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Pulev on Klitschko: It's a Fake Injury, Complete Nonsense
Sofia - Kubrat Pulev has accused world heavyweight champion Wladimir Klitschko of feigning injury to avoid taking on the Bulgarian challenger in an IBF title bout in Hamburg next month.
Klitschko postponed the fight, scheduled for September 6, last week, saying he had torn bicep muscles during training in Austria.
Earlier this week, the 38-year-old Ukrainian said the contest would now take place at the same venue on Nov. 15.
"It's complete nonsense," Pulev told local media on Friday. "If it's a slight injury, you know what medicine can do today and he has a good staff of specialists, he would have been able to recover in time.
"If it's a serious injury he won't recover before Nov. 15. It's a fake injury.
"He knows it's not in his interest to fight. He knows there's a high risk as there's a huge possibility of losing," added Pulev.
"I'm a big threat but I'll continue chasing my goal and I'll be even better prepared."
Klitschko also holds the WBO, WBA and IBO belts and has won 62 of his 65 bouts.
The unbeaten Pulev, 33, who has recorded 11 knockouts from 20 wins, became the IBF international champion in 2011 and European champion in 2012
[QUOTE=bigjavi973;14896160]HAHAHAHA klitschko ducked briggs in 2007 when briggs won the title. They shouldve fought next but wlad fought ray austin instead.[/QUOTE] 2007 was a long time ago. I do believe there was talk of wlad\briggs but that's as far as…Comment by Boxing Goat on 08-30-2014
[QUOTE=bigjavi973;14896160]HAHAHAHA klitschko ducked briggs in 2007 when briggs won the title. They shouldve fought next but wlad fought ray austin instead.[/QUOTE] You know jack [email protected] See the link below where it shows how Wlad was in line to fight Oleg…Comment by crold1 on 08-30-2014
No way Wlad is faking. He's the ultimate professional. Injuries happen. That said, Pulev keeping himself hyped and having a chip when a campo gets blown is no biggie. Look forward to the reschedule. This is an interesting match.Comment by Boxing Goat on 08-30-2014
[QUOTE=LacedUp;14896095]Why didn't he avenge the other two though? If he's never ducked anyone, why didn't he take care of business himself? Remember when Wlad was knocked out by Sanders, Vitali was livid. Jumping into the ring shouting at Sanders as…Comment by Boxing Goat on 08-30-2014
[QUOTE=Weebler I;14896019]Povetkin also says Wlad is faking the injury. I suspect it was a business decision.[/QUOTE] Based on what? There would be no point. The fight financials are already a success.Post a Comment - View More User Comments (44)


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486.542 217.831
The purpose and scope of the International Journal of Thermodynamics is to provide a forum for the publication of original theoretical and applied work in the field of thermodynamics as it relates to systems, states, processes, and both non-equilibrium and equilibrium phenomena at all temporal and spatial scales. The journal, thus, provides a multidisciplinary and international platform for the dissemination to academia and industry of both scientific and engineering contributions, which touch upon a broad class of disciplines that are foundationally linked to thermodynamics and the methods and analyses derived there from. A common thread throughout is that of assessing how both the first and particularly the second laws of thermodynamics touch upon these disciplines.
ECOS Papers
|The IJot will select a limited number of ECOS Conference papers to be reviewed; these paper will be blended with the regular research papers without preparing a special issue or special section.
|Posted: 2015-02-17
IJoT Manuscripts
|The IJoT will accept:
- Novel research that makes a significant advance in improving scientific understanding in a modern area of thermodynamics;
- Novel theoretical methods or experimental techniques in thermodynamics;
- Research with critical procedures toward applications of scientific or technological relevance;
- Scientific advances that generate new avenues of research related to thermodynamics;
The IJoT will need five highlights with all the submissions. These highlights will clearly indicate why the submission is significant, novel, and transformative.
|Posted: 2015-02-17
|More Announcements...
Vol 19, No 2: June 2016
Table of Contents
Regular Original Research Article
|Analysis of a gas system with a recirculation of the flue gases and carbon dioxide capture
|Pawel Monka
|Energetic and exergetic analysis of alternative low-temperature based district heating substations arrangements
|Jose Fiacro Castro Flores
|Entropy analysis of thermoelectric heat pumps including multi-channel heat exchangers: design considerations
|Julien Ramousse
|Numerical approach on the effects of gasoline-hydrogen blends on the cyclic variability in spark ignition engines
|Santiago Daniel Martinez-Boggio, Pedro Luis Curto-Risso, Alejandro Medina, Antonio Calvo
|Entropy function for the teleparallel Kaluza-Klein reduction
|Mustafa SALTI, Oktay Aydogdu
|Predicting The Liquid Phase Equilibrium of Multi-Components Extraction By Thermodynamic Models
|dewi selvia fardhyanti
|Two State Weak and Mean Valued Energy Quantum Systems are Thermodynamically Homologous
|Allen D. Parks

subset: commoncrawl


text:
It is hard to believe that Venezuela's container import business could get any worse — but it has done just that in 2016.
South America
Press Releases
AAPA's Latin American/Caribbean Management Conference to Explore Port Alliances, Development, Productivity
18 Apr 2016
The port of Paranagua, Brazil's second-largest in tonnage terms and third-largest in container traffic, could soon have another container terminal, although some remain skeptical about the Novo Porto project with a capacity of 1.5 million twenty-foot-equivalent units and cost of 4 billion reais ($1.1 billion).
15 Apr 2016
On the back of roaring chicken exports the rapidly growing Terminal de Conteineres de Paranagua will spend $310 million to boost its capacity 1 million 20-foot equivalent units to 2.5 million TEUs after receiving a concession running through 2048. The investment will also allow the port to handle ships with capacities of up to 12,000 TEUs.
14 Apr 2016
Brazil's only surviving container line, Log-In Logistica, may be in deep debt, but that didn't stop it from registering a 21.1 percent increase in Mercosur coastal and Brazilian cabotage movement during 2015.
12 Apr 2016
Container traffic from South America's east coast ports to Europe has rebounded so strongly in recent months that the northbound leg is now the dominant trade on the route, according to Drewry Maritime Research.
11 Apr 2016
Rapidly expanding United Arab Shipping Company announced that it is beefing up its East Coast South America operations with a new joint venture agency in Uruguay as part of a broader strategic push in the region, fueled by expected growth in refrigerated shipments.
07 Apr 2016
Maersk Line's sister company Mercosul Line will beef up its cabotage and coastal operations along the East Coast of South America by adding a new vessel and service to help meet shipper demand for more options to Argentina.
06 Apr 2016
Brazil's passionate Ports Minister Helder Barbalho announced that the recently delayed second tranche of port privatizations valued at more than 2.8 billion reais ($763.3 million) would go forward on June 5 at the Sao Paulo bourse.
05 Apr 2016
The already bleak situation facing the container terminals at Brazil's port of Santos has become even more dire.
29 Mar 2016
The president of an association representing container terminal operators is confident that Brazil will be ready for the Safety of Life at Sea, or SOLAS, Verified Gross Mass rule and has established a Special Technical Group to resolve any final concerns.
28 Mar 2016
Brazil meat exporters had a week of both good and bad news as they seek new markets in Latin America to capitalize on the depreciation of the local currency, the real, which has recently buoyed the country's beef exports.


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Suvarna gets its first Kannadada Kotyadhipati
Suvarna, the Star network's Kannada General Entertainment channel, announced the 1st one crore winner of their show Sunfeast Kannadada Kotyadhipati.
This is the first time in the history of Kannada General Entertainment that a common man has won a prize money of Rs. 1 crore. Hussain Bhasha is the contestant who answered all the 15 questions of the game show and has won the biggest prize money. He is a student and hails from Koppal district.
Sunfeast is the title sponsor of the show, Nugen Kailash is the technology partner, Vijaya Bank is the Banking partner & Airtel is the telecom partner. The host of the show Power Star Puneet Rajkumar says, "I am very happy for Hussain as this show has changed his life, I like his knowledge and confidence. I hope we have more common people who will reach the 1 crore mark."
On this occasion, Anup Chandrasekharan, the Business Head of Suvarna said "We are proud to announce the 1st one crore winner of our show Kannadada Kotyadhipati. We had started this show with a core thought of providing an opportunity to common people to change their lives. There have been contestants who have won prize monies but Hussain has created history by winning the maximum. I would like to congratulate him & his family."


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Vt. Tech ranked 10th among peersSeptember 17,2013The Associated Press
RANDOLPH — Vermont Technical College has been ranked No. 10 among public regional colleges of the North by U.S. News and World Report for the second year in a row.
"The Best Colleges rankings by U.S. News and World Report are an important and respected guide for students and their families," VTC President Phil Conroy said in a statement. "We are thrilled to be ranked among our nation's top colleges for another year and hope this continues to develop our position as a leader in applied education."
