
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The company said pre-tax profit for the first quarter would fall to around £50m, compared to £66m in the same period last year.
The market was shocked by the statement as investors scrambled to dump ICI shares after the news, sending the stock to close 39% lower at 94p.
ICI chief executive Brendan O'Neill said that although it was hard to asses the impact of the war in Iraq, higher oil prices could result in higher production costs.
ICI uses oil products as a feedstock for many of the chemicals it makes.
Raw material
Mr O'Neill said job cuts were inevitable although he would not say how high the numbers would be.
IG index' Freddie Tulloch called ICI's statement to the market "a badly-disguised profit warning."
ICI said it was hurt in the first quarter by weak sales in Europe at its Quest Food unit, which makes food flavourings.
It also blamed rising raw material costs at its National Starch unit, which makes adhesives and food thickeners, for the fall in profits.
More bad news was to follow as ICI also announced the head of its Quest unit, Paul Drechsler, had resigned from the board and would be leaving the company.


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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Cardiovascular disease represents the most common cause of mortality in the developed world but, despite two decades of promising pre-clinical research and numerous clinical trials, cardiovascular gene transfer has so far failed to demonstrate convincing benefits in the clinical setting. In this review we discuss the various targets which may be suitable for cardiovascular gene therapy and the viral vectors which have to date shown the most potential for clinical use. We conclude with a summary of the current state of clinical cardiovascular gene therapy and the key trials which are ongoing.
AAV - Adeno-associated virus
Ad - Adenovirus
CABG - Coronary artery bypass grafting
CAD - Coronary artery disease
CVS - Cardiovascular system
DES - Drug eluting stents
EC - Endothelial cell
ECM - Extracellular matrix
ISR - Instent restenosis
NIH - Neointimal hyperplasia
PAD - Peripheral arterial disease
PCI - Percutaneous coronary intervention
SMC - Smooth muscle cell
SVG - Saphenous vein graft
Although cardiovascular disease is the second most frequently targeted indication in clinical trials of gene therapy, with 137 such studies having received approval by the early part of 2009 (http://www.wiley.co.uk/genmed/clinical/), this is a distant second to studies of cancer-related pathologies, which account for almost 65% of gene therapy clinical trials with close to 1,000 trials initiated or approved at the time of writing. However cardiovascular disease is the most common cause of mortality in the developed world, primarily as a result of obstructive atherosclerosis of the coronary and peripheral arteries, and is associated with an enormous symptom burden, manifesting most commonly as angina pectoris and intermittent claudication when affecting the coronary and lower limb arteries, respectively. Plaque rupture of advanced atherosclerotic lesions leading to acute arterial occlusion is the usual aetiology of myocardial infarction and stroke, which are the commonest causes of mortality associated with atherosclerosis. Heart failure due to left ventricular dysfunction, itself frequently a consequence of myocardial infarction, is increasing rapidly in prevalence in an aging population, partly because of improved therapies for the acute phase of myocardial infarction that result in greater rates of survival from the actual event and more long-term morbidity as a consequence.
At least part of the reason for the relative paucity of clinical studies of gene therapy for cardiovascular diseases resides in the fact that reasonably successful "classical" treatments exist for many cardiovascular pathologies. Substantial symptomatic relief from obstructive atherosclerotic disease affecting the coronary or peripheral arterial trees, for example, can be afforded by balloon angioplasty (with or without stent implantation) or by bypass surgery, but these interventions are in most instances simply symptomatic rather than curative, with no modification of the underlying disease process. Furthermore, such treatments, while having the potential to relieve to a substantial degree the symptoms incumbent upon cardiovascular pathologies, do so at the cost of giving rise to what are in effect a new range of cardiovascular pathologies, including restenosis, stent thrombosis and saphenous vein bypass graft disease, which can result in a recurrence of symptoms in a relatively short time frame. Some pathologies, heart failure being a prime example, are not typically suitable for such interventional approaches to management and rely largely upon pharmacological treatments aimed at symptomatic alleviation, risk factor modification and suppression of disease progression. Although the prognosis for heart failure has improved as a result of such medical therapies, and the use of implantable cardiac devices in carefully selected patients, the condition is still associated with significant morbidity and mortality.
Set in this context, gene therapy has the potential to deliver novel therapies for diseases of the cardiovascular system (CVS) and numerous gene therapy approaches have been investigated to target the different manifestations of cardiovascular disease. These include therapeutic angiogenesis to relieve ischaemia due to severe coronary artery disease (CAD) or peripheral arterial disease (PAD) not amenable to surgery or percutaneous interventions; reducing neointimal hyperplasia (NIH) to prevent accelerated forms of atherosclerosis in stented arteries and in venous bypass grafts; improving cardiomyocyte function for the treatment of heart failure, and providing a long-term treatment for chronic multifactorial cardiovascular disorders such as hypertension and dyslipidaemias. In this review we will discuss the most commonly investigated clinical applications for cardiovascular gene therapy and the potential vector delivery mechanisms for each of these. We will then consider the viral vectors which currently show the most promise for use within the CVS and give an overview of the current field with regards to clinical studies.
As alluded to already, the CVS possesses numerous possible targets for gene therapy. These are outlined in
The vascular wall consists of three layers: the intima, a single layer of endothelial cells (ECs) that lie on the luminal surface of the vessel, overlying a thin layer of connective tissue; the media, consisting of vascular smooth muscle cells (SMCs) and connective tissue; and the adventitia which consists predominantly of loose connective tissue, but also contains fibroblasts. These layers are separated by the internal and external elastic laminae respectively. Gene transfer into the vascular wall was demonstrated first in 1989 [
Choice of vector for clinical application.
|Clinical application
|Potential delivery method
|Desired onset of gene expression
|Desired duration of gene expression
|Target cells
|Possible vectors
|Desirability for repeat dosing
|In-stent restenosis
|Intracoronary infusion/ bound to stent
|Vessel wall (SMC, EC)
|SVG degeneration
|Ex vivo direct application
|Vessel wall (SMC, EC)
|Lentivirus Plasmids
|Heart failure
|Intracoronary infusion; myocardial injection
|Not important
|AAV Lentivirus
|Cardiac angiogenesis
|Intracoronary infusion; myocardial injection
|Not important
|Vessel wall (EC)
|Lentivirus Adenovirus
|Peripheral angiogenesis
|Intra-arterial infusion; intramuscular injection
|Not important
|Vessel wall (EC)
|Plasmids Adenovirus
|Not important
|AAV Lentivirus
|Myocardial injection; coated on pacing wires
|Lentivirus AAV
Since the procedure was first performed in 1977, percutaneous coronary intervention (PCI, also known as angioplasty) has become the predominant method of revascularisation for patients with symptomatic coronary disease. In brief, PCI is performed under local anaesthetic with vascular access obtained via the femoral or radial artery. A catheter is inserted into the ostium of the target coronary artery and a fine guide wire is passed across the stenosis. Further catheters may then be advanced over the guide wire. The stenosis is typically dilated with a balloon followed by implantation of a stent: a metallic expandable coil which is mounted onto a second balloon to allow deployment. Since the mid-1990s, when stent deployment became a routine part of the PCI process, the number of cases has increased dramatically and, in the present day, several million such procedures are performed worldwide each year. However in-stent restenosis (ISR), progressive luminal narrowing as a result of neointimal hyperplasia within the stent, requires further treatment in approximately 14% of patients undergoing PCI with bare metal stents [
Flow chart illustrating the restenotic process
Gene therapy strategies to attain this goal include reducing SMC proliferation and migration, inhibiting thrombosis, reducing ECM deposition and enhancing endothelialisation. Coronary stents provide a very convenient platform for delivering viral vectors [
Coronary artery bypass grafting (CABG) is one of the most commonly performed surgical procedures worldwide, and in spite of the use of arterial grafts where possible, autologous saphenous vein is still the most widely used conduit for CABG [
