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Is The Definitive Edition of DmC Worth The Price?
Frames Per Second isn't graphics. It's gameplay.
Is The Definitive Edition of DmC Worth The Price?
DmC: Devil May Cry: Definitive Edition is a remaster that comes with a visual upgrade for PS4 and Xbox One consoles. Is it worth the $40 when you can get the original for $20?
Huh. Guess PC version won't be getting a patch with those gameplay upgrades like targetable Stinger. The way it handles is so annoying.
BTW They should have called it DmC: Devil May Cry: Definitive Master Correction or something so we can have DMCx3
The original release was not worth full price, so I can't see myself purchasing a copy of this 'Definitive Edition' until it reaches a suitably low price point.
Capcom and NT did good by not shitting on the main audience for once (unlike several media outlets in the past), and this game now actually seems worthwhile if you're really itching for a decent beat 'em up game.
Having said that, I'm much more interested in hearing about DMC4:SE.
So... are any of these changes coming to PC? Because I'm holding out for a PC copy which is actually complete, and the graphical changes are irrelevant in that case.
On a side note, this is pissing me off. It's awesome that upgrades are being implemented into HD versions of games, but the fact that they aren't being put in the PC version is fucking ridiculous. I wouldn't even mind if they upgrades were a bit of DLC, but the fact that they are usually released as an entirely new games really irritates me. The Scholar of the First Sin is doing it, and my best guess is that DMC will be doing it too.
I tend to agree and somehow the Steam version is still priced higher for no reason. Your remark made me chuckle btw, very nice idea.
Character action games, or Spectacle fighters as some call them, live or die based on their framerates. The PS3 version Of Bayonetta is dead in the water due to this fact. But yes the 7th gen console versions almost seem like they never happened with this re-release, if the were in fact lowered to $30 I think it would sell better as well. But that's how Capcom works.
I wouldnt be completely against purchasing that.
Problem is, it doesnt seem to be coming to PC.
This actually sounds acceptable.On the other hand, if the DMC:4 re-release they have in the wings sells better than this one, hopefully they'll wise up and fix things for the next game in the series, so I think I'll just wait, and maybe pick this up pre-owned
The launch trailer was pretty cool, at the very least, if only for one reason.
I heard they got rid of Vergil's stupid hat too. That's a plus, right?
No, it isn't. Why? Because even after doing the basic things they should have done in the first place the game never rises above being mediocre. The real question is this: what can I play besides this? Well, there's Metal Gear Rising, The DMC: HD Collection, DMC4, God of War, Ninja Gaiden 1 and 2, and if you have a Wii U there's Bayonetta 1 and 2 as well as the Wonderful 101. Those are titles with more interesting enemy, fighting, level, weapon, and game design with a lot more flair and are just a lot more fun to play. Heck, at the very least hold your money for DMC4: Special Edition. There's no point in rewarding mediocrity like Ninja Theory's efforts when it's bottom-of-the-barrel in terms of the hack and slash genre. It also doesn't help that NT have made themselves out to be insufferable pricks who think they're God's gift to mankind with storytelling when in fact they've shown nothing but complete ineptitude in that area.
It is censored, so, no.
I loved this game to the point where I might consider buying this... I always liked the series, and I don't really see why everyone was so upset about it. The series as it was, was getting a bit tired honestly. The characters were a little different but you could feel how they might turn into the older characters in the future. I really would be interested to see a sequel if they did one. Is the story stupid? Absolutely! Sniper Rifle abortion? yeah that was a bit of a weird direction, but I didn't feel so weird about it in context, but then again I grew up on south park and worse, and I'm just not offended by creativity in this regard.
They removed Vergil's fedora, gave him a terrible reason for killing an unborn fetus, and censored some of the terribad dialogue. It's good for a laugh if anything!
But in all honesty, just wait for the superior DMC4 Special Edition featuring Vergil from the Devil May Cry Series... you know, a game that's gameplay was great upon release.
It's funny how NT laughed at criticism and told people to chill...but then caved in and did what they should have done in the first place. NT, when you get down to it, are just pathetic as a developer. They're not creative, they're not professional, and now they're forced to compromise on what they claimed was artistic vision because nobody bought their game. Though we all know this version isn't going to sell worth a damn so it seems to me like all that was accomplished was a waste of time, effort, and money. And NT doesn't seem to get it. THis is best exemplified in how they make excuses after every failure; Heavenly Sword flops and it's because it was a PS4 exclusive. Enslaved flops and it's CLEARLY because it's a new IP. Their attempt at a DMC reboot flops and now they're trying to self-publish some other piece of junk on the PS4. What excuse are they gonna make when that flops? I have never seen a dev make so many excuses.
Except everyone knows that's a lie; DMC4 was by far the most successful, financially, critically, and creatively. I still hold it as the benchmark for stylish action games and it had so many places to go with Dante handing off the torch to Nero. NT's efforts on the other hand are just stale. Rote, by-the-numbers junk that any amateur could make, and then is brought down further by a puerile script, unlikable characters, and junk design that impedes the player in the most obnoxious ways possible. And that was reinforced by the game bombing and becoming the least successful DMC in the series, not even reaching half of DMC4's numbers.
None, because once the numbers roll in and this flops, that's it. NT is done. It's pretty much been written in stone as of this day that DMC4 SE will be the money maker in this gamble Capcom is taking to see which direction DMC will go (countless other forums/old fans who grew up with DMC4 whom are hyped and ready to pay up for whatever the new version has to offer).
Honestly we shouldn't be bagging on DmC anymore, because DMC5 might as well be greenlit thanks to it's failure!
Oh they'll make excuses because that's what they've always done. My only guess is that they'll blame gamers as a whole next time because that's the last excuse they have. After the PR nightmare NT and Tam Tam created in the lead up to reboot attempt (seriously, Tam Tam's Twitter was just one juvenile tantrum after another as the weeks rolled on) I doubt anyone wants to work with them anymore. Now with DMC4: SE coming out and CAPCOM clearly even adding new content to it (the teaser was a brand new cinematic) it's safe to say that weird stage in the series' history is dead much like how the X-Men films wiped X Men 3 and Origins: Wolverine out of existence
Is that right? Lol my memory is a bit hazy but I seemed to remember a lot of people hating on 4. But on the other hand you may be right in that regard. But I strongly disagree that it wasn't well made. It may have been poorly written I don't think anyone would fight you on that but that was quite a fun game. Visually awesome, controlled great and was really shows very few cracks gameplay wise. I can't remember any bugs in particular and the ending was pretty alright. I mean I see why earlier dmc fans are upset and maybe it's a bad dmc game but bad game is a bit harsh.
No, it was a mediocre game at best and it selling the worst out of all the entries reinforced that. How people are more excited for DMC4: SE than this game's Definitive Edition speaks volumes. The game SUCKED; it has lousy weapon design, boring enemies with little strategy involved, moves at half-speed until NT was forced to speed it up for the Definitive Edition, and has at best half the depth and breadth of DMC4 (which is played in tournaments to this day). Wearing kid gloves with a mediocre game is not going to somehow turn it good. There's no point in defending a cynically made piece of junk, especially when it's bottom of the barrel in the hack and slash genre. There was no point in buying the game when it came out due to the existence of games like Bayonetta, DMCs 3 and 4, Ninja Gaiden 1 and 2, and the God of War series and the competition has only become more intense with titles like Metal Gear Rising, The Wonderful 101, and Bayonetta 2. It will forever be remembered as the time when CAPCOM had an aneurysm and handed off a great series to a hack developer like NT. No need to try and act like it was good.
For what it's worth, Tameem is busy on Hellblade, and thus had no input in the Definitive Edition. The DE was directed by the combat designer of DmC, Rahni Tucker, and the changelog (which has been released here) is pretty extensive. I'm really against insulting an entire company just for the actions of a select few. In fact, given the censored scenes, lack of stupid fedora, no fanbase insulting and the release of a changelog detailing every single change they've made, Tameems absence is EXACTLY what this game needed from the get-go. If (god forbid) we ever get a sequel, I'd prefer Tucker to take over, and an outside writer to handle the story.
Fortunately I don't think that'll happen, and I suspect we'll be getting some hints in DMC4:SE's trailers that's going to lead to a DMC5 announcement.
I don't mean to be insulting or escalate or trigger anyone when I say this but, I think this might be a bit of a spoiled point of view. I mean if you look at all the slew of big budget games that are completely broken. Your simcity's Diablo 3's Battlefield 4's, Halo's new compilation, games that were part of series that were completely unplayable, I don't think DMC is bad by comparison. And I understand what you're saying honestly, that compared to other games in that genre this game is slow and easy and uninteresting, but honestly compared to how broken, awful and just all around boring some games are today, DMC was a breath of fresh air. I mean play through watchdogs. That game is literally a game that exists without any purpose what so ever. Technically there is nothing wrong with watchdogs, hell some of the mechanics would have made GTAV even better, but story wise the game was so bland that I was pining for some stupid annoying character just to feel something other complete apathy for the plot. DMC at least had character, and when I say technically speaking, I mean it wasn't completely buggy, and didn't have some stupid always online connection or forced microtransactions, and while the combat system may have been the worst in the genre and the game may have sold the worst (incidentally it didn't though, the original re-release of DMC3 did) I think when you and I say cynical it means two different things. You're saying it's uninspired and I'm saying, it wasn't a cash grab.