According to the Carnegie Classification of Institutions of Higher Education, the 367 regional colleges in the ranking focus almost entirely on the undergraduate experience and offer a broad range of programs in the liberal arts like business, nursing and education.MORE IN This Just In
WEATHERSFIELD -- A 29-year-old man died Wednesday night after his motorcycle left... Full StoryThe family of Julia Lathrop will host an all-you-can-eat spaghetti dinner buffet at the Downtown... Full StoryTeen avoids deer, hits utility pole
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Ladies Coats and Jackets
Take on the British weather and win with one of our stylish and high-quality coats. We have parkas, raincoats and showerproof coats, or why not choose a smart coat to top off your work or evening outfit? You'll also find a selection of jackets here - including stylish denim and practical padded jackets.
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Another football match, another head injury – and out come the fawning accolades for a player's bravery, determination and commitment to his team's cause as he plays on.
People who wanted Mascherano substituted after his head knock got their answer, man of the match performance football's a contact sport
— Hughie (@hsharkey63) July 10, 2014
Argentina's Javier Mascherano looked utterly bewildered after hitting his skull against Georginio Wijnaldum's, but insisted he would be fine to continue.
Alvaro Pereira of Uruguay did the same against England earlier in the tournament as his head took the full force of Raheem Sterling's knee, and players' union FIFPro called then for an investigation into how the sport dealt with potential concussions.
Managers, team-mates, fans and the media are doing sportspeople absolutely no good whatsoever with their eagerness to praise anyone who plays on after a knock to the head.
Continuing to play is not a badge of honour; it's a mark of irresponsibility, and, perhaps contrarily and counterintuitively, unprofessionalism.
There is a very strong base of evidence in sports science that demonstrates the dangers of athletic exertion after a head trauma.
Any athlete suspected of having a concussion should - indeed, must - be stopped from playing and assessed thoroughly. An immediate return to the field after a physio has cursorily waved a finger in front of his or her eyes is insufficient.
Concussion can take a while to set in, and management and medical staff should err on the side of caution. An athlete needs to be monitored closely for days – and weeks – afterwards, with a gradual return to competitive play.
Rugby acknowledges it, with proper rules to manage such injuries, and a focus on ensuring the player's wellbeing comes above all else.
Snow sports acknowledge it, with elite competitions requiring protective head gear, with a recommendation extended to leisure participants. The data suggest that helmet use in snow sports reduces the risk of head injury by around 35 per cent.
Even professional wrestling – which consistently gets mocked by sports fans for not being "real", but still entails very real contact and risks – acknowledges it, with WWE now outlawing any deliberate shots at the head, and removing performers from shows to give them recovery time after incurring a head injury. (Indeed, former wrestler Christopher Nowinski now leads the Sports Legacy Institute, which raises awareness about the dangers of sports concussion, and is co-director of a brain injury research centre at Boston University.)
FIFPro are arguing that independent medical professionals should conduct a sideline concussion assessment, whereas FIFA maintains the ultimate responsibility lies with the team doctor – who might have their judgement affected by their investment in the situation.
Above all, it certainly shouldn't be left up to the player.
Pereira apologised for overruling the Uruguay team doctor who had wanted to substitute him, explaining: "It was that moment your adrenaline flowing in your body, maybe without thinking ... what I really wanted to do was to help get the result."
Vincent Kompany of Belgium played on in a World Cup qualifier after breaking his nose, fracturing his eye socket and sustaining a concussion, and afterwards reflected: "I would always listen to what the medical staff has to say but, then again, I would do the opposite of what the medical staff would say… You have to take emotions and adrenaline into account. Unless someone puts on the emergency brake, you are not going to do it yourself."
That final point is key. Football's nebulous "guidelines" have to be turned into hard and fast rules, and those rules have to be enforced.
It's not like football clubs and authorities don't know about this. There's a recent and updated Sport Concussion Assessment Tool (SCAT3 for short) that FIFA recommend should be used for diagnosis.
That FIFA recommend rather than enforce this diagnostic procedure is nothing less than shameful. It shows that they know full well what best practice is, but choose to abdicate responsibility to individual team doctors, knowing that makes it far less likely that teams' stars are withdrawn from action. This failure to ensure the gold standard is followed on football's biggest stage is, quite simply, a disgrace to the game.
SCAT3 recommends treating a head injury as a concussion if a player loses consciousness, if they're lying motionless on the ground, if they're slow to get up, if they look dazed, if they're unsteady on their feet, or if they're confused. Any single one of those symptoms should be enough for someone to be removed from the field of play.
And we very rarely see that in top flight men's football, where the culture of bravado, the pursuit of success and the valorisation of the consequent money trump all - even at the expense of the safety of its players.
Carrie Dunn | @carriesparkle
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- American Football
- Mascherano
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New Clues and Puzzles in Boston Strangler Case
By PHILIP J. HILTS
Published: November 20, 2001
BOSTON, Nov. 19— After nearly 40 years, the perplexing case of the Boston Strangler has come back to life -- a result of forensic science and an unlikely alliance between the families of a victim and the man long thought to have killed her.
For decades it has been widely assumed that the strangler was Albert DeSalvo, who confessed to some of the murders that terrified and transfixed this city in the early 1960's. But he was never convicted of any of them, and the killings are still officially listed as unsolved. DeSalvo was sentenced to life in prison for another crime, and died there in 1973.
Now, forensic scientists hired by the families of DeSalvo and the final victim, Mary Sullivan, have exhumed the bodies and examined them for DNA and other evidence. They say their analysis, nearly complete, has produced enticing new clues -- and some new mysteries.
The forensic team expects to make a detailed report in Washington in a few weeks, said its leader, James E. Starrs, a law professor at George Washington University. The team says it expects to announce these findings, among others:
*DNA found on Miss Sullivan's body is not hers and may be that of her killer -- whether DeSalvo or someone else, the forensic team will not say.
*The forensic team found a hair, missed at the time of the killing, in the young woman's teeth. The scientists say it may be from her killer.
*In a particularly intriguing finding, the team says Miss Sullivan may not have been strangled by hand -- as DeSalvo confessed he had done -- but with her stockings. The finding is based on the condition of a neck bone called the hyoid: it was intact, but would probably have snapped if she had been strangled by hand -- particularly since she had a condition that weakened her bones.
*Much of the belief in DeSalvo's guilt has come from the widely held assumption that he told the criminal lawyer F. Lee Bailey, and later the police, details about the murders that only the killer and investigators could have known. But Elaine and Daniel Sharp, lawyers for the two families, have uncovered transcripts from DeSalvo's first tape-recorded confessions, in 1965, suggesting that he was unfamiliar with many facts of the killings and got some of the most basic ones wrong.
*When DeSalvo's body was exhumed two weeks ago, investigators were stunned to discover that his brain, lungs, heart and liver were missing. Mr. Starrs says he has no idea what happened to the organs; the most innocent explanation is that they were simply misplaced after the first autopsy in 1973.
The case of the Boston Strangler, perhaps the most confounding serial-killer mystery since that of Jack the Ripper, began in 1962. On the evening of June 14, Anna Slesers, a 55-year-old seamstress, was sexually assaulted, then strangled with the cord from her bathrobe.
Within three weeks, two more women were sexually assaulted and strangled with their own clothing, setting off a wave of fear in Boston. Eight to 12 more killings -- depending on whether the police or newspaper reporters were counting -- followed over the next 18 months.
In the news pages, the murders were soon attributed to a single killer; he was dubbed the Phantom Fiend because he seemed able to get into apartments without breaking in, apparently talking his victims into opening their doors.
A manhunt began. The police warned women in the Boston area to be on their guard. Sales of guard dogs and door locks soared. Police leaves were canceled. The killings stopped for several months, then started again, then ended for good after Jan. 4, 1964, with the strangling of 19-year-old Mary Sullivan.
By Jan. 17, with no solution in sight, the Massachusetts attorney general, Edward W. Brooke, started a task force to take over the investigation.
The task force said 11 of the murders might be linked, and over many months, strong suspects were developed in half a dozen cases. But there were no arrests until early 1965, when Albert DeSalvo, 29, an inmate at a state mental hospital, came forward. He had been convicted of talking his way into the apartments of several women and abusing them sexually; after the conviction, he claimed to have committed more than 300 sexual assaults.
He told his lawyer, Jon Asgeirson, that he had the ''biggest story of the century,'' that he had committed not only the 11 murders under investigation but 2 others.
The lawyer was doubtful, but within a short time, a young Boston defense lawyer, F. Lee Bailey, began to listen to DeSalvo's pleas with the aim of arranging book and movie deals. In what became his first prominent case, Mr. Bailey interviewed DeSalvo and on March 6, 1965, collected the first taped confession. Soon, newspapers announced that the strangler had been caught.
Mr. Bailey said he became convinced DeSalvo was the killer because he had given details of the crimes that corroborated those in the police files. Lengthy police interrogations followed.
After that, other suspects were dropped, and the police focused their attention on DeSalvo. He was never charged with the crimes, but in his trial on sexual assault charges, the jury was told he was the strangler, and he was sentenced to life in prison. While behind bars, he tried to market himself by making ''choker'' necklaces and offering to sing on a record called ''Strangler in the Night.'' DeSalvo was stabbed to death in prison in 1973. Three inmates were charged with the killing but never convicted.


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Whenever I start something new that I know nothing about I have to learn as much as possiable. So I am thinking about getting some BF books but I'm not sure where to start. I want something no nonsense and matter of fact. I don't want anything AP ,about parenting, or to preachy if that makes sense. I am confident on my parenting style just don't know what to do about the boobies.