Although advances in surgical and catheter-based techniques now allow revascularisation for the majority of patients with symptomatic CAD and PAD, there exists a proportion of patients in whom these techniques are not applicable either because of excessive procedural risk or because of technical difficulties related to the arterial anatomy. PCI and CABG allow treatment of coronary vessels with a diameter of approximately 2 mm or greater (macrovascular disease), but a significant minority of patients have microscopic coronary disease which is unsuitable for revascularisation by conventional means. Such patients have been studied in many early clinical trials wherein gene therapeutic approaches have utilised pro-angiogenic transgenes in attempts to afford symptomatic alleviation. The induction of therapeutic angiogenesis aims to increase blood flow to ischaemic tissue by the generation of new blood vessels. In the peripheral vasculature, the aim of such therapy is typically the relief of limb pain occurring at rest and the prevention of limb loss in patients with critical ischaemia. In the coronary vasculature, as well as improving exertional angina, coronary angiogenesis has the potential to improve left ventricular function in patients with heart failure: chronically ischaemic regions of myocardium may have poor contractility as a result of hibernation of viable myocardial cells (cardiomyocytes) and these cells may regain normal function with improvement of regional blood flow. As a consequence of the clinical need that these conditions represent – being akin to advanced malignancies in terms of the symptomatic severity and the mortality with which they are associated - they are at the time of writing the most extensively studied application for cardiovascular gene transfer. As well as arterial catheter infusion, direct injection of virus either into skeletal muscle for PAD or into the myocardium at the time of CABG or via a mini-thoracotomy for CAD has been investigated.
Gene delivery to cardiomyocytes, principally within the left ventricle, offers the potential to treat several conditions. As discussed above, pro-angiogenic genes may improve blood supply to the myocardium, and localized delivery of genes involved in the generation and propagation of cardiac electrical activity offers the potential for "biopacemaking" as an alternative to permanent implantable electronic pacemakers [
Heart failure is a clinical syndrome characterized by shortness of breath on exertion, fluid retention and fatigue. It typically occurs as a consequence of left ventricular dysfunction and its prevalence is reaching epidemic levels as the population ages: currently it is estimated that one in five 40 year olds will develop heart failure within their lifetime [
Although heart failure is often considered a permanent progressive condition, significant cardiac dysfunction has been shown to completely resolve in some cases with the temporary use of left ventricular assist devices (LVADs) [
Other putative therapeutic applications of cardiovascular gene therapy include risk factor modifications such as cholesterol lowering or antihypertensive gene therapy. Both high blood pressure and hypercholesterolaemia typically require lifelong oral therapy at the present and while such therapies are often very effective, the potential for gene therapy to act as a one-shot treatment for these chronic pathologies makes them attractive targets for investigation. However we shall confine ourselves for the remainder of this review to a consideration of those viral gene transfer vectors that have been applied to or have potential application to clinical cardiovascular gene transfer, and to a discussion of the current state of clinical virally-mediated gene therapy in the CVS.
The ideal vector for clinical application would be target cell-specific with no expression outwith the target cell type; offer the capacity to transfer large DNA sequences; result in therapeutic levels of transgene expression that are not attenuated by the host immune response; express transgene for a duration appropriate to the clinical problem; pose no risk of toxicity either acutely (as a result of immunogenicity or unregulated transgene expression) or in the long-term (such as oncogenesis); and be cost-effective and easy to produce in therapeutically applicable quantity. Clearly no currently available vector fulfils this wish-list of characteristics, and it is probably unrealistic to suggest that such an ideal vector will ever exist. Several viruses have been considered for use in cardiovascular gene therapy and all represent some compromise of the above features. Adenovirus is the most commonly used virus in clinical trials of cardiovascular gene therapy to date (http://www.wiley.co.uk/genmed/clinical/), although recent advances in the development of recombinant AAVs have led to the initiation of clinical trials using this vector for the treatment of heart failure. Lentiviruses have yet to be used in cardiovascular clinical trials, as a result of concerns over long-term safety, but the recent development of non-integrating lentiviruses may make this vector an appealing option in the future. Other retroviruses, sendaivirus, Semliki forest virus, herpes simplex virus and baculovirus [
Adenoviruses (Ad) were first described in 1953 [
The use of adenoviruses for gene therapy has been reviewed numerously over the last 15 years and it would not serve us well to spend much of the present review discussing the basics of adenovirus biology from this perspective. However, briefly, the adenovirus virion consists of a non-enveloped icosahedral capsid particle containing a 30–40 kb linear dsDNA genome. Located at each of the twelve vertices of the icosahedron is a trimeric fibre shaft terminating in a globular knob domain. The length and flexibility of the fibre shaft varies significantly between adenovirus subtypes and can influence both binding and virus uptake [
Despite its broad natural tropism, when given systemically virtually all Ad5-mediated transduction occurs in the liver, predominantly within resident Kupffer cells [
Recombinant vectors derived from serotype 5 adenovirus (Ad5 – a subgoup C adenovirus) are by far the best characterised and have been used in the majority of clinical trials. First-generation recombinant Ad5 have typically had the E1 and E3 regions (which contain genes that are essential for viral assembly and for evasion of host immunity respectively) removed. Several second-generation recombinant Ad5 have been described that include additional deletions of the adenovirus genome from the E4 locus [
Further modification has given rise to third-generation recombinant adenoviruses, from which all wild-type adenoviral coding sequences have been deleted. These viruses have an increased cloning capacity of approximately 35 kb (compared to around 8 kb in first- and second-generation viruses) and produce no viral proteins in infected cells [
It is almost certain that part of the reason for the surprisingly limited uptake of gutless adenoviruses in pre-clinical studies of cardiovascular gene transfer lies in the relative difficulty of making the helper-dependent vectors. Most such pre-clinical studies are of a relatively short-term nature and it seems that the advantages in duration of transgene expression and reduced host inflammatory responses that are offered by gutless adenoviruses do not outweigh the extra effort of manufacture, particularly as Wen
The immunogenicity of adenoviruses has proven to be a major stumbling block to their clinical use, both by limiting the magnitude and duration of transgene expression and by inducing dose-dependent toxicity. Their broad tropism is also an issue, particularly for systemically administered gene therapy. Both of these problems can potentially be circumvented by modifying Ad targeting
Pseudotyping involves replacing the fibre components of a specific serotype of adenovirus with those from another serotype. Such a manoeuvre can reduce the immunogenicity of the chimeric product and redirect viral transduction to cell types for which the original adenovirus is not normally tropic. In practice, the initial vector that has been subjected to pseudotyping is always Ad5. Earliest reports of pseudotyping of Ad5 included the substitution of the Ad5 fibre head with that from the serotype 3 adenovirus (subgroup B), resulting in a chimera with alterations in tropism that included reduced transduction of human coronary ECs [
Ad5 has been pseudotyped with fibres from the subgroup D serotypes 19p and 37, resulting in chimeric vectors with very low tropism for hepatocytes compared with unmodified Ad5 [
Replacement of adenovirus components with peptides from different classes of virus to form chimeric viruses has been employed as an alternative strategy to pseudotyping [
An alternative approach to pseudotyping is modification of capsid components by selective mutation or by insertion of peptides to alter vector tropism. Mutation of the knob CAR receptor has been shown to reduce transduction of cells expressing CAR
Non-genetic means of transductional targeting involve coating the virus with a bi-specific adaptor which reduces the natural viral tropism and can be coupled to an antibody to selectively target a desired cell type. Examples of these bi-specific molecules include polymers such as polyethylene glycol (PEG) and antibodies. Coating of Ad with PEG coupled to anti-E-selectin-antibody has been shown to both prevent normal binding to the CAR receptor and to target ECs [
Despite significant advances in the understanding of adenovirus transduction and immunogenicity however, and the elegant means by which retargeting strategies have altered very significantly the tropism of the derivative adenoviruses, these targeted adenovirus vectors still remain laboratory tools and, thus far, none have made the transition into the clinical research setting. Furthermore, retargeting aside, these viruses are still basically serotype 5 adenoviruses and come with the problems of innate immunogenicity and pre-existing exposure to their wild-type progenitor in most human communities. As such, it is likely that the best that might be hoped for from these vectors in the state in which they exist now is transient expression of transgene (and consequently transient therapeutic effects) in a carefully targeted population of cells. It is likely that, before widespread clinical usefulness is attained, it will be necessary to further refine adenovirus technology to produce helper-dependent targeted vectors derived from serotypes other than Ad5. And even then, each vector is likely to be useful only once in each patient in whom it might be used. That may, of course, still be enough to be very useful indeed!