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subset: commoncrawl


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Yes, but will they honor Joe Paterno?
MEMBER SINCE August 01, 2016
Recent Activity
I know, right! He just emotes all the right things.
It's been a hell of a ride.
Also, #Purduzzi knows a lot about emojis:
"Oh man, yeah. He's so cool! He even knows so much about emojis, he's good at it, I was kind of surprised. He's so down to earth. When I talk to him, he's just like a dad or an older brother. He's so cool," said Shields.
Maybe because Indiana busted up his ankle in the first half, so he was a little more reticent to keep it?
I don't follow hoops enough. Should an NIT bid be the minimum expectation with the inexperienced, but very talented, freshmen (+Watkins) on this team?
Don't want to get in the playoff? You guys are crazy.
I have a bad feeling about this game. I think Iowa's very much like Minnesota, and somewhat like Pitt. Their offense probably isn't as good as Pitt's, while their defense is probably better than Pitt's.
While the players have never done a night game at Happy Valley, Ferentz has been there done that. With an extra week of prep, he'll have them ready to go. This will be the toughest game left on the slate.
Great to see PSU at #12. Win out and I think they'll be in the NY6.
Also, happy that Purdue is holding off on their announcement.
I think we'll end up higher in the CFP rankings than where we are in the AP and Coaches. That will generate a lot more buzz, which I hope will not be overshadowed by Purdue's big announcement tonight that they have agreed to hire Pat Narduzzi to be their next head coach.
Disappointed that Hall didn't get Smith's thoughts on the big hire that Purdue's going to announce this weekend. Other than that, great interview.
But, what are their starzz????
Seriously though, and this may be a derp on my part, but is that list of players in the table above a list of PSU Hockey commits? Or are they all targets?
Meanwhile, let's also root for another loss or two (or three) for UNL and Wisky so that the Rose Bowl remains on the table for PSU. Need to pass them up in the rankings.
Right you are. Still disappointing for me, but less so.
Can't remember what I predicted, but I think it was a toss-up between 7-5 and 8-4. I'm firmly on 8-4 now, and 9-3 is very possible. 7-5 would be a big disappointment at this point, because it'd mean a loss to either Purdue, Rutgers, or MSU, and they all stink.
I thought he thoroughly outcoached Durkin. This team is far better in the second half, meaning they're able to make adjustments during the game. If anything, I've seen plenty of improvement on the coaching front this season. Talent and depth has a lot to do with that. But these guys are playing hard for Franklin.
With all the injuries, and youth on the roster to begin with, the 4-2 result with a very very close loss to Pitt has me very optimistic on where things are headed.
All the upvotes for Contellus.
It's so subjective, but a signature win just feels like a 'big' win for the program. A win people will talk about for years. A win that you know will boost recruiting. Completing the comeback vs. Pitt for me would have felt that way. But then it would be a win over a Pitt team that at this point would be 2-3. So is that really 'signature'?
If you go by the expectation of a win over a team that finishes in the top-10, then there are only a very small handful of coaches who get such a win each year. And they're not dealing with the sanctions, a hugh schism in the alumni base, and the stigma of IT.
And using that criteria--what's Harbaugh's 'signature' win? What's Larry Fedora's? Tom Herman's?
Would we be allowed to call a win here, given the injury issues and being a home dog, a 'signature' win?
Just don't have a good feeling about this one, but I haven't felt great about any PSU game this year save for Kent and Temple.
I will say I'd rather see PSU go up against a 4-0 MD team than one that's 1-3 with a win over Howard. Makes the games more intereting, and more meaningful wins = more 'croots.
It comes down to these next two weeks. Go 2-0, get some confidence back while heading into a perfectly-timed bye week. Maybe some guys get healthy, and get ready for OSU. Play OSU tough, and then things can really take off over the balance of the season.
But if they go 0-2, then we're realistically looking at a 5-7 or possibly 4-8 season. They could potentially get to 6-6 with guys like Cabinda and Bell coming back healthy. But recruiting will take a huge hit. More importantly, PSU will be trying to get a massive fundraising effort off the ground for this facilities revamp while the FB team is having its worst season in 12 years.
In other words, let's really hope for 2-0, and a better showing vs. OSU than what we saw last weekend.
Agreed on Zane. Not sure why they're once again slow playing a guy at a position they desperately need bodies, just to swing for the fences. If you take Zane and then get a surprise commitment from Hines or Anthony, then figure it out later.
This is a good taek.
PSU is at a crossroads because they didn't win the Pitt game. They could have lost 63-14 to Michigan, but if that came after a 3-0 start then nobody would be talking about being at a crossroads.
They need to go 2-0 these next two weeks, unless they plan on pulling off a stunner vs. MSU to close out the season.
Too lazy to look up, but I thought they had to forfeit that title.
Bill's right. Too late to edit my post. Both of those hires have shown progress so far, so that comment was way off the mark. I was just looking at Dykes' 1-11 debut season when I said that.
That's fair, and I was just coming back to edit my post on that. I saw he went 1-11 his first year there and didn't check the last two years. I should work at Pennlive!
And their BB coach took Cal to the Dance last year, so TBH those hires don't look too bad. And academics has only improved (from a strong starting point) under Sandy, Franklin, Chambers et al.
Very fair.
Let's just hope they go 2-0 the next two weeks and get back on track for a decent season.


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On Sunday afternoon at Iowa Speedway, there was no catching Matheus Leist as after taking the top spot on Lap 32, he drove away from the field en route to scoring the Mazda Iowa 100 Presented by Cooper Tires victory.
Here are some observations from the Indy Lights Presented by Cooper Tires event.
Matheus Dominates
With three victories in the last four races, Matheus Leist is finding his groove in Indy Lights after a rough start to the season with two finishes outside of the top-10. Now with eight straight top-seven finishes, the Carlin Racing driver has moved up to second in points, 13 markers ahead of Kyle Kaiser.
While Leist's wins at Indianapolis and Road America were impressive, the victory on Sunday goes beyond those. He did not have the best starting position, qualifying 10th, and managed to build a gap of 2.93 seconds ahead of Santiago Urrutia by the time the checkered flag flew. The gap could have been larger, but Leist elected to back his lap times down once he got the lead to conserve the tires.
Being almost three seconds ahead was enough to cause some confusion, though, as Urrutia thought he won the event, performing a series of donuts on the frontstretch post-race.
"When I went by (Dalton) Kellett, I thought that I had gotten the lead, so I thought, 'alright' because I had never seen Leist," Urrutia said post-race. "So when I get by Kellett, I tried to save a little and then thought we won at the end. But it's alright, we struggled today so to get back through there and a good solid finish, is a great result, and hopefully, we can run well in Toronto, too."
Rough Day for Rickards
Out of the 14 drivers that started, only one failed to finish the event, which was Garth Rickards. He went around for a quick spin on the backstretch at Lap 23, before pulling off shortly after the restart and retiring from the event.
"Right off the start it didn't feel right," he said. "It was loose. I tried to use the bars to improve the handling, but it just didn't work. It felt good in practice, but it was just undrivable there."
The 14th-place finish adds to the struggles this year for Rickards, who has posted only two top-10's in his rookie campaign.
Colton Leads Early
Before Leist making his way through the field, Colton Herta led the first 32 circuits from the pole and looked set to score his third victory of 2017 possibly. However, he would fade through the second half of the 100 lap event to a fourth-place finish.
"They had it figured out today," he said. "The car went loose on us, and there's not much that you can do on a short oval when that happens."
Herta started off his season well with two wins and a runner-up in the first four races but struggled with only one top-10 in the following four events. Now with back-to-back top-fives, it seems momentum is back on the young driver's side as he heads to the streets of Toronto for the first time in his career. The street circuit could be the right ticket to getting back in victory lane; his first career win came on the streets of St. Petersburg.
Debut Put on Hold
Chad Boat was supposed to make his series debut, but that was delayed till Gateway Motorsports Park.
The 25-year-old was not medically cleared by INDYCAR officials to drive due to injuries sustained during a National USAC midget race on Sunday, July 2.
"To say I'm disappointed doesn't begin to describe how I'm feeling right now, but I trust the doctors and medical staff at INDYCAR and know they have my best interest in mind," said Boat. "I'll continue to follow the instructions I'm receiving for recovery and look forward to being back soon. Thanks to Pristine Auction and Belardi Auto Racing for the opportunity."
Belardi Auto Racing team owner Brian Belardi added that he was "extremely disheartened" by the news, but "remains excited and positive about the future based on his pace in last week's test."
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I don't like seeing little boys in suits for formal events. It creeps me out a bit. I like little boys to look like little boys, not little men. They need to be comfortable – after all, they need to be able to skid across the dance floor on their knees to a hit from the 1980's and play chase with their cousins across a manicured lawn. For our sake too, it makes sense to put them in something a little less formal – when they stuff 20 cakes into their mouths at breakneck speed, followed by a few cocktail sausages dipped in ketchup and egg mayonnaise sandwiches for good measure, it's nice to be able to leave them to it without worrying about the dry cleaning bill.
So if you've got a wedding, christening, anniversary do, or other formal event this summer, here's a few ideas on how to dress your little boys…
1. Trilby Hat, £4.99, H&M (click here)
2. Striped Linen Shirt, from £7, Next (click here)
3. Flat Front Shorts, £12.95, GAP (click here)
4. Striped Sandals, £12.95, GAP (click here)
1. Bow Tie, £8, Mamas and Papas (click here)
2. Striped Shirt, from £40, GANT at John Lewis (click here)
3. Navy Chinos, from £8, Debenhams (click here)
4. Navy TOMS, £23, Office (click here)
1. Navy V Neck Jumper, £49, Ralph Lauren at John Lewis (click here)
2. White Polo Shirt, £3, Mothercare (click here)
3. Beige Chino Shorts, from £7, Next (click here)
4. Slip-on Sneakers, £14.95, GAP (click here)
Are you heading to a formal event this summer? I'd love to see a picture if you try out one of these looks!


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How to Move in Cuba
Transportation is a fundamental service for those who choose Cuba as goal of their vacation, that's why Casas de Cuba offers solutions to move in total freedom and security throughout the Island. Those opportunities that we propose are collective transfers, cars with drivers and also circuits or transfers by minivan or bus. We work with professional and punctual drivers. With the program "Cuba on the Road" We complete our proposals, the rental of motorhomes is a novelty to travel the island comfortably. Contact us and it will be our priority to advise you about the modality that matches your needs.


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Review by Ashley Friedman
Gina Cimmelli, a singer-songwriter out of Brooklyn, NY and Independent Music Award winner, brings us her latest single "Midnight" off of her recently released EP My Little Lies.
The song begins with a very rock and roll vibe. The drumbeat is both rhythmic, yet compelling. The cymbal plays an essential part throughout the piece as it ends the verses going into the pre-chorus and then the refrain. The electric guitar is subtle in the background, playing behind the drumbeat, but is strong enough to make a statement itself.
The song overall gives the listener the feeling that the singer is numb in the life she is living; There seems to be nothing exciting going on. The chorus "I just want to leave the earth / and all its gravity / find new friends in the stars and sleep for eternity, all eternity," is where we see that feeling the most. However, as the piece goes on, both the lyrics and instrumentals get stronger, and it gives the listener a feeling of excitement that the singer is going to get out of this "rut."
"Initially I set out to write a love song, but it just never came – and so the chorus has a different vibe from the verses – which are still sentimental & apologetic. For me, the chorus is about letting go and letting myself be," says Gina.
Gina's voice gives off a very electronic sound. With a touch of Regina Spektor, her voice is in the here and now, but has an old-school feel; a sound that many musicians today try to accomplish, but never quite get there. Gina, however, is an exception.
"I put a big wall / after a giant fall / protecting what's left / my solitude named miss berefted," is a verse that is almost a breaking point for the piece. It's here that Gina is facing the facts of what's happening, how she's living, admitting that there's an issue, and then in the lines that follow "it's alright darling / I'm still here / I'm still here, that's all that matters," is a subtle way of saying, life goes on, and that life isn't a rehearsal, "I'm still here," really puts that idea into perspective.
"This song was written as a way for me to explain myself to the people in my life who were worried about me. I think we all get to a point in our lives where the outside world just seems a bit too heavy and we just want to tuck ourselves away and not have to deal with life," comments Gina.
The song takes us for a ride on an emotional rollercoaster. At one point, we're sitting in a roller coaster, looking at the next hill, trying to prepare ourselves, and then there is that subtle build-up of us going up the hill, and then the drop is a rush of all of the emotions that got us there in the first place. The end of the ride is both reminiscent and invigorating, we're still here, but it took us a whole ride of emotions to get there.
Follow Gina Cimmelli