Any suggestions would be great!


text:
After Hillary Clinton's historic moment on Thursday in which she broke the glass ceiling by becoming the first woman ever to win a major party nomination, some folks were wondering what would become of her husband -- the 42nd president of the United States.
This spring, due to public health concerns surrounding Zika virus, the Oklahoma State Department of Health began a collaborative mosquito surveillance project with Oklahoma State University entomologists to detect the possible presence...
Last week, Brooklyn-based Nick Johnson, who happens to be a friend of mine, publicly declared himself to be the first Pokémon Go player to catch...
Dave Granlund cartoon on Hillary Clinton giving Bernie Sanders holdouts a dose of reality.
Ardmore police have upgraded the pending charge against a 20-year-old Ardmore man accused of the stabbing of a "love triangle" adversary.
Don Landgren cartoon on watering a lawn while in drought conditions.
Take a look at the following disparities from a survey of over 1,000 college-aged students and over 2,000 parents of current and former students:
Chipotle is getting into the burger business. The company said the new restaurant chain will use "high-quality ingredients that are grown and raised with respect for the animals, the land, and the farmers who produce them."
The paperbark maple was introduced to the West more than a century ago by the intrepid plant collector E.H. Wilson, but it has remained a fairly uncommon garden plant, in part because Wilson started with only about 100 seedlings.
People responded more favorably to Hillary Clinton's convention speech than they did to Donald Trump's, according to a CNN/ORC instant poll that compared audience reactions for both.
It was kind of a boring week on Big Brother 18, with
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- Report: #886179
Report - Rebuttal - Arbitrate
Complaint Review: American General / Springleaf Financial
American General / Springleaf FinancialInternet United States of America
American General / Springleaf Financial Krisor and Associates Taking all my money, Every cent, Internet
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Anyone that is thinking about taking out a loan with this company, DONT. They will ruin your lives. I have four kids, no money to my name now. Their attorneys, Krisor and Associates in South bend indiana will back them to the fullest. Things happen in peoples lives to where you are unable to make your payments to your creditors.
The garnishment from my paychecks are understandable, BUT TAKING ALL THE MONEY I HAVE TO MY NAME IN MY CHECKING ACCOUT AFTER THEY TAKE MONEY FROM MY EMPLOYER IS JUST DOWNRIGHT SELFISH OF THIS COMPANY AND THEIR SO CALLED LAWYERS. [continued below]....
They lied about the total amount to regain possession of my vehicle, then gave me a cheesy reciept with the dollar amout "blacked out with marker" to make me believe the total amout paid to the towing company "bower towing". So much anger towards two companies for unethical business practices. This company needs stopped. The people that work for them are just as bad as the administrators of the company....
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|Boxing Champions | Boxing Schedule | Boxing Video | Boxing History | Pound For Pound | Lounge | The Wire | Arcade
|View Poll Results: Did the judges make the right decision, based on the OFFICIAL CRITERIA?
|Voters: 52. You may not vote on this poll
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The judges made the RIGHT decision, and here is why
First off, I had Pac winning the fight. But then again, fans and judges score a fight using different criteria. When you factor that in, I think the judges made the right decision.
So Pacquiao landed the cleaner more effective punches, but that was only 1/4 of the criteria, and Bradley arguably won the other 3. Plus, if a guy controls the action for 2/3 of the round, and the other guy dominates the last 1/3, is it fair to give the round to the other guy?
So overall, maybe the real problem is how fights are scored. But I don't think you can blame the judges for following the official criteria
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If by right you mean wrong, then yeah...
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I kind of agree. I had Pac winning, but I have Bradley winning using that criteria. Kind of like in court when a jury returns an unpopular decision, that they themselves dont believe, but is right according to the law.
As TS said, I think the real problem is the way judges are told to score a fight, not the judges themselves
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Brian Kenny approves this thread
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Bradley didnt do what he said he would do before the fight, so ring generalship goes to Pac. Bradley couldnt do what he originally wanted so surived as best as he could under the circumstances. He originally wanted to take it to Pac, but realized Pac was superior so had to have a different plan to the original.
Everything Pac did better, thats why he recieved less punches than Brad. Bradlesy pitter patter punches shouldnt even have counted if your opponent dont feel it, theres no point in defending it. Brads alll show, no go.
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Okay, I actually bothered to read your post...
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9 rounds pac...1 round even...2 rounds Bradey ,and they were close
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twist it any way you want, but anything less than a scorecard for Pac is borderline criminal. And I'm a Mayweather fan!
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decision went to the wrong person..end of. you have 99.9% of boxing journalists (from ring magazine, espn, maxboxing, etc.), long time critics of pacquiao (mayweathers, teddy atlas, etc.), bradley's manager cameron dunkin, a slew of professional boxers and trainers all saying pac won...
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If someone wanted to find ways to give someone the win, then you can do that with ANY fight.
Bottom line is Pacquiao landed the cleaner effective punches.
Despite what compubox says, Pac landed more than double.
There is a difference between counter punching to a victory, and surviving.
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Why long exposure long to write
I was out last night with my D5100 taking 20 second exposures of cars driving past my house. Why did each exposure take about 20 seconds to write to the memory card? It seems that with most of the picture black, there would be less information that had to be written.
Visit my Nikonians gallery.
#1. "RE: Why long exposure long to write" | In response to Reply # 0BGD600 Registered since 19th Sep 2012Tue 14-May-13 01:11 PM
If you are using in camera noise reduction then the first 20 seconds is your exposure, the second is the camera taking another "black" image to use for NR. HTH
#2. "RE: Why long exposure long to write" | In response to Reply # 0briantilley Nikonian since 26th Jan 2003Tue 14-May-13 01:15 PM
You probably have Long Exposure Noise Reduction turned on. This feature is used to reduce the amount of digital noise in the image. It has to make a second exposure of equal length to the "real" exposure and then do some processing, so that is what you have to wait for. The image itself takes no longer than normal to write to the memory card.
Welsh Nikonian
#3. "RE: Why long exposure long to write" | In response to Reply # 2grnzbra Nikonian since 28th Sep 2011Tue 14-May-13 01:36 PM | edited Tue 14-May-13 01:37 PM by grnzbra
Neat! Thank you for the clarification.
This is the first time I've tried anything like this and got some interresting results. I'll be going out again tonight to see what I can get.
Visit my Nikonians gallery.


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This week UFC FIGHT PASS features Oleg Taktarov, Jon 'Bones' Jones and Victory FC and Shooto live events. read news >>
Ronys Torres had his shot in the UFC in 2010. It didn't go as planned. Today, Torres, Shooto Brazil's lightweight champion, has yet another opportunity to do impress the UFC brass to push closer to a read news >>
The Brazilian Athletic Commission MMA (CABMMA) reports that two fighters from the Aug. 21 Shooto Brazil 56 event tested positive to banned substances. read news >>
The UFC's dance card for its return to Dublin in October is starting to fill up, but at least one more fighter wants on the bill.Filed under: News, UFC read news >>
After three straight stoppage wins, Max Holloway had to go into enemy territory to find his fourth. Check out his decimation of Akira Corassani inside.Filed under: News, UFC, Videos read news >>
LAS VEGAS – Jake Shields won belts with Shooto, Rumble on the Rock, EliteXC and Strikeforce – and he was a win away from a UFC title, as well – but after tonight's WSOF 22 event, he believes he'll ha read news >>
UFC Fight Pass keeps expanding with a live stream of Sunday's Shooto Brazil 54. Then, this summer, the promotion's entire fight library will be added. read news >>
With a win over Alexander Gustafsson in Sweden, Anthony Johnson emerged as the top contender in the light heavyweight division and is expected to be booked for a championship bout opposite Jon Jones read news >>
Following Saturday's UFC on FOX 14 event in Sweden, several of the winning and losing fighters took to social media to react to the event or share a message with supporters. Check out some of those r read news >>
Now that UFC on FOX 14 is in the books, it's time to commence MMAjunkie's "Three Stars" ceremony.Filed under: News, UFC read news >>
At UFC on Fox 14, Anthony Johnson went into Sweden and silenced the second-biggest crowd in UFC history with an opening-round knockout against Alexander Gustafsson. With his victory over The Mauler, read news >>
Anthony Johnson shocked Sweden and their hometown fighter, earning a first-round technical knockout of Alexander Gustafsson at UFC on FOX 14 in Stockholm early Sunday morning. read news >>
Alexander Gustafsson laughs when you ask him what life is like for him in Sweden these days. About to headline the 30,000-seat Tele2 Arena in Stockholm in a fight against Anthony Johnson... read news >>
STOCKHOLM – Ahead of Saturday's UFC on FOX 14 event in Sweden, MMAjunkie lead staff reporter John Morgan takes you inside the card alongside Mike Bohn and Chamatkar Sandhu.Filed under: Featured Video read news >>
When Anthony Johnson faces Alexander Gustafsson this weekend in Stockholm, Sweden, he will have come full circle in a career that has seen many ups and downs. read news >>


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Eosinophil recruitment to the lung in a murine model of allergic inflammation. The role of T cells, chemokines, and adhesion receptors.