AAV is a small member of the parvovirus family with a 4.7 kb single-stranded DNA genome. Wild-type AAV has three unique, potentially beneficial characteristics which distinguish it from other gene therapy vectors: firstly it cannot replicate without the assistance of a helper virus, such as adenovirus or herpes simplex virus; secondly the AAV genome is capable of long-term persistence within the nucleus, either by site-specific integration into the AAVS1 locus on the long arm of chromosome 19 or in episomal form; thirdly, despite the fact that a large proportion of the world's population is seropositive for a variety of AAV serotypes, AAV has never been shown to cause human disease. Since the first infectious clone of AAV serotype 2 was established in 1982 [
As a consequence of loss of the Rep gene, rAAV lose the capacity for site-specific integration into chromosome 19 and acquire the potential for random integration with the risk of oncogenesis, although the available evidence suggests that integration of AAV genomes is inefficient even in wild-type form and nuclear persistence is usually a consequence of episomal maintenance [
Recombinant AAV offers some very advantageous features as a gene therapy vector. As wild-type AAV is not pathogenic it represents the safest of the viral vectors being considered and is significantly less immunogenic than Ad. Recombinant AAV elicit long-term gene expression as the genome persists in the nucleus, largely as circularised dsDNA episomes [
The small packaging capacity of AAV containing an ssDNA genome (approximately 4.6kb) imposes modestly severe limits upon the size of transgene expression cassette that can be inserted. Having said that, 4.6 kb still offers substantial scope for therapeutic gene transfer, and sterling work has been done in minimizing the size of therapeutic gene sequences in order to allow packaging into AAV. This is exemplified by AAV-mediated transfer of dystrophin: the full-length dystrophin cDNA at ≈14kb is far too large for packaging into AAV, yet a functional micro-dystrophin cDNA of 3.8kb has been packaged into a rAAV and used to elicit potentially therapeutic effects in mice [
AAV2 was the first adeno-associated virus to be developed as a gene therapy vector and represents the most extensively investigated of the AAV serotypes. Infection is thought to be primarily mediated by membrane-associated HSPG [
At the present, rAAV are the vector of choice for myocardial gene transfer and the capacity of serotypes 1, 6, 8 and 9 for effective transduction of cardiomyocytes offers the prospect of genuinely effective therapeutic myocardial gene transfer in the clinical setting. Unanswered questions remain about the prospect of integrational oncogenesis, and it is likely that the usefulness of rAAV as therapeutic agents will ultimately be confined by their limited capacity to deliver transgenic material. Nevertheless, rAAV offer the best prospect of breakthrough successes in the field of clinical virus-mediated cardiovascular gene therapy.
Lentiviruses are part of the retrovirus family and consist of a ssRNA genome enveloped in a lipid bilayer; most currently investigated lentiviruses are derived from HIV-1. The primary receptor for lentivirus is the T-cell CD4 receptor and, as opposed to Ad and AAV, cellular entry occurs via membrane fusion. The viral capsid is subsequently released into the cytoplasm where uncoating and reverse transcription of the viral ssRNA to dsDNA occurs followed by nuclear transport via the microtubuli [
Two major developments were required to make lentivirus a possible gene therapy vector. Firstly, self-inactivating lentivirus vectors were generated in which the U3 promoter region of the long terminal repeat had been inactivated [
Potential clinical uses of lentivirus have been demonstrated
Despite the potential that pseudotyped lentiviruses offer as vectors for cardiovascular gene transfer, their use in the clinical setting is very substantially hindered by concerns over their safety. The risk of insertional mutagenesis with integrative vectors has been confirmed in a clinical trial of a gammaretrovirus for the treatment of X-linked severe combined immunodeficiency. Two out of ten patients in this trial developed T-cell leukaemia as a result of integration of the vector in proximity to the LMO2 proto-oncogene [
In addition to manipulating vector tropism to target those tissues to which gene delivery is desirable, it is possible to use conditional regulatory elements to confer a further level of specificity upon the manner in which gene therapies are applied to the cardiovascular system. Transcriptional targeting, by the inclusion of cell-specific promoters within the transgene expression cassette, offers the potential to increase vector safety by minimizing expression of transgene outwith specific cardiovascular cell types. Transgene expression in clinical trials has typically been driven by strong constitutively-active viral promoters. The most frequently used of these is the major intermediate-early enhancer/promoter from human cytomegalovirus (MIEhCMV), which is also the promoter most likely to be found in vectors used for studies of pre-clinical cardiovascular gene therapy [
Multiple endothelial-specific promoters have been identified including fms-like tyrosine kinase-1 (flt-1) [
The murine SM22α promoter regulates transgene expression in SMCs following adenovirus-mediated gene transfer
The ventricle-specific myosin light chain-2v promoter and the α-myosin heavy chain promoter have been demonstrated to result in cardiac specificity with both adenoviral [
Having discussed some of the potential targets for cardiovascular gene therapy, and considered some aspects of the vectorology of cardiac and vascular gene transfer, we shall now take a brief look at the current state of cardiovascular gene therapeutics from a clinical perspective.
As we stated at the start of this article, cardiovascular diseases are the second most common target for clinical trials of gene therapy. Studies have been performed to investigate gene therapy to reduce neointima formation following PCI and for systemic cardiovascular diseases, but the large majority of clinical trials of cardiovascular gene therapy that have to date progressed to completion have investigated the induction of therapeutic angiogenesis within the peripheral vasculature and within the myocardium. Given the scope of potential targets within the cardiovascular system, it may seem initially surprising that one therapeutic objective should so dominate this field of study, but the simple fact is that the participants in these studies of angiogenesis are otherwise at a therapeutic dead-end, beyond further percutaneous or operative intervention, with only limb amputations or persistent symptomatic myocardial ischaemia (with the incumbent impositions on quality of life that these burdens convey) to countenance.
Despite the preponderance of studies of viral gene transfer in the pre-clinical setting, a substantial proportion of clinical trials of cardiovascular gene therapy have employed non-viral gene transfer in preference to virus-mediated methods. As the remit of this article is confined to virus-mediated gene therapy, we shall defer from comment on such clinical studies of plasmid-mediated gene delivery. The reader who is interested in the outcomes of the those clinical trials in which non-viral means of gene transfer were employed is referred to the review by Rissanen and Yla-Herttuala, which nicely summarizes the state of play in early 2007 [
The induction of angiogenesis as a therapeutic strategy for both coronary and peripheral arterial disease has been investigated in a series of clinical randomised clinical trials, primarily using vascular endothelial growth factor (VEGF) or fibroblast growth factor (FGF) as the proangiogenic transgene. Most research on PAD has employed plasmid vectors for gene transfer, although studies of viral gene therapy have been published: in a phase II study of intra-arterial injection of AdVEGF165 following peripheral angioplasty an increase in new vessels distal to the site of vector delivery was demonstrated, but this was not accompanied by improved healing of ischaemic ulcers, resolution of rest pain or increased ankle-brachial index by comparison with controls [
In contrast to studies of PAD, the majority of studies of angiogenic gene transfer for myocardial ischaemia have used virus-mediated (specifically, adenovirus-mediated) gene transfer – presumably it is easier to convince regulatory authorities of the life-saving potential of viruses in this setting than in the limb vasculature (patients with PAD do not typically die of their peripheral arterial problems, but of myocardial infarction or stroke).
In the earliest study of intracoronary injection of AdFGF-4 (AGENT-2), delivery of active vector by subselective coronary catheterization of culprit arteries resulted in a borderline significant reduction in the size of the region of myocardium demonstrating stress hypoperfusion eight weeks post-delivery [
Further studies of intracoronary injection of AdFGF-4, in the guise of the AGENT-3 and AGENT-4 studies, have given rise to the largest experience to date of cardiovascular gene therapy, with over 500 patients with chronic angina having undergone enrolment [
In addition to intracoronary administration of viruses, direct intramyocardial injection of adenovirus has been investigated following thoracotomy in human studies. Administration of Ad5-VEGF121 hinted at clinical efficacy in a phase I study, with "suggested" improvements in regional ventricular wall motion, severity of angina and exercise tolerance [
All considered, adenovirus-mediated myocardial gene transfer of pro-angiogenic genes has provided little cause for enthusiasm about the potential for widespread clinical application of such therapy. However, the fact that it has been possible to elicit clinically useful effects (albeit restricted to women) by delivery of adenoviruses, which – it must be remembered – are likely to give rise to appreciable transgene expression for only two or three weeks post-delivery, does raise the possibility that more useful clinical effects may arise from the use of vectors that will elicit transgene expression of longer duration. In this respect, it will be interesting to see whether studies of angiogenic gene transfer using AAV, gutless adenoviruses or lentivirus will ever see the light of day.
A vast number of potentially therapeutic transgenes have been studied in animal models of restenosis [