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Package Includes
- 1 x Electric Hand Blenders


text:
SecPod – Our 12 Year Experimental Journey
It has been 12 years since the inception of SecPod, The Company that aims towards implementing "Cyber Hygiene" across enterprises. Our journey has been all about experiments. Experiments and thoughts of various kinds: Can we build a company organically, become better each day and grow along? Can we build a respected Technology Company which […]Read More →


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JR Smith involved in three-way trade
The former Chicago Bulls coach confirmed the trade after the Knicks' loss to the Memphis Grizzlies, with the Cleveland Cavaliers and the Oklahoma City Thunder the other teams involved in the NBA trade.
The deal will see guards Smith and Iman Shumpert move from the Knicks to the Cavs with Lou Amundson, centre Alex Kirk and a 2019 second-round draft pick moving in the other direction.
New York will also waive Samuel Dalembert.
Additionally, Lance Thomas will swap Oklahoma for New York, guard Waiters will move from the Cavs to the Thunder, with Oklahoma sending Cleveland a future first-round draft pick.
The Knicks have a 5-32 win-loss record this season and Jackson said the trade should improve the team's fortunes moving forward, while also allowing them to regain control of their salary cap.
"As our journey moves through this season, we will search for the type of players that fit the style we hope to exhibit for our fans," Jackson told the Knicks website.
"Our desire is to improve our ability to compete. In addition, these transactions improve our flexibility to the current roster and the salary cap for future seasons."


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Prince's Estate Puts A Stop To The Release of EP
April 20, 2017
Tomorrow marks the one year anniversary of Prince's death and if you thought we were getting new music from him - not so fast! Prince's estate has sued the producer to stop the release of Deliverance, a new EP of unreleased songs that was supposed to come out Friday, November 21st. Their argument? They say that the producer is violating a signed agreement that says the songs belong to Prince. We knew this was going to happen…..oh well.


text: Each year upperclassmen studying World Languages at Kittatinny Regional High School in Newton create a World Languages Village. The village has a bank, ethnic restaurants, gift shops and tourist attractions so the underclassmen can practice their French, Spanish and German in a fun yet challenging atmosphere. Students are awarded Euros and grades based on how well they interact using their target language.