Gonzalo, J A
Lloyd, C M
Kremer, L
Finger, E
Martinez-A, C
Siegelman, M H
Cybulsky, M
Gutierrez-Ramos, J C
Journal of Clinical Investigation
Eosinophil accumulation is a distinctive feature of lung allergic inflammation. Here, we have used a mouse model of OVA (ovalbumin)-induced pulmonary eosinophilia to study the cellular and molecular mechanisms for this selective recruitment of eosinophils to the airways. In this model there was an early accumulation of infiltrating monocytes/macrophages in the lung during the OVA treatment, whereas the increase in infiltrating T-lymphocytes paralleled the accumulation of eosinophils. The kinetics of accumulation of these three leukocyte subtypes correlated with the levels of mRNA expression of the chemokines monocyte chemotactic peptide-1/JE, eotaxin, and RANTES (regulated upon activation in normal T cells expressed and secreted), suggesting their involvement in the recruitment of these leukocytes. Furthermore, blockade of eotaxin with specific antibodies in vivo reduced the accumulation of eosinophils in the lung in response to OVA by half. Mature CD4+ T-lymphocytes were absolutely required for OVA-induced eosinophil accumulation since lung eosinophilia was prevented in CD4+-deficient mice. However, these cells were neither the main producers of the major eosinophilic chemokines eotaxin, RANTES, or MIP-1alpha, nor did they regulate the expression of these chemokines. Rather, the presence of CD4+ T cells was necessary for enhancement of VCAM-1 (vascular cell adhesion molecule-1) expression in the lung during allergic inflammation induced by the OVA treatment. In support of this, mice genetically deficient for VCAM-1 and intercellular adhesion molecule-1 failed to develop pulmonary eosinophilia. Selective eosinophilic recruitment during lung allergic inflammation results from a sequential accumulation of certain leukocyte types, particularly T cells, and relies on the presence of both eosinophilic chemoattractants and adhesion receptors.
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Constitutive and allergen-induced expression of eotaxin mRNA in the guinea pig lung
The Journal of Experimental Medicine
Eotaxin is a member of the C-C family of chemokines and is related during antigen challenge in a guinea pig model of allergic airway inflammation (asthma). Consistent with its putative role in eosinophilic inflammation, eotaxin induces the selective infiltration of eosinophils when injected into the lung and skin. Using a guinea pig lung cDNA library, we have cloned full-length eotaxin cDNA. The cDNA encodes a protein of 96 amino acids, including a putative 23-amino acid hydrophobic leader sequence, followed by 73 amino acids composing the mature active eotaxin protein. The protein-coding region of this cDNA is 73, 71, 50, and 48% identical in nucleic acid sequence to those of human macrophage chemoattractant protein (MCP) 3, MCP-1, macrophage inflammatory protein (MIP) 1 alpha, and RANTES, respectively. Analysis of genomic DNA suggested that there is a single eotaxin gene in guinea pig which is apparently conserved in mice. High constitutive levels of eotaxin mRNA expression were observed in the lung, while the intestines, stomach, spleen, liver, heart, thymus, testes, and kidney expressed lower levels. To determine if eotaxin mRNA levels are elevated during allergen-induced eosinophilic airway inflammation, ovalbumin (OVA)-sensitized guinea pigs were challenged with aerosolized antigen. Compared with the lungs from saline-challenged animals, eotaxin mRNA levels increased sixfold within 3 h and returned to baseline by 6 h. Thus, eotaxin mRNA levels are increased in response to allergen challenge during the late phase response. The identification of constitutive eotaxin mRNA expression in multiple tissues suggests that in addition to regulating airway eosinophilia, eotaxin is likely to be involved in eosinophil recruitment into other tissues as well as in baseline tissue homing.
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Monocyte chemotactic protein 3 is a most effective basophil- and eosinophil-activating chemokine
The Journal of Experimental Medicine
CC chemokines constitute a novel class of cytokines that attract and activate monocytes and lymphocytes, as well as basophil and eosinophil leukocytes, with distinct target cell profiles, and are believed to be involved in the regulation of different types of inflammation. The action of the recently identified monocyte chemotactic protein 3 (MCP- 3) on human basophil and eosinophil function was studied and compared with that of other CC chemokines. In basophils, MCP-3, MCP-1, RANTES, and macrophage inflammatory protein (MIP)-1 alpha all induced cytosolic- free calcium concentration ([Ca2+]i) changes and, with different efficacies, chemotaxis (RANTES = MCP-3 >> MCP-1 > MIP-1 alpha), histamine release (MCP-1 = MCP-3 >> RANTES > MIP-1 alpha), and leukotriene C4 formation, after IL-3 pretreatment (MCP-1 = MCP-3 >> RANTES > MIP-1 alpha). Thus, MCP-3 was as effective as MCP-1 as an inducer of mediator release, and as effective as RANTES as a stimulus of basophil migration. In contrast to MCP-1, MCP-3 was also a stimulus for eosinophils, and induced [Ca2+]i changes and chemotaxis as effectively as RANTES, which is the most potent chemotactic cytokine for these cells. Desensitization of the transient changes in [Ca2+]i was used to assess receptor usage. In basophils, stimulation with MCP-3 prevented responsiveness to MCP-1 and RANTES, but not to MIP-1 alpha. No single CC chemokine (except for MCP-3 itself) affected the response to MCP-3, however, which was prevented only when the cells were prestimulated with both MCP-1 and RANTES. In eosinophils, by contrast, cross-desensitization between RANTES and MCP-3 was obtained. RANTES and to a lesser extent MCP-3 also desensitized eosinophils toward MIP-1 alpha. The desensitization data suggest the existence of three chemokine receptors: (a) a MCP-1 receptor expressed on basophils but not eosinophils that is activated by MCP-1 and MCP-3; (b) a RANTES receptor in basophils and eosinophils that is activated by RANTES and MCP-3; and (c) a MIP-1 alpha receptor that is activated by MIP-1 alpha, RANTES and, more weakly, by MCP-3. This study shows that MCP-3 combines the properties of RANTES, a powerful chemoattractant, and MCP-1, a highly effective stimulus of mediator release, and thus has a particularly broad range of activities toward both human basophil and eosinophil leukocytes.
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Effects of Respiratory Mycoplasma pneumoniae Infection on Allergen-Induced Bronchial Hyperresponsiveness and Lung Inflammation in Mice
Chu, Hong Wei
Honour, Joyce M.
Rawlinson, Catherine A.
Harbeck, Ronald J.
Martin, Richard J.
Infection and Immunity
Airway mycoplasma infection may be associated with asthma pathophysiology. However, the direct effects of mycoplasma infection on asthma remain unknown. Using a murine allergic-asthma model, we evaluated the effects of different timing of airway Mycoplasma pneumoniae infection on bronchial hyperresponsiveness (BHR), lung inflammation, and the protein levels of Th1 (gamma interferon [IFN-γ]) and Th2 (interleukin 4 [IL-4]) cytokines in bronchoalveolar lavage fluid. When mycoplasma infection occurred 3 days before allergen (ovalbumin) sensitization and challenge, the infection reduced the BHR and inflammatory-cell influx into the lung. This was accompanied by a significant induction of Th1 responses (increased IFN-γ and decreased IL-4 production). Conversely, when mycoplasma infection occurred 2 days after allergen sensitization and challenge, the infection initially caused a temporary reduction of BHR and then increased BHR, lung inflammation, and IL-4 levels. Our data suggest that mycoplasma infection could modulate both physiological and immunological responses in the murine asthma model. Our animal models may also provide a new means to understand the role of infection in asthma pathogenesis and give evidence for the asthma hygiene hypothesis.
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Chemokines in the limbal form of vernal keratoconjunctivitis
El-Asrar, A.
Struyf, S.
Al-Kharashi, S.
Missotten, L.
Van Damme, J.
Geboes, K.
The British Journal of Ophthalmology
BACKGROUND/AIMS—Chemokines are a family of low molecular weight cytokines that attract and activate leucocytes. The CC chemokines act on eosinophils, basophils, monocytes, and lymphocytes, suggesting that they play an important part in allergic diseases. The aims of this study were to investigate the expression of the CC chemokines, RANTES, eotaxin, monocyte chemotactic protein (MCP) 1, MCP-2, and MCP-3 in the conjunctiva of patients with vernal keratoconjunctivitis (VKC) and to determine the cellular source of these chemokines. METHODS—Conjunctival biopsy specimens from nine subjects with active VKC, and six control subjects were studied by immunohistochemical techniques using a panel of monoclonal and polyclonal antibodies directed against RANTES, eotaxin, MCP-1, MCP-2, and MCP-3. The phenotype of inflammatory cells expressing chemokines was examined by sequential double immunohistochemistry. RESULTS—In the normal conjunctiva, superficial epithelial cells showed a constitutive, weak cytoplasmic expression of eotaxin. Few inflammatory cells in the perivascular areas expressed RANTES, MCP-1, MCP-2, and MCP-3. In VKC specimens, the epithelium showed intense cytoplasmic eotaxin staining in all cells, and cytoplasmic RANTES staining mainly in the superficial layers. Furthermore, RANTES and eotaxin were expressed on the vascular endothelium mainly in the upper substantia propria. Compared with normal controls, VKC specimens showed significantly more inflammatory cells expressing RANTES, eotaxin, MCP-1, and MCP-3 (p<0.001, 0.0028, 0.0092, and <0.001, respectively). In VKC specimens, the numbers of inflammatory cells expressing RANTES were significantly higher than the numbers of inflammatory cells expressing eotaxin, MCP-1, and MCP-2 (all p values <0.001). Colocalisation studies revealed that the majority of inflammatory cells expressing chemokines were CD68 positive monocytes/macrophages. CONCLUSIONS—These results demonstrate an increase in the expression of RANTES, eotaxin, MCP-1, and MCP-3 in the conjunctiva of patients with VKC compared with control subjects. These data suggest a potential role for these chemokines in the pathogenesis of VKC. Antagonists of chemokine receptors may provide new therapeutic modalities in VKC.