Gene-eluting stents using both adenovirus and plasmid vectors have been investigated
The only completed clinical trials of myocardial gene therapy to date have been of proangiogenic factors, and as already discussed, the outcomes of these studies have been less than impressive. However myocardial gene therapy has recently become the focus of renewed interest due to the initiation of clinical studies using an AAV vector for the treatment of heart failure. Two excellent recent reviews discuss this field in more detail [
It is expected that these studies will provide important information on both the suitability of AAV as a vector and whether SERCA2a is a beneficial transgene in human heart failure. Although the results are eagerly awaited there are several reasons to be cautious. The vectors chosen for these studies may not be the optimal vectors for myocardial gene delivery; as discussed earlier, the AAV8 and AAV9 serotypes have been shown to exhibit greater myocardial tropism than the AAV1 and AAV6 serotypes, and the human CMV promoter, whilst efficacious in cardiomyocytes, runs the risk of being rendered quiescent in the long-term as a consequence of DNA methylation. There are also some safety concerns with the use of SERCA2a. Overexpression of SERCA2a in rat myocardium leads to an increased rate of fatal arrhythmia [
It is difficult to write a review of gene therapy with regard to any of its spheres of application without being constrained eventually to resort to talk of its "promise" or "potential" in the clinical translation of that setting; a brief scout through PubMed reveals that the oldest hit for "gene therapy" and "promise" dates from as far back as 1981 [
Firstly, it is possible that we have been misled about the potential for gene therapy. The talk of promise and potential is, after all, based upon pre-clinical studies. Until some unequivocal clinical benefit is obtained from the extrapolation of results obtained
At the present, efficient gene transfer in clinically-applicable exposure times is typically reliant upon the use of viruses (although gene therapy for peripheral arterial disease is an exception in this regard and much of the currently ongoing clinical research uses non-viral gene transfer), and those viruses that are available (or at least those that have been used in clinical trials of cardiovascular diseases) are either potently immunogenic and pro-inflammatory or difficult to generate at high titres. This naturally begs the question, why have investigators not used better vectors for clinical gene transfer? Why have there, alluding specifically to the cardiovascular system, been no studies of clinical gene transfer using helper-dependent adenoviruses, for example? Gutless adenoviruses offer a lot of very tempting features as clinical gene transfer vectors. They can be expected to elicit transgene expression of similar magnitude to that achieved by first-generation vectors, but for longer and with less concomitant inflammation, yet so far the authors are aware of no plans to use them in a clinical setting. Similarly, the two recent studies of AAV-mediated gene transfer of SERCA2a have employed (or will employ) AAV serotypes that, whilst effective for use in cardiomyocyte gene transfer, are not the most effective vectors for this purpose. Once again, it isn't immediately apparent why clinical investigators are relying on suboptimal gene transfer strategies. It might be argued, of course, that we simply don't know if the methods being employed
It may be that this problem is more closely related to commercial issues than technical matters. Compared to classical pharmacological agents (with regard to which a lone company can generate, develop, investigate and eventually market a unique molecule) gene therapy agents are complex. Multiple components are required to generate a vector that can be delivered to a target tissue, and give rise to expression of a therapeutic protein in humans. The simplest virus vector requires the therapeutic transgene itself, a promoter of transgene expression, a polyadenylation signal and the apparatus necessary to package them into the chosen viral agent. This typically represents four separate patented technologies and four separate parties who have to be reconciled with the development of a product for clinical trials. Against this backdrop it should perhaps come as no surprise that not all technologies are available for all investigators, and it is probably not adopting too cynical a posture to say that the widely dispersed intellectual properties that underlie viral gene therapy vectors are a discouragement to the involvement of big pharmaceutical companies in clinical trials of these agents. Until it becomes clear that gene therapies can be transferred effectively into the clinic with profit-making potential, clinical trials of gene therapy are likely to be forced to accept compromises in their implementation.
Another of the problems that gene therapies face in the cardiovascular setting is the need to compete in many therapeutic areas with classical pharmacological therapies that are, in fact, adequate (albeit sometimes little more than adequate) for their clinical purposes. Gene therapy, and particularly virus-mediated gene therapy, has still to contend with the widely-held belief that it is a risky therapeutic approach to a problem comparable, for example, with systemic chemotherapy. This is reinforced by infamous failures of the past: the most widely-known recipient of virus-mediated gene therapy was the first person to die as a direct consequence of the agent he received. Speaking from personal experience, many experienced medical practitioners who know almost nothing else of gene therapy are aware that Jesse Gelsinger died as a result of a large dose of recombinant adenovirus vector. Perhaps because of this gene therapies tend still to be reserved for application to clinical situations in which no adequate classical pharmacological therapies exist. Certainly within the cardiovascular system, trials of gene therapy have been predominantly directed at angiogenesis in patients who are symptomatic despite best medical care and for whom revascularization is no longer a viable option. There can be no doubt that a therapy that proves successful in these patients will be very welcome indeed, but the fact that these patients have exhausted those therapies that are currently available does mean that a lot is being asked of gene therapy to succeed where well-established therapies have failed. In that respect, it seems that cardiovascular gene therapies are going to have to be proved successful in some of the most very demanding of clinical situations before they are applied to settings where they might more reasonably be expected to achieve clinical usefulness.
The perception of gene therapy as a high-risk option naturally accounts for the preponderance of clinical studies that are aimed at treating malignant diseases. It ought to be stressed however that the prognosis of certain cardiovascular diseases, severe left ventricular dysfunction for example, is not so very different from that of some malignancies and, while drug treatments are available that modify the disease course and prolong life expectancy of patients with heart failure, there are no cures for the large majority of patients. As such these patients are in need of novel therapies to no lesser extent than are victims of cancer. Where one of the most important differences between severe heart failure and cancer, however, is that once the cellular targets of oncological gene therapies have been successfully targeted there is no virtue in persistence of gene expression, as the purpose of gene expression is to kill the cell in which expression occurs. In contrast, some cardiovascular targets for gene therapy may require long-term transgene expression. Studies of cancer gene therapy can therefore make effective use of simple, easy-to-produce vectors such as first-generation recombinant adenoviruses, which are not likely to find a useful clinical application in cardiovascular gene therapy. Certainly, the evidence available to date shows that very little clinical benefit has accrued in any cardiovascular setting from use of first-generation adenoviruses.
As a result of the issues discussed above, successful virus-mediated gene therapy for cardiovascular disease is harder to achieve than, say, cancer gene therapy, and the rewards are often regarded as being less. Despite this, at the time of writing, recombinant viral vectors still offer the greatest potential to apply gene therapy strategies to cardiovascular disease and it is new developments in viral vectors that are likely to reap the earliest rewards in the clinical setting. Vectors that are available now (for instance pseudotyped AAV), despite the reservations voiced above, offer the realistic proposition of myocardial gene therapies for heart failure. The first iteration of these therapies is not going to be the definitive iteration thereof (as is always the case when new technologies are applied to therapeutics) and the population being studied in these early trials manifest extreme degrees of the disease state, so it is unrealistic to expect dramatic benefits, but any beneficial effect will be a step forward.
Similarly, despite the problems inherent in the application of recombinant adenoviruses to the cardiovascular system, the
Whilst at the present all that gene therapy has to offer in the setting of cardiovascular disease is potential or promise (whichever is your preference), the prospect is implausible that gene therapies will not at some time in the future become a routine part of everyday therapeutics. And while it is equally likely that when this time arrives we will not be using virus vectors as we recognize them today, recombinant viruses represent the most important pathway by which gene therapy will gain initial credibility as a therapeutic modality in the setting of cardiovascular disease. Viruses have taken millions of years to evolve the means by which they deliver their nucleic acids to the nuclei of the cells that they infect. Gene therapists might reasonably ask for something more than 28 years to turn the promise that virus–mediated gene transfer offers into effective gene therapies.