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Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) encodes a G-protein-coupled receptor (GCR) homolog. This protein is a potent, constitutively active signalling molecule that can influence both proliferation and angiogenesis when ectopically expressed in fibroblasts in vitro. Here we have examined the expression of the KSHV GCR gene in virus-infected lymphoid cells and in KS tumors. Our results show that in both situations the gene is expressed primarily during lytic replication; its transcription is unaffected by inhibition of viral DNA synthesis, indicating that it is expressed in the early phases of the lytic program. The major transcript bearing GCR sequences is bicistronic, harboring coding sequences for another viral gene, K14, at its 5′ end. Extensive searches for monocistronic GCR mRNAs using nuclease mapping and reverse transcription-PCR failed to detect such species. The 5′ end of K14/GCR mRNA maps to nucleotide (nt) 127848, and its poly(A) addition site maps to nt 130546; a 149-nt intron is present in the K14/GCR intergenic region. These results suggest that the KSHV GCR is translated by unconventional mechanisms involving either translational reinitiation, internal ribosomal entry, or leaky ribosomal scanning. The restriction of GCR expression to the lytic cycle has important implications for the potential role(s) of the GCR in KS pathogenesis.
Kaposi's sarcoma (KS), an endothelial tumor with neoangiogenic and inflammatory components, is a common neoplasm of AIDS patients. The epidemiology of KS strongly implicates a sexually transmitted cofactor other than human immunodeficiency virus in its pathogenesis (3). In recent years, a novel human herpesvirus, KS-associated herpesvirus (KSHV; also called human herpesvirus 8), has emerged as the leading candidate for this cofactor (8; reviewed in references13 and 37). KSHV DNA is found in all KS tumors, localized to the endothelial (spindle) cells of the lesion (5, 40). Infection is found at high rates in groups at high KS risk and much lower rates in the general population; in individual subjects, infection precedes KS development and is strongly correlated with increased KS risk (14, 15, 21, 26, 45). KSHV is a member of the lymphotropic gammaherpesvirus subfamily, which includes herpesvirus saimiri and Epstein-Barr virus. In keeping with this classification, KSHV has been linked to at least two lymphoproliferative disorders: primary effusion lymphoma (PEL) and multicentric Castleman's disease (6, 39). In the majority of KS spindle cells and PEL cells, the KSHV genome exists in a latent state, with only a small subpopulation of cells in either tumor displaying lytic viral replication (28, 34, 35, 40).
The viral gene products responsible for KS pathogenesis remain to be defined. Genes known to be expressed in latency (9, 10) include those encoding (i) LANA, the latency-associated nuclear antigen (20, 22, 33); (ii) v-cyclin, a homolog of cellular D-type cyclins (16, 24, 41); (iii) v-FLIP, a protein whose homologs impair caspase activation and programmed cell death (30, 42); and (iv) products of the K12 locus (46), whose biochemical activities are unknown but which may influence cell proliferation in vitro (29). In addition, KSHV harbors numerous additional genes that bear homology to cellular functions involved in growth control, signal transduction, and other regulatory processes (4, 13, 30-32, 36). One of these, open reading frame (ORF) 74, encodes a protein with homology to known G-protein-coupled receptors (GCRs), in particular several human chemokine receptors and an interleukin-8 receptor homolog encoded by herpesvirus saimiri (7). The KSHV GCR has been demonstrated to be a constitutively active receptor that signals through the phosphoinositide-inositoltrisphosphate-protein kinase C pathway (1). Mouse fibroblasts stably transfected with the KSHV GCR gene form foci, and these foci are tumorigenic in nude mice (2). Furthermore, expression of the KSHV GCR in such fibroblasts has been shown to induce secretion of vascular endothelial growth factor, a known mediator of angiogenesis (2). Based on these findings, it has been proposed that the KSHV GCR may be a key mediator of both the proliferative and angiogenic components of KS (2).
Here we examine the structure and expression of the mRNAs encoding ORF 74, which is located immediately rightward of a previously described cluster of latently expressed genes (Fig.1A) (10). We show that in the PEL cell line BCBL-1, ORF 74 is expressed as an early lytic gene. In keeping with this, in situ hybridization of BCBL-1 cells and KS tumors reveals that ORF 74 is transcribed predominantly in the subpopulation of cells that express lytic cycle genes. A detailed analysis of the fine structure of this transcript reveals that ORF 74 is the downstream gene of a bicistronic message whose 5′ gene encodes ORF K14, a homolog of the cellular OX-2 protein (36). The implications of these findings for the potential role(s) of GCR in KS are discussed.
Cell lines, plasmids, and probes.BCBL-1 cells, a B-cell lymphoma line latently infected with KSHV (23, 35), were cultured in RPMI 1640 supplemented with 10% fetal bovine serum, 2 mM penicillin, streptomycin and l-glutamine, 1 mM sodium bicarbonate, and 0.05 mM 2-mercaptoethanol at 37°C in 5% CO2. BJAB cells, an Epstein-Barr virus-negative (25) and KSHV-negative B-cell lymphoma line, were cultured in the same medium and conditions as BCBL-1 cells.
The KSHV GCR gene was subcloned from phage lambda 4, a genomic KSHV clone derived from a pulmonary KS tumor (46). A 1-kbBamHI fragment from clone lambda 4 (nucleotide [nt] 129211 to 130212, based on the sequence of Russo et al. [36]) was subcloned into the BamHI site of pBluescript SKII+ (Stratagene) to create plasmid pML14. pML14 was linearized withEcoRI within the polylinker and transcribed with T3 RNA polymerase and [32P]UTP to produce an antisense riboprobe for ORF 74. For a double-stranded DNA probe for ORF 74, the 1-kbBamHI fragment from pML14 was gel purified and labeled with DNA polymerase by using a random priming procedure (Rediprime; Amersham). The ORF K14-specific probe was made by cutting clone lambda 4 with SmaI (at nt 127909) and NdeI (nt 128320) to release a ∼400-bp fragment; following gel purification, this fragment was labeled by random priming as above. A probe for the K14/ORF 74 intergenic region was created by cutting a cDNA clone that contained the 5′ untranslated region of ORF 74 with AvrII (within KSHV sequences) and EcoRI (within the plasmid backbone) to release a fragment containing KSHV nt 128948 to 129214; following gel purification, the fragment was labeled by random priming as described above. To create a GCR expression vector for the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, the AvrII (nt 129215)-SacII (nt 130405) fragment from lambda 4 containing the entire GCR ORF and 156 bp upstream of the ATG was cloned into theXbaI-SacII sites of pBluescript (Stratagene) to create pML16. The insert of pML16 was subsequently cloned into an expression plasmid under the control of the SRα promoter (composed of the simian virus 40 [SV40] early promoter and part of the human T-lymphotropic virus type 1 [HTLV-1] long terminal repeat) to create plasmid pML17.
RNA preparation and Northern blotting.BCBL-1 cells were diluted to 2.5 × 105 cells/ml 12 h prior to treatment with 0.7 mM phosphonoformic acid (PFA) (19, 27) or mock treatment; 12 h later, half were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA; 20 ng/ml), and half were mock treated for 12 h. At that point, cells were washed and then maintained at a constant PFA level for another 48 h, at which time RNA was isolated by using RNAzol B (Tel-Test, Inc., Friendswood, Tex.) as recommended by the manufacturer. A 50-μg aliquot of each RNA sample was used for poly(A) enrichment using the Oligotex mRNA purification system (Qiagen) as recommended by the manufacturer; 1.5 μg of polyadenylated RNA that resulted from this purification was separated on a 1% agarose–17% formaldehyde gel and transferred to Hybond-N membrane for 12 h in 10× SSC (1× SSC is 0.15 M NaCl plus 0.015 M sodium citrate). The blot was then UV cross-linked and hybridized with the ORF 74 riboprobe in hybridization buffer (0.5 M NaCl, 5% sodium dodecyl sulfate [SDS], 6% polyethylene glycol 8000, 250 μg of salmon sperm DNA per ml, 50% formamide) at 72°C. After overnight hybridization, the blot was rinsed and then washed with 2× SSC–0.1% SDS for 15 min, with 0.5× SSC–0.1% SDS for 15 min, and finally with 0.1× SSC–0.1% SDS for 15 min. Subsequently, the blot was exposed to Kodak XAR5 film for 72 h.
cDNA cloning.The cDNA clones containing ORF 74 were isolated from a poly(dT)-primed library made by R. Renne from induced BCBL-1 cells in Lambda Zap (Stratagene). Screening was performed with the genomic ORF 74 BamHI fragment described above.
RNase protection assay.For ORF 74, plasmids to make riboprobes were constructed by using PCR to amplify fragments of genomic DNA from the lambda 4 subclone. For probe G1, primers KG1 (5′ GCGGTGCATCACCTACTTCAG) and GK2 (5′ CTCACACACGCTCSCTTCTAGGC) were created. For probe G2, the primers used were GCR2 (5′ CCCCTTCTGATTCTGACAGACAAC) and GK2 (see above). The PCR products were cloned into pCR2.1 (Invitrogen). The plasmids were linearized with the HindIII site from the polylinker and transcribed with T7 RNA polymerase in the presence of radiolabeled [32P]UTP. The riboprobes were purified on a 4% denaturing acrylamide gel and eluted from the gel for 12 h at 37°C in elution buffer (2.5 M sodium acetate, 0.5 mM EDTA, 0.5% SDS). The probes were precipitated with ethanol and resuspended in 10 μl of Tris-EDTA, and specific activity was determined. The RNase protection assay was performed essentially as described in reference1a. In brief, 5 × 105 cpm of each probe was added to 10 μg of total RNA that had been precipitated and resuspended in hybridization buffer. Hybridization was carried out overnight at 37°C, and then 300 μl of RNase solution (10 mM Tris [pH 7.6], 5 mM EDTA, 300 mM NaCl, 40 μg of RNase A per ml, 0.4 U of RNase T1 per μl) was added for 1 h at 60°C. The reactions were stopped with SDS and proteinase K addition, and the products were purified by phenol-chloroform extraction and ethanol precipitation. The samples were separated on an 5% denaturing acrylamide gel and exposed to film for 72 h.
5′ RACE.5′ rapid amplification of cDNA ends (5′ RACE) was performed on 2 μg of 24-h TPA-treated BCBL-1 total RNA. Primer KR5 (5′ CTGCAAAGCAGACACGCCTTCTT) was used for cDNA synthesis; primers K5-2 (5′ GATATAACTCCGCCCTCCACTACG) and 7306 (5′ CGCGGCGCCCGGGACAATC) were used for subsequent PCR steps as instructed by the manufacturer (Boehringer Mannheim Inc.). RACE products generated after two rounds of PCR were cloned into pCR2.1 (Invitrogen) and sequenced.
Primer extension.Primer extension was performed as described by Zhong et al. (46); 10 μg of total RNA from BCBL-1 cells that were either uninduced or induced for 24 h with TPA were used with the primer K5-1 (5′ GGCACCAATCAGAAAGTAGCTTG); 10 μg of yeast RNA was used as a control. The reaction mixtures were loaded on a 6% denaturing acrylamide gel and then exposed to Kodak Biomax MS film for 5 days.
S1 nuclease assay.S1 nuclease mapping was performed with an S1 mapping kit from Ambion (Austin, Tex.) according to the manufacturer's instructions; 10 μg of total RNA from BCBL-1 cells or BJAB cells treated with TPA for 24 h was used with the end-labeled primer SK3 (5′ GGAGGCAGCTGCGCCACGAAGCAGTCACGTCCCCAAGAGCAGCAGCTTGGTCCATT). Hybridization (12 h) and S1 nuclease digestion (30 min) were performed at 37°C. After the reactions were complete, the samples were separated on a 6% denaturing acrylamide gel and exposed to Kodak Biomax MS film for 5 days.
Reverse transcription-PCR (RT-PCR).Total RNA (0.5 μg) from TPA-treated BCBL-1 cells was first treated with RQ1 DNase (Promega) as recommended by the manufacturer. The RNA was then reverse transcribed with 10 pmol of primer GCRcR (5′ GAGTTTCATTCCAGGATTCATCATC) and 200 U of Moloney murine leukemia virus reverse transcriptase (Gibco BRL) for 35 min at 42°C as described by Dittmer et al. (10). The cDNA was then purified and resuspended in 100 μl, using a High Pure PCR purification kit (Boehringer Mannheim) according to the manufacturer's instructions; 10 μl of this cDNA was used in a PCR with primers K9 (5′ GCAGCTGCCTCCAAATGATACACAC) and GCR1 (5′ GAAGATGGTTAGGAAATCCTCGGC) plus 1 U of Taq polymerase and buffer (Perkin-Elmer). The amplification conditions were 30 cycles of 1 min at 94°C, 1 min at 65°C, and 1.5 min at 72°C followed by 10 min at 72°C. The amplification products were cloned into pCR2.1 (Invitrogen) and sequenced.
In situ hybridization.Riboprobes were generated by runoff transcription of linearized plasmid DNA containing ORF 74 (pML14), K12 (T0.7) (46), or nut-1 (46) inserts. Radiolabeled (to a specific activity of ∼109 dpm/μg) and nonisotopic probes were synthesized with 35S- and digoxigenin-labeled UTP, respectively. In situ hybridization protocols described in detail by Haase (18) were used for both tissue specimens and cultured cells. Briefly, 6-μm sections of a formalin-fixed paraffin-embedded dermal KS lesion from an HIV-infected individual were deparaffinized and pretreated in a series of solutions containing 0.2 N HCl, 0.15 M triethanolamine (pH 7.4), 0.005% digitonin, and 5 μg of proteinase K per ml. Slides with sections of BCBL-1 cells were pretreated with 0.2 N HCl–2× SSC at 70°C plus 1 μg of proteinase K per ml. The slides were then acetylated and hybridized for 16 to 18 h at 45°C with a solution containing 10% dextran sulfate, 50% deionized formamide, 20 mM HEPES (pH 7.4), 1 mM EDTA, 1× Denhardt's medium, poly(A) (1 mg/ml), 0.6 M NaCl, 100 mM dithiothreitol, yeast RNA (250 μg/ml), and 35S-labeled riboprobe (105 cpm/μl) or digoxigenin-labeled riboprobe (0.15 ng/μl). The slides were then treated with RNase, washed under conditions of increasing stringency, dehydrated, coated with photographic emulsion, and exposed at 4°C (40). For double labeling, slides were hybridized with a mixture of radiolabeled and nonisotopic probes. Following the posthybridization wash, digoxigenin was detected with alkaline phosphatase-conjugated antibody and nitroblue tetrazolium–5-bromo-4-chloro-3-indolylphosphate substrate (Boehringer Mannheim). The slides were then coated with photographic emulsion and exposed at 4°C to develop the radiolabel signal. The slides were stained with standard hematoxylin-and-eosin protocols or, in the case of the double label, briefly with hematoxylin alone.
MTT assay.Subconfluent Cos7 cells were transfected with a GCR expression plasmid (pML17) or the empty vector, using Lipofectamine (Gibco BRL) according to the manufacturer's instructions. At 48 h posttransfection, cells were trypsinized and resuspended in medium; MTT (0.3 mg/ml) was added with occasional mixing for 2.5 h. Cells were pelleted and lysed in 10% Triton X-100–0.1 N HCl in isopropanol. The A570 and A690 were determined spectrophotometrically. The assay was performed on two separate transfections, and the results are displayed as the means and standard deviations of these measurements.
Size and expression of ORF 74 mRNA.Because of the proposed role(s) of the ORF 74 gene product in the pathogenesis of KS (1, 2), we sought to determine the structure and temporal class of its mRNA. To characterize the expression of this mRNA, we examined polyadenylated RNA from BCBL-1 cells by Northern blotting with a probe specific for ORF 74. BCBL-1 is a B-cell line derived from an AIDS-related body cavity-based lymphoma that is latently infected with KSHV (23, 35); it can be induced to undergo lytic replication upon addition of phorbol esters such as TPA (35). The drug PFA is known to selectively inhibit viral DNA synthesis, leading to suppression of late gene transcription while immediate early and early genes remain unaffected (19, 27). BCBL-1 cells were mock treated or treated with TPA alone, PFA alone, or TPA plus PFA, and RNA was isolated from these cells 48 h later; 1.5 μg of RNA poly(A)-purified from each of the samples was separated on a 1.2% agarose–17% formaldehyde gel and transferred to a Hybond-N membrane. An antisense riboprobe for the coding region of ORF 74 was used to detect the ORF 74-containing mRNA. Figure2A shows a major mRNA species of approximately 2.8 kb hybridizing to the ORF 74 probe, as well as a much less abundant larger species of about 9 kb. The 2.8-kb mRNA is strongly upregulated by TPA (lane 3), suggesting that it is a lytic gene, and is unaffected by treatment with PFA (lane 4), indicating that it is not a late gene but rather an immediate-early or early gene. The same kinetics were observed when a duplicate filter was probed for a known early gene, the thymidine kinase gene (data not shown). The small amount of mRNA that hybridizes to ORF 74 in the absence of TPA (lane 1) comes from the 1 to 3% of cells in the BCBL-1 culture in which KSHV is spontaneously reactivated to lytic replication. The larger 9-kb mRNA is temporally coregulated with the major 2.8-kb species. We speculate that it may be derived by readthrough of the 2.8-kb RNA past its poly(A) site into 3′ sequences, since the poly(A) signal of the 2.8-kb species is a variant (AUUAAA) from the consensus AAUAAA (see below) that is known to result in a modestly reduced efficiency of polyadenylation (38). However, we have not characterized this RNA in detail, and other models for its structure are not excluded.