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High expression of the chemokine receptor CCR3 in human blood basophils. Role in activation by eotaxin, MCP-4, and other chemokines.
Uguccioni, M
Mackay, C R
Ochensberger, B
Loetscher, P
Rhis, S
LaRosa, G J
Rao, P
Ponath, P D
Baggiolini, M
Dahinden, C A
Journal of Clinical Investigation
Eosinophil leukocytes express high numbers of the chemokine receptor CCR3 which binds eotaxin, monocyte chemotactic protein (MCP)-4, and some other CC chemokines. In this paper we show that CCR3 is also highly expressed on human blood basophils, as indicated by Northern blotting and flow cytometry, and mediates mainly chemotaxis. Eotaxin and MCP-4 elicited basophil migration in vitro with similar efficacy as regulated upon activation normal T cells expressed and secreted (RANTES) and MCP-3. They also induced the release of histamine and leukotrienes in IL-3-primed basophils, but their efficacy was lower than that of MCP-1 and MCP-3, which were the most potent stimuli of exocytosis. Pretreatment of the basophils with a CCR3-blocking antibody abrogated the migration induced by eotaxin, RANTES, and by low to optimal concentrations of MCP-4, but decreased only minimally the response to MCP-3. The CCR3-blocking antibody also affected exocytosis: it abrogated histamine and leukotriene release induced by eotaxin, and partially inhibited the response to RANTES and MCP-4. In contrast, the antibody did not affect the responses induced by MCP-1, MCP-3, and macrophage inflammatory protein-1alpha, which may depend on CCR1 and CCR2, two additional receptors detected by Northern blotting with basophil RNA. This study demonstrates that CCR3 is the major receptor for eotaxin, RANTES, and MCP-4 in human basophils, and suggests that basophils and eosinophils, which are the characteristic effector cells of allergic inflammation, depend largely on CCR3 for migration towards different chemokines into inflamed tissues.
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Ca2+-Activated K+ Channel–3.1 Blocker TRAM-34 Attenuates Airway Remodeling and Eosinophilia in a Murine Asthma Model
Girodet, Pierre-Olivier
Ozier, Annaig
Carvalho, Gabrielle
Ilina, Olga
Ousova, Olga
Gadeau, Alain-Pierre
Begueret, Hugues
Wulff, Heike
Marthan, Roger
Bradding, Peter
Berger, Patrick
American Journal of Respiratory Cell and Molecular Biology
Key features of asthma include bronchial hyperresponsiveness (BHR), eosinophilic airway inflammation, and bronchial remodeling, characterized by subepithelial collagen deposition, airway fibrosis, and increased bronchial smooth muscle (BSM) mass. The calcium-activated K+ channel KCa3.1 is expressed by many cells implicated in the pathogenesis of asthma, and is involved in both inflammatory and remodeling responses in a number of tissues. The specific KCa3.1 blocker 5-[(2-chlorophenyl)(diphenyl)methyl]-1H-pyrazole (TRAM-34) attenuates BSM cell proliferation, and both mast cell and fibrocyte recruitment in vitro. We aimed to examine the effects of KCa3.1 blockade on BSM remodeling, airway inflammation, and BHR in a murine model of chronic asthma. BALB/c mice were sensitized with intraperitoneal ovalbumin (OVA) on Days 0 and 14, and then challenged with intranasal OVA during Days 14–75. OVA-sensitized/challenged mice received TRAM-34 (120 mg/kg/day, subcutaneous) from Days −7 to 75 (combined treatment), Days −7 to 20 (preventive treatment), or Days 21 to 75 (curative treatment). Untreated mice received daily injections of vehicle (n = 8 per group). Bronchial remodeling was assessed by histological and immunohistochemical analyses. Inflammation was evaluated using bronchoalveolar lavage and flow cytometry. We also determined BHR in both conscious and anesthetized mice via plethysmography. We demonstrated that curative treatment with TRAM-34 abolishes BSM remodeling and subbasement collagen deposition, and attenuates airway eosinophilia. Although curative treatment alone did not significantly reduce BHR, the combined treatment attenuated nonspecific BHR to methacholine. This study indicates that KCa3.1 blockade could provide a new therapeutic strategy in asthma.
asthma; KCa3.1; ion channel; remodeling; smooth muscle
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Arsenic trioxide, a potent inhibitor of NF-κB, abrogates allergen-induced airway hyperresponsiveness and inflammation
Zhou, Lin-Fu
Zhu, Yi
Cui, Xue-Fan
Xie, Wei-Ping
Hu, Ai-Hua
Yin, Kai-Sheng
Respiratory Research
Overactivation of nuclear factor κB (NF-κB) orchestrates airway eosinophilia, but does not dampen airway hyperresponsiveness in asthma. NF-κB repression by arsenic trioxide (As2O3) contributes to apoptosis of eosinophils (EOS) in airways. Here we provide evidence that As2O3 abrogates allergen (OVA)-induced airway eosinophilia by modulating the expression of IκBα, an NF-κB inhibitory protein, and decreases the airway hyperresponsiveness.
Using a murine model of asthma, the airway hyperresponsiveness was conducted by barometric whole-body plethysmography. Airway eosinophilia, OVA-specific IgE in serum, and chemokine eotaxin and RANTES (regulated upon activation, normal T cell expressed and secreted) in bronchoalveolar lavage fluid were measured by lung histology, Diff-Quick staining, and ELISA. Chemokine-induced EOS chemotactic activity was evaluated using EOS chemotaxis assay. Electrophoretic mobility shift assay and Western blot analysis were performed to assess pulmonary NF-κB activation and IκBα expression, respectively.
As2O3 attenuated the allergen-induced serum IgE, chemokine expression of eotaxin and RANTES, and the EOS recruitment in bronchoalveolar lavage fluid, which is associated with an increased IκBα expression as well as a decreased NF-κB activation. Also, As2O3 suppressed the chemotaxis of EOS dose-dependently in vitro. Additionally, As2O3 significantly ameliorated the allergen-driven airway hyperresponsiveness, the cardinal feature underlying asthma.
These findings demonstrate an essential role of NF-κB in airway eosinophilia, and illustrate a potential dissociation between airway inflammation and hyperresponsiveness. As2O3 likely exerts its broad anti-inflammatory effects by suppression of NF-κB activation through augmentation of IκBα expression in asthma.
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Bronchial hyperresponsiveness in lung transplant recipients: lack of correlation with airway inflammation
Liakakos, P.
Snell, G. I.
Ward, C.
Johns, D. P.
Bamford, T. L.
Williams, T. J.
Walters, E. H.
BACKGROUND: Bronchial hyperresponsiveness (BHR) to methacholine has been reported to occur in most lung transplant recipients. BHR to physical stimuli such as exercise and non-isotonic aerosols has not been as extensively studied in this subject population. This report aims to assess the presence and degree of BHR to methacholine and hypertonic saline in stable lung transplant recipients and to relate it to the presence of airway inflammation. METHODS: Ten patients undergoing bilateral sequential lung transplantation and six heart-lung transplant recipients, all with stable lung function, were recruited 66- 1167 days following transplantation. Subjects underwent a methacholine challenge and bronchoscopy for sampling of bronchoalveolar lavage fluid, transbronchial and endobronchial biopsy tissues. Hypertonic saline challenge was performed six days later. RESULTS: Nine of the 16 transplant recipients had positive methacholine challenges (geometric mean PD20 0.18 mg, interquartile range 0.058-0.509) and three of these subjects also had positive hypertonic saline challenges (PD15 = 2.3, 33.0, and 51.5 ml). No clear relationship was found between BHR to either methacholine or hypertonic saline and levels of mast cells, eosinophils or lymphocytes in samples of biopsy tissue or lavage fluid. CONCLUSIONS: Most of the lung transplant recipients studied were responsive to methacholine and unresponsive to hypertonic saline. BHR was not clearly related to airway inflammation, suggesting an alternative mechanism for BHR following lung transplantation from that usually assumed in asthma.