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First introduced in 1983, the 2WD racing buggy Frog made a huge splash with its eye catching design and high performance running. The Frog now makes a comeback, updated for a new age, but with its basic structure essentially unchanged. Preserving its characteristic space frame, the oil dampers for trailing arm type rear suspension have been updated to diaphragm type. The rear drive shaft features dogbone type joints for secure power transmission. The sleek polycarbonate body remains the same, while the 3-piece wheels feature front grooved and rear spike tyres for excellent off-road running.The electric R/C racing buggy features an ABS space frame and nylon suspension and bumper for a lightweight yet rugged form that is perfect for off road running. The Battery is held in an ultra-low position, giving this car the stability and weight balance to handle rough terrain and wild jumps. The advanced 4-wheel independent suspension comprises of a front double wishbone type featuring in-board spring and durable steel radius arm. Rear trailing arm type features horizontally mounted aluminum cylinder oil dampers for effective shock absorbtion. The sealed differential gearbox ensures high speed cornering, while full gearbox ball bearings and 3-step gear ratio secures maximum transmission efficiency.
540 MotorElectronic speed control (ESC)Oil filled dampersPolycarbonate bodyIncludes re-designed side aluminum dampers inspired by TRF shock designIncludes re-designed dog-bone style drive train with original rubber bootsIncludes straight ribbed racing front tires and high-grip rear spiked tyresWheels are realistic 3-piece typeIncludes diff gear
2 Channel RC Unit7.2v Race pack and chargerPaint and tools to build kit
© 2003-2017 Fusion Hobbies Limited | Registered in England number: 4523506 PO Box 6531, Kettering, Northants, NN15 5ZU
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tag:blogger.com,1999:blog-1409654809690469042.post4121792569216732124..comments2017-07-13T16:22:06.710-04:00Comments on I Heart Robotics: Fastners for 3D Printing: Screw it, we'll use science. Part 2 of nI Heart email@example.com:blogger.com,1999:blog-1409654809690469042.post-15586659959585474872011-10-29T19:26:36.504-04:002011-10-29T19:26:36.504-04:00That is actually a really complicated question. A...That is actually a really complicated question.