Since the ORF 74 coding region is only 1.0 kb, the 2.8-kb transcript was presumed to contain sequences for an adjacent gene. The best candidate for this gene is ORF K14, which encodes an OX-2 homolog, as it is the only adjacent ORF whose coding region has the same polarity as ORF 74 (Fig. 1A). To determine whether K14 is in fact part of the 2.8-kb mRNA, 5 μg of total RNA from TPA- and PFA-treated BCBL-1 cells was examined by Northern blotting using probes for K14 and for the K14/ORF 74 intergenic region. Figure 2B shows that the same 2.8-kb transcript anneals with probes for the K14 gene (lane 1), the intergenic region (lane 2), and the ORF 74 coding region (lane 3). The low-abundance 9-kb band is not seen here, presumably owing to the lower amount of RNA used in this experiment and the lower specific activity of the probes used. These results suggest that K14 and ORF 74 mRNAs are contained in a single 2.8-kb lytic transcript that is expressed early in viral replication.
In situ hybridization confirms that ORF 74 is a lytic cycle gene.The above population analyses were performed with RNA extracted from the PEL cell line BCBL-1. To determine the profile of ORF 74 transcription at the single-cell level, we performed in situ hybridization with antisense riboprobes. We found that only a few percent of the cells in uninduced BCBL-1 cultures contained detectable levels of ORF 74 RNAs (Fig. 3E). These cells, which colabel with probes for lytic genes (e.g.,nut-1 and the major capsid protein gene [not shown]), are the source of the low levels of ORF 74 mRNAs seen in the Northern analysis of comparable uninduced cultures (Fig. 2). As expected, TPA treatment induces ORF 74 transcription, consistent with lytic expression in these cells (Fig. 3F). To explore the relevance of these findings for KS, we examined primary KS tumors. Figure 3A shows that few cells in the tumor express ORF 74 mRNA, and these cell numbers are comparable to those expressing the known lytic gene, nut-1(Fig. 3B). In contrast, hybridization to a subjacent section with probe for the viral K12 (T0.7) gene that is transcribed in both lytically and latently infected cells reveals the large number of infected cells within the lesion (Fig. 3C). Double labeling with radiolabeled ORF 74 probe and digoxigenin-labeled nut-1 (whose expression is confined to lytic infection) probe confirmed that the ORF 74 transcripts are produced predominantly in those cells which are in the lytic cycle (Fig. 3D). This result accords well with that for BCBL-1 and suggest that most of the spindle cells in KS tumors do not express ORF 74.
Fine structure of the 3′ portion of K14/GCR RNA.To begin the study of the fine structure of the GCR transcript, we screened an oligo(dT)-primed cDNA library prepared from TPA-induced BCBL-1 cells, using a DNA probe specific for ORF 74. Six clones that contained ORF 74 sequences were isolated and sequenced; none was full length. The two longest clones (1.6 kb) were identical and included the entirety of the GCR coding region, together with additional 5′ and 3′ sequences. At the 3′ end of the clones was a run of T residues corresponding to the poly(A) tail; 29 nt 5′ to this poly(A) tail was a likely poly(A) addition signal, AUUAAA, at nt 130517. At the 5′ end of the two clones, just upstream of the initiator AUG codon for GCR, comparison of the cDNA sequence with the genomic sequence revealed the presence of a small intron of 149 nt, with a splice donor at nt 129219 and splice acceptor at nt 129367 (Fig. 1B). The splice donor and acceptor sites conform to consensus splice sites found in higher eukaryotes. (Of the four remaining cDNA clones, one was similarly polyadenylated but shorter, while the others bore evidence of 3′ deletions most likely due to rearrangements during cloning.)
To confirm the presence of this intron and to see if any unspliced RNAs were also generated from this region, we performed an RT-PCR analysis. Primers spanning the putative intron were used to amplify randomly primed cDNAs from both total and oligo(dT)-selected RNA from TPA treated BCBL-1 cells. Sequencing of the major RT-PCR product revealed that it was indeed spliced and confirmed the splice donor and acceptor sites determined by cDNA cloning (not shown). No products corresponding to unspliced RNA were detected.
Searching for monocistronic GCR mRNAs.Although the major RNA containing GCR sequences appears to be a K14/GCR bicistronic transcript, we were concerned that a minor monocistronic GCR mRNA might initiate within the K14/ORF 74 intergenic region. To search for such an RNA, we performed RNase protection across this region, using the antisense riboprobes (G1 and G2) depicted in Fig.4B. Both were transcribed from genomic KSHV DNA and shared a common 5′ end within GCR sequences, but they terminated at different sites within ORF K14 or the intergenic region. Each probe was hybridized to total RNA from BCBL-1 cells that were either untreated or treated with PFA and TPA. After hybridization, the samples were treated with RNases A and T1 for 1 h at 37°C and separated on a 6% denaturing acrylamide gel. As shown in Fig. 4A (lanes 1 and 4), hybridization with both probes G1 and G2 resulted in protection of a common 120-nt fragment representing the sequence 3′ to the intron. Each probe also generated a larger protected fragment (Fig. 4A); as depicted in Fig. 4B, these correspond exactly to the sizes predicted from protection by RNA segments arising from the spliced RNA in the region 5′ to the splice donor. No other protected species were detected in this analysis. Additional RNase mapping studies of this region, including studies using cDNA probes bearing the 149-nt splice (not shown), similarly yielded no evidence for any transcripts other than the spliced bicistronic RNA discussed above. In particular, we detected no start sites corresponding to the 5′ end of the 1.6-kb ORF 74-containing cDNAs that emerged from our cDNA cloning analyses; these are therefore incomplete cDNAs derived by premature termination during cDNA synthesis.
The 5′ end of K14/GCR mRNA.Given the location of the poly(A) addition site at nt 130546 and the approximate size of the transcript (2.8 kb), we estimated that the 5′ end of the RNA would lie just upstream of the K14 ORF. To search for the start site of the 2.8-kb transcript, we used primer extension, 5′ RACE, and S1 nuclease analysis. For the primer extension analysis, we used a labeled oligonucleotide (K5-1) located 81 nt downstream of the ATG of K14 (Fig.5B). Following annealing of this end-labeled primer to RNA from TPA-induced BCBL-1 cells and extension with reverse transcriptase, a single product of 116 bp was detected (Fig. 5A, lane 6); as expected, the amount of this extension product was greater with RNA from TPA-induced cells than with RNA from uninduced cells (Fig. 5A, lanes 5 and 6). There was no extension product in the control reaction with yeast RNA (Fig. 5A, lane 7). The size of this product, determined by comparison to the sequencing ladder generated by using the same primer, indicates a potential start site at nt 127848. A confirmatory 5′ RACE analysis (see Materials and Methods for details) yielded four clones, two of which terminated precisely at nt 127848, in excellent agreement with the primer extension (the sequences of the remaining two clones indicated that they resulted from mispriming).
Since both primer extension and 5′ RACE rely on the use of reverse transcriptase, which can prematurely terminate at RNA secondary structures, we used S1 nuclease analysis to further confirm the mapping. This was done by using an oligonucleotide of 53 nt (probe SK3 [Fig. 5C]) that spanned the putative start site at nt 127848. RNA from TPA-induced BCBL-1 and BJAB (a KSHV-negative Burkitt's lymphoma cell line) was hybridized to the 53-bp 5′-end-labeled probe and then treated with S1 nuclease. The resulting 32 ± 1-nt protected fragment, seen only in the BCBL-1 sample (Fig. 5B), confirms nt 127848 as the presumed start site and implies that the 5′ noncoding region upstream of ORF K14 is only ca. 35 nt. Transcripts initiating from this start site and polyadenylated at nt 130546 would result in a mRNA of 2,698 bp, which accords well with the estimated size of the transcript by Northern blotting. Importantly, this start site is 30 bp downstream of a recognizable TATA box. By scanning the region 5′ to this start site, we found several potential transcription factor binding sites, including an Sp1 site at nt 127755 and an AP-1 site overlapping the TATA box (Fig. 5C). Interestingly, the latency promoter directing ORF 73 (LANA) expression (10) lies in the body of the K14 ORF on the opposite strand. This finding raises the possibility that lytic cycle K14/GCR mRNAs have the potential to serve as antisense RNA regulators of the latency transcripts from the ORF 71–73 cluster, and tests of this hypothesis are in progress.
Searching for alternatively spliced GCR RNAs from the K14 promoter.Another potential way to generate a monocistronic mRNA for ORF 74 would be by alternative splicing from a putative splice donor within the K14 5′ noncoding region to a splice acceptor site 5′ to ORF 74 (for instance, the known splice site at nt 129368, just 5′ to the GCR AUG). To search for such spliced RNAs, we used a sensitive RT-PCR assay. cDNA was prepared from TPA-induced BCBL-1 RNA by using a primer in the body of the GCR coding region. PCR amplification from this template was carried out with an upstream primer from the K14 5′ noncoding region (K9) and a downstream primer just 3′ to the GCR AUG (GCR1). As shown in Fig. 6, the only PCR products detected were of a size expected from amplification of the full-length, bicistronic RNA species; no smaller species reflecting the splicing out of K14 coding sequences was observed. Sequencing of these products confirmed that they corresponded to the intact sequence between the primers. The longer species corresponded to the genomic sequence and may have resulted from the presence of nuclear pre-mRNA; the shorter species is identical in sequence except for the excision of the 149-nt intron previously described.
Consequences of GCR overexpression.The positioning of GCR coding sequences at the 3′ end of a bicistronic mRNA would seem designed to ensure their inefficient expression. To examine what would occur if the GCR gene was strongly expressed, we constructed an expression vector in which the SRα promoter (composed of the SV40 early promoter and part of the HTLV-1 long terminal repeat) was used to drive transcription of a monocistronic GCR message. This plasmid was transfected into Cos7 cells, which allow for additional amplification of expression based on SV40 DNA replication. Cell viability was assayed by the MTT assay, which measures the ability of viable cells to metabolize the compound MTT to formazan, which is detected spectrophotometrically (see Materials and Methods). As shown in Fig.7, substantial cell death was observed when GCR was overexpressed.
These studies demonstrate that the principal KSHV mRNA bearing GCR coding sequences is a lytic transcript composed of the coding regions of both ORF K14 and ORF 74, with the K14 gene located in the 5′ position. Extensive searches (by sensitive RNase mapping and RT-PCR approaches) for alternatively initiated or alternatively spliced RNAs in which ORF 74 would be the sole (or at least the 5′) coding region revealed no evidence for such transcripts, though of course the existence of such RNAs at levels below the detection thresholds of our methods cannot be formally excluded. The evidence points instead to the conclusion that the 2.8-kb RNA is likely functionally bicistronic, with the K14 gene translated by conventional initiation mechanisms and the GCR gene translated by nonclassical strategies, e.g., modified ribosomal scanning, translational reinitiation, or internal ribosome entry. Although unusual, this arrangement may not be without logic. Published data indicate that the KSHV GCR is a powerful and constitutively active signalling molecule (1). Presumably even modest levels of KSHV GCR would suffice to carry out its signalling functions, and overexpression of such a potent activity might even be deleterious. Indeed, in our hands, overexpression of the GCR in transiently transfected COS cells triggers cell death (Fig. 7). Thus, relegation of the GCR to the 3′ position in the transcript, where its translation would be expected to be inefficient, may be a strategy for ensuring levels of expression commensurate with cell survival.
The finding that KSHV GCR is a lytic cycle gene is consistent with observations in other herpesvirus infections. For example, cytomegalovirus encodes several GCR homologs as lytic genes (43, 44). The limitation of KSHV GCR expression to the lytic cycle has implications for its potential role(s) in KS tumorigenesis. Since most lytically infected cells eventually die, it is unlikely that cells expressing detectable GCR transcripts in KS will go on to proliferate—consistent with the observation that most spindle cells in KS tumors do not express GCR mRNA. Of course, it is formally possible that abortively infected cell types express some lytic cycle genes yet escape destruction; but even assuming that every spindle cell expressing GCR in a KS lesion is abortively infected (a proposition for which there is no evidence), this would still represent only a tiny fraction of proliferating spindle cells in the tumor. Still another model for how GCR expression could be linked to proliferation involves the induction and secretion of growth-inducing factors from GCR-expressing cells. However, proliferative effects from this mechanism would be expected to operate on uninfected as well as infected cells. As such, this model would fail to explain one of the central features of KS: that most proliferating spindle cells are latently infected with KSHV (5, 40). We therefore find it improbable that the viral GCR is principally responsible for spindle cell proliferation in KS tumors, despite its demonstrated ability to deregulate growth in 3T3 cells (1).
On the other hand, expression of GCR in lytically infected cells could have numerous and profound pathologic consequences for the two other components of a KS lesion: neoangiogenesis and inflammatory cell infiltration. Bais et al. (2) have clearly shown that GCR signalling initiates a program of cellular gene expression that culminates in synthesis and release of vascular endothelial growth factor. Clearly, paracrine release of such potent angiogenic factors from even a small subpopulation of cells could trigger dramatic neovascularization, a hallmark of KS histology. It is also conceivable that paracrine mediators released under the influence of GCR signalling have effects on inflammatory cell infiltration. We think it much more likely that GCR plays its role in KS pathogenesis by these paracrine mechanisms than by cell-autonomous effects of GCR expression.
Finally, regardless of any potential role in KS pathogenesis, lytic cycle GCR expression likely plays additional roles in the KSHV life cycle—a cycle which in normal immunocompetent hosts is largely played out in lymphoid rather than endothelial cells. The cellular chemokine receptor, Burkitt's lymphoma receptor 1, is known to regulate the migration of B cells both systemically and within lymphoid organ microenvironments (11, 12, 17). If the product of ORF 74 shares this function, then perhaps its expression during lytic reactivation would provide a mechanism to home virus-laden cells to lymphoid organs, where the released viral progeny could more readily infect other susceptible B cells. Alternatively, GCR-activated signalling pathways may result in the activation or induction of host and/or viral proteins that upregulate lytic growth. Decisive tests of the role of the GCR in viral growth and KS pathogenesis will likely require the development of genetic systems for constructing and propagating mutations in individual viral genes.
We thank Dirk Dittmer and Rolf Renne for technical assistance and the remainder of the Ganem lab for helpful discussions.
J.R.K. was supported by funds from the National Institutes of Health (grant T32GM08568). D.G. is an investigator of the Howard Hughes Medical Institute.
- Received 25 January 1999.
- Accepted 25 March 1999.
- Copyright © 1999 American Society for Microbiology