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Bronchial Hyperresponsiveness to Methacholine and AMP in Children With Atopic Asthma
Kang, Sung Han
Kim, Hyung Young
Seo, Ju-Hee
Kwon, Ji-Won
Jung, Young Ho
Song, Young Hwa
Hong, Soo-Jong
Allergy, Asthma & Immunology Research
Bronchial hyperresponsiveness (BHR) is typically measured by bronchial challenge tests that employ direct stimulation by methacholine or indirect stimulation by adenosine 5'-monophosphate (AMP). Some studies have shown that the AMP challenge test provides a better reflection of airway inflammation, but few studies have examined the relationship between the AMP and methacholine challenge tests in children with asthma. We investigated the relationship between AMP and methacholine testing in children and adolescents with atopic asthma.
The medical records of 130 children with atopic asthma (mean age, 10.63 years) were reviewed retrospectively. Methacholine and AMP test results, spirometry, skin prick test results, and blood tests for inflammatory markers (total IgE, eosinophils [total count, percent of white blood cells]) were analyzed.
The concentration of AMP that induces a 20% decline in forced expiratory volume in 1 second [FEV1] (PC20) of methacholine correlated with the PC20 of AMP (r2=0.189, P<0.001). No significant differences were observed in the levels of inflammatory markers (total eosinophil count, eosinophil percentage, and total IgE) between groups that were positive and negative for BHR to methacholine. However, significant differences in inflammatory markers were observed in groups that were positive and negative for BHR to AMP (log total eosinophil count, P=0.023; log total IgE, P=0.020, eosinophil percentage, P<0.001). In contrast, body mass index (BMI) was significantly different in the methacholine positive and negative groups (P=0.027), but not in the AMP positive and negative groups (P=0.62). The PC20 of methacholine correlated with FEV1, FEV1/forced vital capacity (FVC), and maximum mid-expiratory flow (MMEF) (P=0.001, 0.011, 0.001, respectively), and the PC20 of AMP correlated with FEV1, FEV1/FVC, and MMEF (P=0.008, 0.046, 0.001, respectively).
Our results suggest that the AMP and methacholine challenge test results correlated well with respect to determining BHR. The BHR to AMP more likely implicated airway inflammation in children with atopic asthma. In contrast, the BHR to methacholine was related to BMI.
AMP; atopic asthma; bronchial hyper-responsiveness; methacholine
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T cell-dependent regulation of eotaxin in antigen-induced pulmonary eosinophila
The Journal of Experimental Medicine
T lymphocytes have been implicated in controlling the recruitment of eosinophils into the lung in murine models of allergic asthma. The mechanism by which T cells assist in the recruitment of eosinophils to the lung in these models is not completely understood. We hypothesized that eosinophil-active chemokines might be regulated by antigen (Ag)- induced T cell activation in vivo and thereby mediate T cell-dependent eosinophil recruitment. To test this hypothesis, we examined the effect of an anti-CD3 mAb on Ag-induced pulmonary eosinophilia and correlated this with the expression of three eosinophil-active chemokines: eotaxin, macrophage inflammatory protein (MIP)-1 alpha, and RANTES. We found that Ag-induced pulmonary eosinophilia was associated with the induction of eotaxin and MIP-1 alpha, but not RANTES mRNA. Prechallenge treatment with anti-CD3 mAb inhibited eotaxin, but not MIP-1 alpha and RANTES mRNA induction, and significantly reduced eosinophil accumulation in the lung. In addition, Ag-specific antibody responses and mast cell degranulation after Ag challenge in sensitized mice were not affected by T cell elimination, and were not sufficient to induce the expression of eotaxin and cause pulmonary eosinophilia. These findings suggest that eotaxin is one of the molecular links between Ag- specific T cell activation and the recruitment of eosinophils into the airways.
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Distinct expression and function of the novel mouse chemokine monocyte chemotactic protein-5 in lung allergic inflammation
The Journal of Experimental Medicine
We have cloned a novel mouse CC chemokine cDNA from the lung during an allergic inflammatory reaction. The protein encoded by this cDNA is chemotactic for eosinophils, monocytes, and lymphocytes in vitro and in vivo. Based on its similarities in sequence and function with other CC chemokines, we have named it mouse monocyte chemotactic protein-5 (mMCP- 5). Under noninflammatory conditions, expression of mMCP-5 in the lymph nodes and thymus is constitutive and is generally restricted to stromal cells. Neutralization of mMCP-5 protein with specific antibodies during an allergic inflammatory reaction in vivo resulted in a reduction in the number of eosinophils that accumulated in the lung. Moreover, mMCP- 5 mRNA expression in vivo is regulated differently from that of other major CC chemokines in the lung during the allergic reaction, including Eotaxin. The presence of lymphocytes is essential for expression of mMCP-5 by alveolar macrophages and smooth muscle cells in the lung, and the induction of mMCP-5 RNA occurs earlier than that of the eosinophil chemokine Eotaxin during allergic inflammation. In contrast to Eotaxin, mRNA for mMCP-5 can be produced by mast cells. From these results, we postulate that mMCP-5 plays a pivotal role during the early stages of allergic lung inflammation.
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Murine lung eosinophil activation and chemokine production in allergic airway inflammation
Rose, C Edward
Lannigan, Joanne A
Kim, Paul
Lee, James J
Fu, Shu Man
Sung, Sun-sang J
Cellular and Molecular Immunology
Eosinophils play important roles in asthma and lung infections. Murine models are widely used for assessing the functional significance and mechanistic basis for eosinophil involvements in these diseases. However, little is known about tissue eosinophils in homeostasis. In addition, little data on eosinophil chemokine production during allergic airway inflammation are available. In this study, the properties and functions of homeostatic and activated eosinophils were compared. Eosinophils from normal tissues expressed costimulation and adhesion molecules B7-1, B7-2 and ICAM-1 for Ag presentation but little major histocompatibility complex (MHC) class II, and were found to be poor stimulators of T-cell proliferation. However, these eosinophils expressed high levels of chemokine mRNA including C10, macrophage inflammatory protein (MIP)-1α, MIP-1γ, MIP-2, eotaxin and monocyte chemoattractant protein-5 (MCP-5), and produced chemokine proteins. Eosinophil intracellular chemokines decreased rapidly with concomitant surface marker downregulation upon in vitro culturing consistent with piecemeal degranulation. Lung eosinophils from mice with induced allergic airway inflammation exhibited increased chemokines mRNA expression and chemokines protein production and upregulated MHC class II and CD11c expression. They were also found to be the predominant producers of the CCR1 ligands CCL6/C10 and CCL9/MIP-1γ in inflamed lungs. Eosinophil production of C10 and MIP-1γ correlated with the marked influx of CD11bhigh lung dendritic cells during allergic airway inflammation and the high expression of CCR1 on these dendritic cells (DCs). The study provided baseline information on tissue eosinophils, documented the upregulation of activation markers and chemokine production in activated eosinophils, and indicated that eosinophils were a key chemokine-producing cell type in allergic lung inflammation.
allergy; chemokines; eosinophils; lung; mouse
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Murine lung eosinophil activation and chemokine production in allergic airway inflammation
Rose, C Edward
Lannigan, Joanne A
Kim, Paul
Lee, James J
Fu, Shu Man
Sung, Sunsang J
Cellular & molecular immunology
Eosinophils play important roles in asthma and lung infections. Murine models are widely used for assessing the functional significance and mechanistic basis for eosinophil involvements in these diseases. However, little is known about tissue eosinophils in homeostasis. In addition, little data on eosinophil chemokine production during allergic airway inflammation are available. In this study, the properties and functions of homeostatic and activated eosinophils were compared. Eosinophils from normal tissues expressed costimulation and adhesion molecules B7-1, B7-2 and ICAM-1 for Ag presentation but little major histocompatibility complex (MHC) class II, and were found to be poor stimulators of T-cell proliferation. However, these eosinophils expressed high levels of chemokine mRNA including C10, macrophage inflammatory protein (MIP)-1α, MIP-1γ, MIP-2, eotaxin and monocyte chemoattractant protein-5 (MCP-5), and produced chemokine proteins. Eosinophil intracellular chemokines decreased rapidly with concomitant surface marker downregulation upon in vitro culturing consistent with piecemeal degranulation. Lung eosinophils from mice with induced allergic airway inflammation exhibited increased chemokines mRNA expression and chemokines protein production and upregulated MHC class II and CD11c expression. They were also found to be the predominant producers of the CCR1 ligands CCL6/C10 and CCL9/MIP-1γ in inflamed lungs. Eosinophil production of C10 and MIP-1γ correlated with the marked influx of CD11bhigh lung dendritic cells during allergic airway inflammation and the high of CCR1 on these dendritic cells (DCs). The study provided baseline information on tissue eosinophils, documented the upregulation of activation markers and chemokine production in activated eosinophils, and indicated that eosinophils were a key chemokine-producing cell type in allergic lung inflammation.
allergy; chemokines; eosinophils; lung; mouse
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Low dose of Mycoplasma pneumoniae (Mp) infection enhances an established allergic inflammation in mice: Role of prostaglandin E2 (PGE2) pathway
Wu, Qun
Martin, Richard J.
LaFasto, Spencer
Chu, Hong Wei
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
Over 40% of chronic stable asthma patients have evidence of respiratory Mycoplasma pneumoniae (Mp) infection as detected by polymerase chain reaction (PCR), but not by serology and culture, suggesting a low-level Mp involved in chronic asthma. However, the role of such a low-level Mp infection in regulation of allergic inflammation remains unknown.