A material like aluminum or injection molded plastic will generally have a uniform density and attributes such as the modulus of elasticity and yield strength do not change with respect to orientation.

3D printed parts however are anisotropic and the maximum tensile load in the Z axis could be several orders of magnitude less than if you applied the same load along the X or Y axis. The Z axis in this case would be the vertical axis through the extruder head.

The problem with trying to scientifically measure the mechanical properties is that most of the test equipment is designed to apply much larger loads so the measurements are often within the noise margins of the tensile test machine. If you are really interested I can try to find the test data I have, though I'm not sure how much insight can be gained from it.

Looking at it qualitatively instead of quantitatively he biggest problem fused filament fabrication machines such as the MakerBot, RepRap and StrataSys Prodigy Plus have for producing robust 3D printed parts is interlayer bonding. Different process such as SLS may be able to produce more isotropic parts.I Heart Roboticshttps://email@example.com:blogger.com,1999:blog-1409654809690469042.post-11135876483341683562011-10-29T17:17:36.704-04:002011-10-29T17:17:36.704-04:00This is of interest for building things. Do you k...This is of interest for building things. Do you know of anyone who has performed load tests on printed parts in general compared to molded or extruded parts?

The big question would be how much heavier a printed part would have to be to match the strength of the other.Lorenhttps://email@example.com


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Altered Book: purple.blue rev 2.0/
Is it OK to absolutely love your art journal? This book, this art journal. I love the look and feel, the textures, the colors, the quotes, I'm so happy with it! This quote inspires me (I would say "resonates" but... that's not my lingo), and it is something I am so guilty of... thinking about something, imagining it happening, yet not taking action. Lists. I make lists of things to do, pros and cons, the steps in a project. At work, I liked developing and tweaking and sorting and prioritizing the elaborate project plans (for process redesign) more than carrying out the plans. Right now there are a bunch of "wishes" swirling around my head, yet I don't take action. How do you kick yourself into higher gear?
You can see the original pages at purple.blue rev 1.1.