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Diaper Drive: Communities come together in Conway | News
CONWAY, Ark. (KTHV) -- We are in the home stretch of the THV Diaper Drive. Cabot and Maumelle collected more than 44,000 diapers, and now it's Conway's turn.
Liz Massey was live at the Walmart on Highway 65 North trying to raise 100,000 diapers. And communities all over the state are contributing in a big way.
Immanuel Baptist Church in Little Rock recently held a diaper shower to help out. And workers from Kimberly Clark plants in Maumelle and Conway held a friendly competition to see who could donate more. They've got a special delivery of about 10,000 diapers and 20 pallets of wipes.


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Kaisha Murzamadiyeva
Ornek is a display typeface in the newly proposed Kazakh Latin alphabet. The word Ornek translates to ornament in Kazakh. This typeface and these specimen posters are inspired by the patterns and colors found in traditional Kazakh tapestry.
In 2017, my country, Kazakhstan transitioned from a Cyrillic to a Latin-based alphabet. This isn't the first time the country has switched alphabets. At one point, the official language was Arabic. When the new alphabet was announced, I saw an opportunity to create a new typeface.
Throughout history, my country's culture has constantly been influenced and shaped by other cultures. As a result, many of our traditions have been lost. I wanted to create Ornek, not only as a tool for people but also to preserve the essence of Kazakh culture during this transition period.
I drew inspiration from the ornamental patterns found in traditional wool rugs known as "Shyrdak," which are felted by Kazakh women. The crafting of wool rugs is a very labor-intensive tradition, that is still done today. These rugs are known to be vibrant in color and embellished with patterns, which I tried to emulate within my letterforms and specimen posters.


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New York, NY (PRESS RELEASE – August 19, 2009) – Twenty entrepreneurs have advanced to the second stage of Forbes.com's third annual "Boost Your Business" editorial contest, available at http://www.forbes.com/byb.
Visitors to Forbes.com can now vote for the five companies most poised for growth among the 20 semi-finalists. Their submissions, including self-recorded 30-second "elevator-pitch" videos, are available for review at http://www.forbes.com/byb. Voting for this round runs through September 30.
Contestants represent businesses in various industries–from nurse-concierge services and online book rental, to enterprise software and yoga accessories–and are headquartered around the country.
"The quality of our contestants gets better with each passing year," said Brett Nelson, Entrepreneurs Editor at Forbes. "We wish them luck in the second round. Captivating our savvy readers in only 30 seconds on video is no mean feat."
In the first round of the contest, which began in May, entrants submitted a 500-word write-up about their small business, including a description of the business model, current capitalization and theoretical plan for investing the prize money. From the 20 semi-finalists who made it to the second round of the contest, five finalists will be selected to compete for the grand prize.
Those five finalists will be flown to New York City to give live presentations to an expert panel of judges. The winner will receive $50,000 in cash and $50,000 in advertising on Forbes.com. The 2009 BYB contest is sponsored by Comcast.
Forbes Media
Forbes Media encompasses Forbes and Forbes.com, the #1 business site on the Web that reaches more than 18 million people monthly. The company publishes Forbes and Forbes Asia, which together reach a worldwide audience of more than 5.5 million readers. It also publishes ForbesLife and ForbesWoman magazines, in addition to licensee editions in China, Croatia, India, Israel, Japan, Korea, Poland, Romania, Russia and Turkey. Other Forbes Media Web sites are: ForbesTraveler.com; Investopedia.com; RealClearPolitics.com; RealClearMarkets.com; RealClearSports.com; and the
Forbes.com Business and Finance Blog Network. Together with Forbes.com, these sites reach nearly 40 million business decision makers each month.
- Onsite Nurse Concierge Dove Canyon CA
- Green Paper Studio Bethesda MD
- Naturally Bamboo Mankato MN
- i-Nalysis Concord MA
- NuBarter Savannah GA
- Plank Charlestown MA
- NuClimate Air Quality Systems, Inc. East Syracuse NY
- Audissey Guides Boston MA
- GreenSoul Shoes New York NY
- GiftCardRescue.com Ellicott City MD
- Base Brands Atlanta GA
- Healthy Life Screening Akron OH
- BookSwim Newark NJ
- INeedAPencil.com Cambridge MA
- Earthborn Studios, Inc. Leeds AL
- Plastic Jungle Mountain View CA
- ReadyPing Chicago IL
- I Want A Better House Nashville TN
- Encore Path Baltimore MD
- Ksplice Cambridge MA


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Five months before Bon Iver, A$AP Rocky and Jorja Smith are welcomed to the City of Iron from 19-21 July 2019, Melt, once again, proves its unique standing on the European festival circuit with Kaytranada, Virgil Abloh, FKJ, Yung Lean and HVOB completing this year's lineup, a standing based on the innovative and diverse fusion of the Ferropolis backdrop with a musical zeitgeist which omits any kind of genre definitions. This year, Melt welcomes over 120 artists on the peninsula at Lake Gremmin, anticipating a unique diversity which only emerges here in Ferropolis – the ultimate reason for fans from across the world to travel to Melt Festival each year. Want to come along? We're giving away 2×2 tickets for the weekend. Just email email@example.com to enter.
Naturally, Melt's lineup includes female representatives of their generation, like soul singer Mahalia, techno DJ Honey Dijon and dream pop duo Ider. Aside from the musical programme, Melt spreads the idea of limitless freedom and love: at the Melt Forest, one of last year's highlights, Pornceptual and drag queen icon Pansy take the wheel.
Above all, Canadian producer Kaytranada, whose musical scent you can smell even five kilometres against the wind, will celebrate his only festival gig at #melt2019 with his debut album "99.9%" and his current "Nothing Like U/Chances" EP in tow. We can already tell you one thing: Kaytranada has never failed to lure a crowd to the dance floor.
He might be young, but he's got stories to tell. Yung Lean conquered the world with his take on cloud rap starting in Sweden, becoming one of the most defining rappers of generation internet. Within six years after the release of "Ginseng Strip 2002", he has expanded his horizons and, alongside his new song "Creeps Creeps", released a classic indie/rock record under the guise of Nectar breaking down all genre borders. Yung Lean will only play one show in Europe, and it's going to be at #melt2019.
Through running his own clothing label Off-White and working for Louis Vuitton as creative director, Virgil Abloh has arrived on the Olympus of fashion. When it comes to music, the multi-talent has also made an impact working together with his buddy Kanye West. At #melt2019, we can look forward to one of his rare appearances and a smashing DJ set packed with hip hop, grime, trap and soul, which will no doubt echo as far as Berlin.
Also, one-of-a-kind experiences await off the main stages. The Black Madonna will curate the entire Sunday lineup at the "Big Wheel" stage under the banner of "We Still Believe" featuring Jennifer Cardini amongst others. On Saturday, DIYNAMIC label owner Solomun will take over the Sleepless Floor together with his crew comprising Magdalena and Adana Twins followed by the Hessle Audio-Takeover with Ben UFO and Shanti Celeste on Sunday. This year, we'll celebrate our pre-party with Bonobo (DJ), Kink (live) and many more. On top, we welcome up-and-coming artists such as slowthai, Flohio, Nilüfer Yanya, Benjiflow and Duckwrth on the "Highsnobiety Soundsystem" Stage.
Over the past years, the Melt Forest has become one of the festival's outstanding highlights. From early afternoon until the wee hours of the morning, the forest is a hub of music, love, freedom and adventure. After last year's huge success, drag queen Pansy and the artist collective Lotenheim will return, and with Pornceptual, we'll finally create a space for sexual self-discovery Berlin style. A takeover by Wilde Renate promoters Paper is, of course, an absolute must, too.
Complete lineup at a glance:
A$AP Rocky, Adana Twins, Agar Agar, Ama Lou, Angel-Ho, Arca, Auntie Flo, BenjiFlow, Bilderbuch, Bluestaeb B2B Melodiesinfonie B2B S. Fidelity, Bon Iver, Bonobo (DJ), Boy Pablo, Cari Cari, Cashu, Charlotte De Witte, D.Y.A, David August, Denis Sulta B2B Eclair Fifi, Die Achse, DJ Lag, Donna Leake, Dr. Rubinstein B2B Tijana T, Dubfire, Duckwrth, Elderbrook, Ellen Allien, Emma Isabella, Erotik Toy Records, FJAAK (Live), FKJ, Flohio, Four Tet, Giant Rooks, Giant Swan (Live), Gus Dapperton, HAAi, Helena Hauff, Hessle Audio (Ben UFO, Pangaea, Pearson Sound, Shanti Celeste), Honey Dijon, HVOB, Ider, Inga Mauer, ItaloJohnson, James Vickery, JASSS, Jennifer Cardini, Jimothy, Job Jobse, Johannes Albert, Jorja Smith, Kampire, Kaytranada, KiNK (Live), Kobosil, Kollektiv Turmstrasse, Lehar & Musumeci, Lemaitre, Leon Vynehall, Live From Earth Klub (Bauernfeind, DJ Gigola B2B Wolfram, MCR-T), Lyzza (DJ), Magdalena, Magit Cacoon, Mahalia, Mall Grab, Mano Le Tough, Mareike Bautz, Masego, Modeselektor (Live), Monolink (Live), Mor Elian, Moxie, Myss Keta, Nilüfer Yanya, No Vacation, Normal 4 & Bufiman (Live), Octo Octa, Octavian, Oshun, Ozelot (Abdel Hady aka Iceman, Manuel Fischer, Prioleau), Pardon Moi (Live), 박혜진Park Hye Jin, Parra For Cuva, Peach, Peak & Swift, Perel, Rin, Ross From Friends (Live), Sally C, Skepta, Slowthai, Solomun, SRVD (Live), Stephan Bodzin (Live), Sudan Archives, Tereza, The Black Madonna, Tiffany Calver, Tom Trago (Live), Tornado Wallace, TRP, Tua, Vaal, Virgil Abloh, Virginia, Yung Lean
Bonobo pres. Outlier: Bonobo (DJ), KiNK (Live), Mano Le Tough, Perel, Sally C; Forest Stage pres. by Paper; Pansy's Playhouse; Pornceptual pres. The Secret Garden of PORN; Sensi Stage pres. by Lotenheim; Solomun pres. Diynamic Takeover: Solomun, Adana Twins, Dubfire, Kollektiv Turmstraße, Lehar & Musumeci, Magdalena, Magit Cacoon; The Black Madonna press. We Still Believe: The Black Madonna, HAAi, Jennifer Cardini, Octo Octa; Salon – Zur Wilden Renate Takeover: Alison Swing, Marlon Hoffstadt, Peak & Swift, Sebastian Voigt
Early Bird Tickets (price level 1) have already sold out. Tickets to Melt Festival 2019 are currently available at EUR 129 or as 4 Friends Tickets at EUR 479. Day Tickets are available at EUR 69 and VIP Tickets at EUR 239, which include VIP camping, VIP area access at the festival grounds and more.
To check out all ticket categories as well as our lineup, go to www.meltfestival.de