To determine the impact of a low-level Mp infection in mice with established airway allergic inflammation on allergic responses such as eosinophilia and chemokine eotaxin-2, and the underlying mechanisms (i.e., prostaglandin E2 [PGE2] pathway) since PGE2 inhalation before allergen challenge suppressed eosinophil infiltration in human airways.
BALB/c mouse models of ovalbumin (OVA)-induced allergic asthma with an ensuing low-dose or high-dose Mp were used to assess IL-4 expression, BAL eosinophil, eotaxin-2 and PGE2 levels, and lung mRNA levels of microsomal prostaglandin E synthase-1 (mPGES-1). Primary alveolar macrophages (pAMs) from naïve BALB/c mice were cultured to determine if Mp-induced PGE2 or exogenous PGE2 down-regulates IL-4/IL-13-induced eotaxin-2.
Low-dose Mp in allergic mice significantly enhanced IL-4 and eotaxin-2, and moderately promoted lung eosinophilia, whereas high-dose Mp significantly reduced lung eosinophilia and tended to decrease IL-4 and eotaxin-2. Moreover, in both OVA-naïve and allergic mice, lung mPGES-1 mRNA and BAL PGE2 levels were elevated in mice infected with high-dose, but not low-dose Mp. In pAMs, IL-4/IL-13 significantly increased eotaxin-2, which was reduced by Mp infection accompanied by dose-dependent PGE2 induction. Exogenous PGE2 inhibited IL-4/IL-13-induced eotaxin-2 in a dose-dependent manner.
This study highlights a novel concept on how differing bacterial loads in the lung modify the established allergic airway inflammation, and thus interact with an allergen to further induce Th2 responses. That is: Unlike high-level Mp, low-level Mp fails to effectively induce PGE2 to down-regulate allergic responses (e.g., eotaxin-2), thus maintaining or even worsening allergic inflammation in asthmatic airways.
asthma; Mycoplasma pneumoniae; eotaxin-2; PGE2; alveolar macrophages
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Ca2+-signaling in airway smooth muscle cells is altered in T-bet knock-out mice
Bergner, Albrecht
Kellner, Julia
Kemp da Silva, Anita
Gamarra, Fernando
Huber, Rudolf M
Respiratory Research
Airway smooth muscle cells (ASMC) play a key role in bronchial hyperresponsiveness (BHR). A major component of the signaling cascade leading to ASMC contraction is calcium. So far, agonist-induced Ca2+-signaling in asthma has been studied by comparing innate properties of inbred rat or mouse strains, or by using selected mediators known to be involved in asthma. T-bet knock-out (KO) mice show key features of allergic asthma such as a shift towards TH2-lymphocytes and display a broad spectrum of asthma-like histological and functional characteristics. In this study, we aimed at investigating whether Ca2+-homeostasis of ASMC is altered in T-bet KO-mice as an experimental model of asthma.
Lung slices of 100 to 200 μm thickness were obtained from T-bet KO- and wild-type mice. Airway contraction in response to acetylcholine (ACH) was measured by video-microscopy and Ca2+-signaling in single ASMC of lung slices was assessed using two-photon-microscopy.
Airways from T-bet KO-mice showed increased baseline airway tone (BAT) and BHR compared to wild-type mice. This could be mimicked by incubation of lung slices from wild-type mice with IL-13. The increased BAT was correlated with an increased incidence of spontaneous changes in intracellular Ca2+-concentrations, whereas BHR correlated with higher ACH-induced Ca2+-transients and an increased proportion of ASMC showing Ca2+-oscillations. Emptying intracellular Ca2+-stores using caffeine or cyclopiazonic acid induced higher Ca2+-elevations in ASMC from T-bet KO- compared to wild-type mice.
Altered Ca2+-homeostasis of ASMC contributes to increased BAT and BHR in lung slices from T-bet KO-mice as a murine asthma model. We propose that a higher Ca2+-content of the intracellular Ca2+-stores is involved in the pathophysiology of these changes.
Related Articles
Anti-Malarial Drug Artesunate Attenuates Experimental Allergic Asthma via Inhibition of the Phosphoinositide 3-Kinase/Akt Pathway
Cheng, Chang
Ho, W. Eugene
Goh, Fera Y.
Guan, Shou Ping
Kong, Li Ren
Lai, Wen-Qi
Leung, Bernard P.
Wong, W. S. Fred
PLoS ONE
Phosphoinositide 3-kinase (PI3K)/Akt pathway is linked to the development of asthma. Anti-malarial drug artesunate is a semi-synthetic derivative of artemisinin, the principal active component of a medicinal plant Artemisia annua, and has been shown to inhibit PI3K/Akt activity. We hypothesized that artesunate may attenuate allergic asthma via inhibition of the PI3K/Akt signaling pathway.
Methodology/Principal Findings
Female BALB/c mice sensitized and challenged with ovalbumin (OVA) developed airway inflammation. Bronchoalveolar lavage fluid was assessed for total and differential cell counts, and cytokine and chemokine levels. Lung tissues were examined for cell infiltration and mucus hypersecretion, and the expression of inflammatory biomarkers. Airway hyperresponsiveness was monitored by direct airway resistance analysis. Artesunate dose-dependently inhibited OVA-induced increases in total and eosinophil counts, IL-4, IL-5, IL-13 and eotaxin levels in bronchoalveolar lavage fluid. It attenuated OVA-induced lung tissue eosinophilia and airway mucus production, mRNA expression of E-selectin, IL-17, IL-33 and Muc5ac in lung tissues, and airway hyperresponsiveness to methacholine. In normal human bronchial epithelial cells, artesunate blocked epidermal growth factor-induced phosphorylation of Akt and its downstream substrates tuberin, p70S6 kinase and 4E-binding protein 1, and transactivation of NF-κB. Similarly, artesunate blocked the phosphorylation of Akt and its downstream substrates in lung tissues from OVA-challenged mice. Anti-inflammatory effect of artesunate was further confirmed in a house dust mite mouse asthma model.
Artesunate ameliorates experimental allergic airway inflammation probably via negative regulation of PI3K/Akt pathway and the downstream NF-κB activity. These findings provide a novel therapeutic value for artesunate in the treatment of allergic asthma.
Related Articles
Chemokine-induced eosinophil recruitment. Evidence of a role for endogenous eotaxin in an in vivo allergy model in mouse skin.
Teixeira, M M
Wells, T N
Lukacs, N W
Proudfoot, A E
Kunkel, S L
Williams, T J
Hellewell, P G
Journal of Clinical Investigation
Selective eosinophil recruitment into tissues is a characteristic feature of allergic diseases. Chemokines are effective leukocyte chemoattractants and may play an important role in mediating eosinophil recruitment in various allergic conditions in man. Here, we describe a novel mouse model of eosinophil recruitment in which we have compared the in vivo chemoattractant activity of different C-C chemokines. Furthermore, we describe the use of antibodies to chemokines and receptor blockade to address the endogenous mechanisms involved in eosinophil recruitment in a late-phase allergic reaction in mouse skin. Intradermal injection of mEotaxin and mMIP-1alpha, but not mMCP-1, mRANTES, mMCP-5, or mMIP-1beta, induced significant 111In-eosinophil recruitment in mouse skin. Significant 111In-eosinophil recruitment was also observed in an active cutaneous anaphylactic reaction. Pretreatment of skin sites with antieotaxin antiserum, but not an antiMIP-1alpha antibody, suppressed 111In-eosinophil recruitment in this delayed-onset allergic reaction. Similarly, desensitization of the eosinophil eotaxin receptor CCR3 with mEotaxin, or blockade of the receptor with metRANTES, significantly inhibited 111In-eosinophil recruitment in the allergic reaction. These results demonstrate an important role for endogenous eotaxin in mediating the 111In-eosinophil recruitment in allergic inflammation, and suggest that blockade of the CCR3 receptor is a valid strategy to inhibit eosinophil migration in vivo.
Related Articles
γδ T Lymphocytes Coordinate Eosinophil Influx during Allergic Responses
de Oliveira Henriques, Maria Das Graças Muller
Penido, Carmen
Frontiers in Pharmacology
Tissue eosinophil infiltration, which is a hallmark of allergic and helminthic diseases, is mainly coordinated by T lymphocytes, via the production of eosinophilotactic chemokines. Among T lymphocyte subsets, lymphocytes expressing γδ T cell receptor have been determined as a key factor for eosinophil accumulation via direct and indirect mechanisms. This knowledge is strongly supported by the fact that, in different experimental models of eosinophilic airway inflammation and helminth-induced Th2 lung inflammation, an evident tissue accumulation of γδ T lymphocytes is observed. In addition, the depletion of γδ T lymphocytes is correlated with the impairment of eosinophil accumulation in inflamed tissue. γδ T lymphocytes are non-conventional T lymphocytes, which comprise a minor T lymphocyte subset, mainly distributed in the tissue, and present crucial roles in innate and acquired immune responses. γδ T lymphocytes recognize several danger- and pathogen-associated molecular pattern molecules and stress antigens in a MHC-independent fashion and can provide rapid tissue-specific responses, via the production of a wide range of chemical mediators capable to modulate other cell populations. These mediators include chemoattractant cytokines and chemokines that attract eosinophils into the tissue by either direct recognition (such as IL-5, CCL11/eotaxin), or indirect mechanisms via the modulation of αβ T lymphocytes and macrophages (through the production of interferon-γ, IL-4, and CCL2/Monocyte chemoattractant protein-1, MCP-1, for example). The present review presents an overview of how γδ T lymphocytes coordinate eosinophil accumulation in allergy, by focusing on their role in airway inflammation and by discussing the involvement of cytokines and chemokines in this phenomenon.
integrin α4β1; selectins; MCP-1; IL-17; leukotriene B4
Related Articles
320 Development of a Questionnaire for the Assessment of Bronchial Hyperresponsiveness in Korea
Lim, Seong Yong
Yoo, Kwang HA
Shim, Jae-Jeong
Kim, Kwan Hyung
The World Allergy Organization Journal
2012;5(Suppl 2):S120.