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Possibly as triumphant as ending World War II with a bomb made from plutonium developed here.
Eve Conant reports on the controversial mixture of uranium and plutonium—and the likelihood of its dispersal into the air.
I drank an International Proton Pale Ale and opted not to follow it up with a plutonium Porter.
When my oldest child was a toddler, I treated illuminated screens like plutonium.
In that time, we might give up our plutonium reprocessing plant but retain our newer uranium enrichment facilities.
They put the thorium block which contained the plutonium into the hole, the plutonium facing outward.
Now the conversion mass is all gone, and the plutonium's all spent.
Los Alamos scientists devised two designs for an atomic bomb--one using the uranium and another using the plutonium.
I wonder if he has any idea of what else plutonium can be used for?
After letting the temperatures of the plutonium and casing equalize the core slid smoothly into place.
transuranic element, 1942, from Pluto, the planet, + element ending -ium. Discovered at University of California, Berkeley, in 1941, the element named on suggestion of Seaborg and Wahl because it follows neptunium in the periodic table as Pluto follows Neptune in the Solar System. The name plutonium earlier had been proposed for barium and was sometimes used in this sense early 19c.
plutonium plu·to·ni·um (plōō-tō'nē-əm)
Symbol Pu
A naturally radioactive, metallic transuranic element, occurring in uranium ores or produced artificially by neutron bombardment of uranium. Its longest-lived isotope is Pu 244 with a half-life of 77 million years. Atomic number 94; melting point 640°C; boiling point 3,228°C; specific gravity 19.84; valence 3, 4, 5, 6.
Symbol Pu
A silvery, radioactive metallic element of the actinide series that has the highest atomic number of all naturally occurring elements. It is found in minute amounts in uranium ores and is produced artificially by bombarding uranium with neutrons. It is absorbed by bone marrow and is highly poisonous. Plutonium is used in nuclear weapons and as a fuel in nuclear reactors. Its longest-lived isotope is Pu 244 with a half-life of 76 million years. Atomic number 94; melting point 640°C; boiling point 3,232°C; specific gravity 19.84; valence 3, 4, 5, 6. See Periodic Table.
A radioactive chemical element that is artificially derived from uranium.
Note: Plutonium is used in nuclear reactors.


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King pips Forde in Golden Shears Speedshear
From Doug Laing, media officer, Shearing Sports New Zealand
February 27, 2014.
King pips Forde in Golden Shears Speedshear
Hastings shearer Dion King has drawn first-blood among the Open-class stars at the Golden Shears in Masterton by winning the event's first in-stadium Speedshear tonight.
King, among the favourites to win the 20-sheep Golden Shears Open final on Saturday, tonight shore a two-tooth ewe carrying about 2.2kg of wool in 24.7 seconds, to beat fellow finalist Darin Forde, of Winton, by just four-hundredths of a second in the Speedshear final front of about 500 people in Masterton's War Memorial Stadium.
The 2006 Golden Shears Open champion, he is the World nine-hour lambshearing record holder, with a tally of 866, shorn in 2007. Forde once set a nine-hour ewe-shearing record of 720, and the third placegetter, New Zealand-based Irish shearer Ivan Scott, holds the eight-hour lambshearing record, with a tally of 744, shorn in 2012.
King won $1000, Forde $600, Scott $400 and fourth semi-finalist John Kirkpatrick, of Napier, $200.
The big surprise was the quarterfinal elimination of veteran Te Kuiti shearer David Fagan who, having won about 10 other speedshears this summer, was more than three seconds quicker than the next-fastest in the heats, when his 27.6sec was the only time under 30 seconds.
Golden Shears Open championship favourite Rowland Smith, of Hastings, did not compete in the Speedshear, a short version of competition shearing most commonly seen as a pub sport.
Southland shearer Brett Roberts, of Mataura, won $500 as Senior Speedshear winner, with a final time of 29.1sec. Runner-up Kane Kapene, of Martinborough, shore 29.82sec in their showdown. South Island-based Masterton shearer and first-year senior Ethan Pankhurst had his event's fastest first-round time but was eliminated at the next stage.
The Speedshear was a warm-up to Friday's real action, including the Golden Shears Open and Senior championship heats.


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My name is Josh Frank, I currently am enrolled at Ohio University Lancaster. I am in the Business Mangement Technology program. I have only 3 classes left to take and I will be finishing them up after this Fall quarter. It has taken me 3 years to compelete a associates degree just because I have a lot of other stuff going on.
I currently am working at Lancaster Bingo Company. I have been there for a little over 3 years. It is a great job especially because they work around your schooling. The only bad thing about working around your schooling you have to work the hours of 3-11. However it is a great place for college students to work. They don't work you to much because they know school come first then work. Normally I work 3-4 nights a week, so it is just enough to keep me busy.
I also about a month ago recieved my real estate license and have been doing that a bunch lately. I am working for Century 21 Darfus Realty in Lancaster. My mom Melissa Frank is the top real estate agent at Century 21 so I didn't really get to slowing get welcomed I had no choice but to jump right in. I do really like real estate though and I believe after I have 20 transcations and after my 2 year degree I will go back to school for a few more classes and get my brokers license so I can have my own real estate company 1 day very soon.