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Tips for Perfectly Melted Chocolate in the Microwave
Whether you're making chocolate covered strawberries or you're making chocolate truffles, melting chocolate in the microwave is a time-saver. We have a few tips to doing it well.
Melting chocolate in the microwave can be tricky even if it sounds simple. Chocolate burns easily — and chocolate going to waste would be a shame, right?
If you want to melt chocolate the right way, you should use a double-boiler. It's the most reliable way of melting chocolate — but it's not the fastest method. With a double boiler, you heat the chocolate in a heat-safe bowl over hot water so the chocolate slowly and gently melts without burning. But we don't always have time for the best method for melting chocolate. Sometimes what you want is the fastest good method. Using the microwave is definitely a time-saver and it works well if you follow these simple steps.
Melting Method
- Set your microwave oven to 50 percent power. Chocolate is very easy to overheat, and low heat makes the melting process much more manageable.
- Place your chocolate chips or chocolate bars in a microwave-safe bowl. Microwave the chocolate in 20 to 30-second intervals, mixing the bowl of chocolate with a completely dry utensil between every heating session*. Chocolate retains its shape when heated this way, so you need to mix it to test its structural integrity. If you are able to mix most of your chocolate pieces, just keep mixing until it has a smooth consistency. The remaining chips will gradually melt.
- Decrease the time intervals in which you heat the chocolate with every session. Start with 30 seconds, go to 20, and 15, and 10, and so on.
- Use a rubber spatula to remove all of the melted chocolate from the bowl.
*If enough water comes in contact with your chocolate, it will become grainy and unusable.
Tips and Tricks
- Find a good, microwave-safe bowl that doesn't retain too much heat. Glass bowls work well. If your bowl gets too hot, it could overheat your chocolate, too. This has more significance with large batches of chocolate.
- Overheated chocolate can be extremely dry and unpleasantly chunky. If your chocolate is only slightly overheated, you might be able to save it by adding in a little vegetable oil, but it's not a guarantee.
- Dropping a little bit of vegetable oil onto the chocolate before you microwave it will give you a bit more room for error.
Get Melting
Now that you know the tricks to melting chocolate, there are thousands of recipes on Yummly to explore with your new skill. Here are some for inspiration.


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TV Series Hidden Identity Seasons 1,2 All Episodes for Download
Hidden Identity seasons list:
Looking for the Hidden Identity TV Show? Seasons 1,2 are available for downloading in good and high hd quality, select the season number below.
Hidden Identity screencaps
The ideal crime is certainly a myth that is unlikely to be debunked. Elusive criminals do not happen, but there are those who are very difficult to catch, because they skillfully confuse the tracks and continue to kill innocent people while the police are trying to find at least one clue. For such cases, there is a Department-detectives, which are not in any list. They do not appear on the post and live all his life under cover. Nor present behalf of, nor fate – and meanwhile they are building family, give birth to children and even work on simple positions. And only in extreme cases, when the search for another maniac come to a standstill, they are activated and begin their investigation. A young guy named Gong Woo has always been a simple policeman. He guarded the city and watched over the safety, but failed to protect the only girl he loved with all his heart. Her death was a fatal blow in the fate of our hero. He tried to find the criminals, but all was in vain, however, soon appeared in the case of an unusual lead. Brother of the deceased shared with our hero that hired a special team of detectives who are now investigating the case. So gon met with a special Department, which soon fascinated him so that the guy even asked him to work. Now he is part of an unusual team of professionals who investigate the most serious crimes.
Televison show Hidden Identity seasons available for download - 1,21 seasons
Hidden Identity Season 116 EpisodesDownload


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"In the Ljubljana of the eighties, one could trace projects that were based on the idea of reconstruction of famous art works of the avant-garde art tradition. The examples of such happening are the projects that took place in 1986 in Galerija ŠKUC – The Last Futuristic Performance by Kazimir Malevič, the international exhibition of modern art (Armory Show) and the lecture Walter Benjamin: Mondrian '63 – '96. The author (authors?) of the projects remains unknown to the wider public; he namely uses the names of famous, but already deceased artists. The whole affair is a trend and research in the field of contemporary art, that is totally parallel to the world trends – artistic concepts. The author (authors?) has presented himself in New York in the nineties with the concept Salon de Fleurus, a project of paintings reconstruction and the ambient of a Paris apartment (on the Fleurus street – Rue de Fleurus) of Gertrude Stein from the beginning of the 20th century. In this case, the issue is an extraordinary fictionalization of history, an almost theatrical staging of a literary myth from the beginning of the century, that nevertheless poses key questions about the birth of modern art and the present system of observation of art production."
From the Introduction, by Marina Gržinić Mauhler
Marina Gržinić Mauhler is a philosopher, media artist and theoretician from Ljubljana. She works as a researcher at the SAZU Institute of philosophy.
Marina Gržinić: Salon de Fleurus in the private lot in Soho, New York: from fiction to virtuality
Marina Gržinić: W. Benjamin, Kazimir Malevich, Mondrian and other contemporary spectral figures and icons – theses
Timothy Druckrey: Stop playing these games as well
Hito Steyerl: Babylon abyss
Georg Schöllhammer: Trade roads after the sixties of the 20th century. Seven sketches on the exchange of cultural goods
Maria Klonaris, Katerina Thomadaki: Cinematography of the body: metabody art. Retrospective view
Goran Djordjevič: Cubism and abstract art. The first ethnological exhibition of modern art
0100101110101101.org: Talk with 0100101110101101.org
Michael Fehr: Mounting from the ruins
Borut Vogelnik: IRWIN Retroavantgarde
Marina Gržinić: Does contemporary art still need museums?
Lev Manovich: Avantgarde as software
English - Slovene edition.
184 pages, 170 x 240 mm, 20 b&w reproductions, paperback


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Do you know your computer which program are connecting internet? Here will showing you two sets of free-to-use network monitoring program – Currports and Moo0 ConnectionWatcher, which allows you to easily understand the program using which port and the network traffic .
1.Currports is a standalone executable program ( 55KB ) .It displays the list of all currently opened TCP/IP and UDP ports on your local computer and allows you to view a list of ports that are currently in use, and the using application . You can close a selected connection , terminate the process and export all or selected items to a HTML or text report. Additional information includes the local port name, local/remote IP address, highlighted status changes and more.
Download Currports and supports Window 2000/2003/XP/Vista .
2.Moo0 Connectionwatcher is developed by a Japanese that enables you to watch over any TCP/UDP connection from/to your PC.using this software,you may discover which software sends/receive information with whom in details.
Right click on the item of connection process will showing you 'locate program' , 'disconnect' , 'Close program' and ' Kill program' in details.
Download Moo0 connectionwatcher and supports window XP/Vista.


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Dana M. Edwards
Digital Media Strategist | Integrated Communications Marketer | Graphic Designer
About Me
Book Recs
Work Examples
viral videos
Scheduling In-Text Videos on Twitter
July 19, 2016
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How using a video to promote an event set a record social media engagement rate
October 27, 2015
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Federico Delbonis beat Paolo Lorenzi 4-6, 6-3, 6-4 to win the Brazil Open 2014 title.
Delbonis broke Lorenzi's serve to start the decisive set and held on to close the match in 2 hours, 6 minutes after converting on his second match point.
Delbonis celebrated a nearly perfect week in which he also reached the semifinals in the doubles tournament.
"To tell you the truth, I have no words," Delbonis said. "I played well match after match. It was a great result in the end."
The 23-year-old lefty was playing only in his second ATP final. He had lost to Fabio Fognini last July after upsetting Roger Federer in the semifinals in Hamburg.


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Andrea Rossouw - What has HIV Aids shown us about ourselves
Add to Cart Gift to Someone
Price: €1.00
Price: €1.00
Our physical bodies are in the process of supporting us one and equal in aligning ourselves here as the physical. Within this we will find that when we participate in the mind according to realities of the mind and disregard the actuality of the physical – this is where we will find ourselves faced with illness, disease and accidents.
This product is delivered electronically. There's no shipping involved.