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Home > Transportation > Bicycle Accessories > size 21.5x17x14.5 (l x w x h)cm bicycle bags boxes
|Product Name:
size 21.5x17x14.5 (l x w x h)cm bicycle bags boxes
|Packaging Details:
|Packing Method
|Delivery Detail:
|25-45 days after order confirmation
size 21.5x17x14.5 (l x w x h)cm bicycle bags boxes
bicycle handlebar bag Article No. B1018
Material: 600D
Size: 21.5X17X14.5 (L X W X H)CM
1.Three Velcro mounting straps
2.shoulder belt
3.Mesh pockets on the two sides
4. can be used waist bag
Professional Service
1 Reply your enquiry in 24 working hours.
2 Experienced staffs answer all your questions in professional and fluent English.
OEM Service
1 MOQ is 500 pcs/style.
2.Customized logo is acceptable. AI file is best choice. PDF, JPG is ok.
3 Exclusive and unique solution can be provided to our customer by your our well-trained and professional engineers and staffs.
4. Special instruction: some products can be MOQ 300pcs/tyle. But customized logo will has some cost of printing film.
Shanghai Zhifa Company Limited is the oversea sale office of Zhifa packaging company limited and Ningbo KT bicycle accessories factory. Our bike bag factory was found in 2010 and Ningbo KT bicycle accessories factory was found in 2006. Our company is focus on bike accessories for more than 10 years.
To bring more value to our customer, we are focus on designing and producing bike bags & bike tools. There are hundreds of new products are customized sold to our customer. We sincerely do our best to achieve win-win cooperation.
Our products have ROHS, REACH, MSDS and other certificate. Quality is the soul of our company. We believe stable quality with reasonable price.
To enable you to get a good understanding of our quality and service, we would like to can offer free sample (sample charge can be refunded).
Q:Can you offer free sample?
A: We offer some free sample to our old customer. Customized product will collect some charge.For new customer, we will collect some charge, if the formal order achieve MOQ, we can refund it from formal order.
Q:What about the leading time?
A:In general, the leading time is about 20 to 40days. But please confirm the exact delivery time
with us as different products and different quantity will have different leading time.
Q:How about the packing and shipping?
A:Normaly, product is individually packed into a polybag, then we use hard carton for packaging. Some small tools are put into a carton without polybag, such as tyre levers, tyre patches, etc. If you have any other special requirements, please feel free to contact with us.
Q:Can I have our own logo on the products?
A:That\'s ok to have your own logo on the products. Please contact with us to make sure the
detailed things before placing order.
Q:Can you make products obey my request?
A:Yes, we have a development team who has great experience in developing new products.
OEM/ODM are highly welcomed.
1. Before confirming the order, material and color should be check strictly through sample
2. Quality will be controlled from the beginning.
3. Every bell will be checked and cleaned before packing into the carton
4. Before shipping the clients could send a QC or point to the third party to check the quality.
1. We accept T/T, Paypal, and China domestic bank (RMB).
2. For small amount, if all in stock, we will arrange shipment in 3 days after payment.
For the sample not in stock, it needs around 7 days to make it.
For quanity amount, 30% pre-payment and the rest of payment needs to be done before delivery.
3. Make sure that you have completed all the detailed infomation such as contact person, address, post code. and phone number.
4. There are stock for bike tools which only takes around 3 days to deliver.
For the products not in stock, bike tools takes around 3 weeks to finish production and bike bags takes around 5-7 weeks to finish production.


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How simple is it to create an account with QuestionPro? Are you able to create a login within mere seconds? Once you're logged onto your account and ready to make your first survey, how easy is it to begin the process? Is it straightforward and simple to use, or are you bogged down by a confusing interface? Are you given various questionnaire designs to choose from to help?
With QuestionPro, you can do everything above and more!


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Baker's lung?
Does anyone know anything about Baker's lung/flour lung? I've been having some respiratory problems for the past three or four weeks - not like asthma, there's no wheezing - just tightness/constriction in my throat and chest. My DH made a link between when I got my grain mill...and I've been grinding wheat every day since then...and the coughing/constriction. It comes and goes, but it seems to be getting worse. Went to the doctor, and he didn't detect anything (wouldn't ya know...) and told me I'm perfectly healthy. It makes it tough to breathe. Does anyone have experience with this or links for more info?


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Search results for 'craftsman 27 inch 12 drawer vintage tool storage combo blue&12.5 - 22.0 Gal. tank size'
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text: Hey Folks, I've been tasked with upgrading a bunch of cvs clients on Win32. The old version we ran was cvs 1.11 (not CVSNT), the new version we want to run is CVSNT 2.0.51d. We've been hit with a permission denied error when people attempt to use CVSNT 2.0.51d to update a sandbox that was created with cvs 1.11. I have been able to resolve that problem by removing the readonly flags from all the files. (They were checked out with CVSREAD=1) It's strange that cvs 1.11 was able to understand this and CVSNT was not (regardless of CVSREAD being set)- and this is what led me start to worry a bit about sandbox compatibility between CVSNT 2 and cvs 1.11. I have a hunch that CVSNT is more than just slightly different than cvs 1.11. I noticed that CVSNT does create some extra files in the CVS directories that don't appear under cvs 1.11 (Entries.Extra, Entries.Old) Are we going to run into any problems if we have users use CVSNT 2.0.51d on sandboxes that were checked out with cvs 1.11? Is that supposed to work? Can you mix and match clients? Ideally I'd prefer if I could get all our users to just do a fresh checkout once they're upgraded, but I've been told that in some cases that is not practical. If I forego that step, am I setting myself up for a migraine in a few weeks? Thanks in advance, --adam


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Capital City Gastropub
261 New Scotland Ave. (Grove Ave.) Send to Phone
518-459-5077 | Make Restaurant Reservations
OpenDinner nightly
Open late Thurs.-Sat.
- Dress code: Casual
- Full bar
- Wheelchair accessible
* Click here for rating key
Capital City Gastropub Restaurant Review: This cozy spot with red walls and dark wood offers wines by the glass and craft beers on tap to complement an ever-changing menu. Owner-chef Kevin Everleth goes to great ends to obtain regionally-produced ingredients and lists source names to prove it. One might encounter house-smoked Sweet Tree Farm chicken; Berlin's Best rainbow chard tossed with buttermilk and horseradish, with compressed sweet potatoes; and Kilcoyne Farms beef Bolognese, gnocchi, Grana Padano, bone marrow and herbs.
Find out which restaurants and chefs top the list of GAYOT's 2016 Annual Restaurant Awards.


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Iced Audio has updated AudioFinder to v4.6.
- Added the ability to select and play a portion of audio in the AudioViewer.
- Added Export Selection to the Process menu.
- Added Control Key/Drag of selected AudioViewer audio to create new clips based on the selection.
- Fixed Autopilot stopping issue.
- Fixed Session Favorites bug.
- Other bug fixes.