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Dandong Nondestructive Testing Equipment Co., Ltd.
X Ray Tube Inspection,X Ray Inspection,RTR Inspection Tube
|Payment Type:
|L/C,T/T,D/P,Western Union
|Min. Order:
|1 Set/Sets
|Delivery Time:
|15 Days
Model No.: XYG-320
Portable: Portable
Form: Portable
Application: Industrial
Type: Industrial High-definition X-ray Detector
Certification: CE, ISO
Customized: Customized
Alarm Form: Display Alarm
Working Way: Continuous Working
Cooling Way: Oil
Radiation Method: Filming/RTR
Voltage: 320KV
Packaging: WOODEN PACKAGE
Productivity: 100
Brand: JUXING
Transportation: Ocean,Land,Air
Place of Origin: DANDONG
Supply Ability: 100
Certificate: ISO9001
HS Code: 90221990.00
Port: DALIAN,SHENYANG,BEIJING
Metal Ceramic X Ray Tube Inspection Product Line
The RTR Inspection Tube which shown on pic is one of mainly part of industrial DR machine. it is exposure producing part of machine. with over 30years experience, DNDT can cooperates with many international brand X Ray Tube Inspection supplier, meanwhile we have our own production,testing and repairing line of this important part. the famous brand such as Thales, Amerian Varian, Switerland COMET and x ray source from some Japan company.
DR machine brief configuration and data:
Pic of unit:
Product Categories : X Ray Tube


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|Property is theft
|Property is sacred
|Any government is bad
|Capitalists are baby-eating villains
|Capitalists are noble Nietzchean heroes
|Workers should rule
|Worker activism is evil
|The poor are oppressed
|The poor are pampered good-for-nothings
For the longer version, you can read What's wrong with libertarians.
Or again, for a shorter version, here's my only slightly tongue-in-cheek take:
- Anarchist
- Unemployed Libertarian
- Libertarian
- Employed Anarchist
I might add that I pulled the link from this discussion. It's really sad how completely incapable people are of reading something and seeing past the little things which cause knee-jerk reactions. There wasn't much intelligent rebuttal in that thread.
My favorite comment in that thread was where a poster claimed that corruption in a Libertarian society could be avoided by keeping a clear separation of business and government because -- make sure you're not drinking anything when you read this -- "corruption only spreads to areas in which they can obtain both political and economic power".
Of course, if you're the captain of the U.S.S. Make Shit Up, you can steer to any port you want. Comments like that are worthy of the Randroids.


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This is a full cleansing amulet that will radiate the follicles of power in your body through connecting this piece with your brain waves --this will break down any potential blockages caused by negative energies and strong forces of emissivity.
Designed to implement your body with one week, you will relinquish all viable components that have brought forth the negative energies that have entered you ... and they will be extracted from within~!
Great piece, especially this time of the year -- as this is when the levels of energetic spirits is heightened!


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taskYIELD() is used to request a context switch to another task. However, if
there are no other tasks at a higher or equal priority to the task that calls
taskYIELD() then the RTOS scheduler will simply select the task that called
taskYIELD() to run again.
If configUSE_PREEMPTION
is set to 1 then the RTOS scheduler will always be running
the highest priority task that is able to run, so calling taskYIELD() will never
result in a switch to a higher priority task.
If the port in use supports the configMAX_SYSCALL_INTERRUPT_PRIORITY (or
configMAX_API_CALL_INTERRUPT_PRIORITY) constant, then taskDISABLE_INTERRUPTS will either
disable all interrupts, or mask (disable) interrupts up to the configMAX_SYSCALL_INTERRUPT_PRIORITY setting.
Check the implementation of taskDISABLE_INTERRUPTS for the port in use.
If the port in use does not support the configMAX_SYSCALL_INTERRUPT_PRIORITY constant
then taskDISABLE_INTERRUPTS() will globally disable all maskable interrupts.
Normally this macro would not be called directly and taskENTER_CRITICAL() and
taskEXIT_CRITICAL() should be used in its place.
Macro to enable microcontroller interrupts.


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I already bought the nissian Altima sv 2018 38k mil at the enterprise renter I'm not sure if should return it or not
Thank you for writing in. Typically, purchasing a pre-owned vehicle that was used as a rental car is a fairly good deal. The vehicles are sold before the mileage drops its value to a point where the model can't be sold for profit to the rental company, yet you don't have to pay depreciation on an almost new vehicle. The vehicle is always kept clean, well maintained, and you can almost guarantee it hasn't been smoked in. Ask yourself it the vehicle meets your needs. Does it have enough power? Does it have enough space? Was it a good price? Can you pay it off soon or is it already paid for? How easy would it be for you to upgrade? Weigh your options. Often seeing it on paper in front of you drives home facts better than simply thinking about it. Nissan Altimas have a fairly strong reputation for being reliable. Good luck!


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- As noted, Elias and Kevin Owens received major heat from the WWE fans in Seattle this past Monday when they mentioned how the city no longer has an NBA team. Above is a new WWE Now video with Cathy Kelley looking at backlash from fans & players of the former Seattle Supersonics team, which relocated to Oklahoma City a few years back. WWE is calling it the longest boo in RAW history.
- The following Hidden Gems were added to the WWE Network this week:
Legendary Lou
NWA World Heavyweight Champion Lou Thesz puts his title on the line against the dangerous Wild Bill Longson. (6/17/52)
The Great Gotch
Karl Gotch makes his impact felt on U.S. soil when he teams with Rene Goulet to face The Rugged Russians at Madison Square Garden. (1/31/72)
To Catch a Model
Billy Robinson, accompanied to the ring by WWE Hall of Famer Lord Alfred Hayes, takes on Rick Martel in Canada. (10/18/84)
Oklahoma's Favorite Son
The highly revered Danny Hodge joins forces with wild man Jos LeDuc to battle the dastardly duo of Pak Song and Toru Tanaka. (11/12/74)
Japanese Pride
Before becoming one of Japan's most controversial figures in MMA, Nobuhiko Takada traveled to Canada to face Athol Foley. (8/12/83)
- Triple H has been doing media in Melbourne, Australia to promote tomorrow's WWE Super Show-Down match with The Undertaker. He tweeted the following and included a photo from the Melbourne Cricket Ground, noting that there will be more than 65,000 fans in attendance:
Dropped by the @MCG this afternoon on the way to speak at Bastion Collective in Melbourne. This city is abuzz about #WWESSD. Spoke with @theheraldsun about what it'll feel like with over 65,000 fans in the stadium ... tomorrow night is gonna be LOUD. pic.twitter.com/XsDSfSszQJ Triple H (@TripleH) October 5, 2018


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Women's Center promotes bystander intervention
October 22, 2015
Last year, there was a rise of reported sexual assaults at Grand Valley State University, which has subsequently led to an increase in efforts to educate the GVSU community about what they can do to help.
One initiative that GVSU has started is training students, faculty and staff on how to be active bystanders. An active bystander is someone who takes action when they see an incident happen, whether that is as simple as a rude comment or something as serious as an attack.
The Women's Center hosted a bystander intervention training session last Friday. The event, titled "Bringing in the Bystander," took place in the Mary Idema Pew Library and was open to all GVSU community members.
For this training, GVSU partnered up with the Michigan Coalition to End Domestic and Sexual Violence (MCEDSV). The two organizations aimed to prepare the attendees to be active bystanders toward gender-based violence in the GVSU community.
"When (attendees) see a bias incident, somebody telling a racist, sexist, homophobic joke or a potential sexual assault, they know how to recognize that and step in and hopefully prevent that from happening," said Aubrey Dull, the Violence Against Women Act Grant graduate assistant.
Bringing in the Bystander started off with a presentation about rape culture. This presentation was lead by Mary deYoung, professor of sociology and a GVSU Title IX investigator.
After deYoung concluded her portion of the training, the floor was turned over to two members of the MCEDSV, the senior program director Lisa Winchell-Caldwell and the interim assistant director Sarah Prout Rennie.
"Our priority was for students to feel empowered to use their existing skills, leadership and opportunities to build on the incredible work already being done to create the violence-free campus community they want," Winchell-Caldwell said.
However, the event was not solely for students.
"It was designed to be an afternoon training for student leaders, faculty, student engagement staff, and other interested parties to further build up the bystander engagement and response already present on campus," Winchell-Caldwell said.
The training was lecture-based with short videos and small group discussions mixed in. The idea was to keep students and faculty engaged in what was going on in order for them to pass their learning on to others in the community. The coordinators hope for a butterfly effect to lead others to being active and effective bystanders.
"I think it was really empowering for the students to realize that they can make a difference and they can make change on campus," Dull said.
The event was only one of many attempts by the university to do as much as possible to inform the campus community about sexual misconduct.
"We've had a couple of campus organizations get in touch with (the Women's Center) being interested in doing more," Dull said. "Eyes Wide Open (is) interested in perhaps doing one next semester."
More events and trainings like this could be coming in the near future. The event was considered successful by its organizers, so they are staying hopeful that they will continue to be able to educated the GVSU community on how to make an impact.
"The participants were clearly passionate about the issue and had a great deal of knowledge about both sexual assault and their campus community," Winchell-Caldwell said.
For more information about future events, visit www.gvsu.edu/womenscen.


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A recent study out of Turkey found that in those with alopecia areata, low vitamin D levels are common and may relate to a more severe disease state.
Vitamin D has a well-established effect on the immune system and is linked to a variety of autoimmune diseases. Researchers have found that vitamin D may be able to help in some aspects of autoimmune diseases, such as multiple sclerosis, lupus, and type 1 diabetes. That being said, there hasn't been any research looking at the relationship between vitamin D and AA.
Recently, researchers at the Şişli Etfal Eğitim ve Araştırma Hastanesi (Training and Research Hospital) in Turkey conducted a study to determine if vitamin D levels relate to AA and how vitamin D may affect disease severity.
They wanted to know how vitamin D levels differed between the three groups and how vitamin D levels related to disease severity in those with AA and vitiligo.
The researchers found that 90.7% of patients with AA had vitamin D levels at or less than 20 ng/ml compared to 70.5% of patients with vitiligo and 32.8% of the healthy participants. Furthermore, they found that lower vitamin D levels were significantly related to an increased percentage of hair loss on the scalp, but they found no significant relationship between vitamin D levels and BSA in vitiligo.
"We found that [vitamin D] levels were significantly lower in patients with AA than in patients with vitiligo and in healthy controls," the researchers stated.
"In addition, our results show that there is a significant inverse correlation between low [vitamin D] levels and severity of AA according to SALT scores."
Source: Aksu Cerman, A., Sarikaya Solak, S. and Kivanc Altunay, I. (2014), Vitamin D deficiency in alopecia areata. British Journal of Dermatology, 170: 1299–1304. doi: 10.1111/bjd.12980] {http://