Bronchial hyperresponsiveness (BHR) is an important pathophysiological feature of asthma. In addition to the diagnostic significance, BHR is associated with the severity of airway inflammation and BHR- based treatment approaches has been shown to be effective. Nevertheless, challenge tests are time consuming, inconvenient to patients, and are not accessible in every primary care physicians. We aimed to develop a questionnaire for the assessment of BHR in Korean subjects.
From the 24 University-affiliated hospitals, we recruited 149 adults between age 20 and 40 years with more than one asthmatic symptom (cough, sputum or dyspnea) and who had bronchial provocation test. A list of 33 symptoms, past history of allergy or smoking and 10 provoking stimuli were selected for the BHR questionnaire. After a methacholine challenge test patients were asked to complete each questionnaire. For each item of questionnaire, diagnostic odds ratios for the presence of BHR were calculated and multiple logistic regression analysis was performed to select final questionnaire items. Receiver operating characteristic (ROC) curve analysis was used to evaluate the sensitivity and specificity of the selected questionnaire items.
Methacholine challenge test was positive in 36 patients (24.2%). Eleven symptoms and 2 provoking stimuli items were statistically significant by the results of diagnostic odds ratio. According to the result of multiple logistic regression analysis, 4 items were finally selected for the significant BHR questionnaire: the presence of wheezing episode, past history of physician-diagnosed asthma, family history of asthma. The psychiatric stress was negatively associated provoking stimuli item for the presence of BHR. The area under the ROC curve was 0.80 (95% CI, 0.72-0.86). Sensitivity was 84.9% (95% CI, 68.1-94.9) and specificity was 65.5% (95% CI, 55.8-74.3).
Four BHR questionnaire items including wheezing episode, past history of physician-diagnosed asthma, family history of asthma and psyachiatric stress stimuli were able to assess the presence of BHR in Korean adults.
Related Articles
Nasal eosinophilic inflammation contributes to bronchial hyperresponsiveness in patients with allergic rhinitis.
Jang, An-Soo
Journal of Korean Medical Science
There are increasing evidences that allergic rhinitis (AR) may influence the clinical course of asthma. We conducted methacholine challenge test and nasal eosinophils on nasal smear to patients with allergic rhinitis in order to investigate the mechanism of connecting upper and lower airway inflammation in 35 patients with AR during exacerbation. The methacholine concentration causing a 20% fall in FEV1 (PC20) was used as thresholds of bronchial hyperresponsiveness (BHR). Thresholds of 25 mg/dL or less were assumed to indicate BHR. All patients had normal pulmonary function. Significant differences in BHR were detected in the comparison of patients with cough or postnasal drip and without cough or postnasal drip. There were significant differences of PC20 between patients with cough or postnasal drip and those without cough or postnasal drip (3.41+/-3.59 mg/mL vs 10.2+/-1.2 mg/mL, p=0.001). The levels of total IgE were higher in patients with seasonal AR than in patients with perennial AR with exacerbation (472.5+/-132.5 IU/L vs. 389.0+/-70.9 IU/L, p<0.05). Nasal eosinophils were closely related to log PC20 (r=-0.65, p<0.01). These findings demonstrated that nasal eosinophilic inflammation might contribute to BHR in patients with AR.
Related Articles
Effects of steroid treatment on lung CC chemokines, apoptosis and transepithelial cell clearance during development and resolution of allergic airway inflammation
Uller, L.
Lloyd, C. M.
Rydell-Törmänen, K.
Persson, C. G. A.
Erjefält, J. S.
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
Steroid treatment of allergic eosinophilic airway diseases is considered to attenuate cell recruitment by inhibiting several chemokines and to cause eosinophil clearance through inducement of apoptosis of these cells. However, roles of these mechanisms in the actions of steroids in vivo have not been fully established. Also, as regards clearance of tissue eosinophils other mechanisms than apoptosis may operate in vivo.
This study explores anti-inflammatory effects of steroids instituted during either development or resolution of airway allergic inflammation.
Immunized mice were subjected to week-long daily allergen challenges (ovalbumin). Steroid treatment was instituted either amidst the challenges or exclusively post-allergen challenge. CC chemokines, goblet cell hyperplasia, occurrence of eosinophil apoptosis, and airway tissue as well as lumen eosinophilia were examined at different time-points.
Daily steroids instituted amid the allergen challenges non-selectively attenuated a range of chemokines, permitted egression of tissue eosinophils into airway lumen to increase, and reduced development of lung tissue eosinophilia. Steroid treatment instituted post-challenge selectively inhibited the CC-chemokine regulation upon activation, normal T cell expressed and secrted (RANTES), permitted continued egression of eosinophils into airway lumen, and resolved the tissue eosinophilia. Eosinophil apoptosis rarely occurred at development and resolution of the allergic eosinophilic inflammation whether the animals were steroid treated or not. However, anti-Fas monoclonal antibodies given to mice with established eosinophilia post-challenge produced apoptosis of the tissue eosinophils indicating that apoptotic eosinophils, if they occur, are well detectible in vivo.
Airway tissue eosinophils are likely eliminated through egression into airway lumen with little involvement of apoptosis and phagocytosis. Our data further suggest that therapeutic steroids may resolve airway inflammation by permitting clearance of tissue eosinophils through egression and inhibiting RANTES-dependent cell recruitment to lung tissues.
apoptosis; asthma; chemokines; glucocorticoids
Related Articles
Nonhematopoietic NADPH oxidase regulation of lung eosinophilia and airway hyperresponsiveness in experimentally induced asthma
Abdala-Valencia, Hiam
Earwood, Julie
Bansal, Shelly
Jansen, Michael
Babcock, George
Garvy, Beth
Wills-Karp, Marsha
Cook-Mills, Joan M.
American journal of physiology. Lung cellular and molecular physiology
Pulmonary eosinophilia is one of the most consistent hallmarks of asthma. Infiltration of eosinophils into the lung in experimental asthma is dependent on the adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells. Ligation of VCAM-1 activates endothelial cell NADPH oxidase, which is required for VCAM-1-dependent leukocyte migration in vitro. To examine whether endothelial-derived NADPH oxidase modulates eosinophil recruitment in vivo, mice deficient in NADPH oxidase (CYBB mice) were irradiated and received wild-type hematopoietic cells to generate chimeric CYBB mice. In response to ovalbumin (OVA) challenge, the chimeric CYBB mice had increased numbers of eosinophils bound to the endothelium as well as reduced eosinophilia in the lung tissue and bronchoalveolar lavage. This occurred independent of changes in VCAM-1 expression, cytokine/chemokine levels (IL-5, IL-10, IL-13, IFNγ, or eotaxin), or numbers of T cells, neutrophils, or mononuclear cells in the lavage fluids or lung tissue of OVA-challenged mice. Importantly, the OVA-challenged chimeric CYBB mice had reduced airway hyperresponsiveness (AHR). The AHR in OVA-challenged chimeric CYBB mice was restored by bypassing the endothelium with intratracheal administration of eosinophils. These data suggest that VCAM-1 induction of NADPH oxidase in the endothelium is necessary for the eosinophil recruitment during allergic inflammation. Moreover, these studies provide a basis for targeting VCAM-1-dependent signaling pathways in asthma therapies.
endothelium; gp91 phox; eosinophils; VCAM-1
Related Articles
Relationship Between Atopy and Bronchial Hyperresponsiveness
Suh, Dong In
Koh, Young Yull
Allergy, Asthma & Immunology Research
Both atopy and bronchial hyperresponsiveness (BHR) are characteristic features of asthma. They are also found among non-asthmatic subjects, including allergic rhinitis patients and the general population. Atopy and BHR in asthma are closely related. Atopy induces airway inflammation as an IgE response to a specific allergen, which causes or amplifies BHR. Moreover, significant evidence of the close relationship between atopy and BHR has been found in non-asthmatic subjects. In this article, we discuss the relationship between atopy and BHR in the general population, asthmatic subjects, and those with allergic rhinitis. This should widen our understanding of the pathophysiology of atopy and BHR.
Allergic rhinitis; asthma; atopy; bronchial hyperresponsiveness; patients; population
Related Articles
Rhinovirus infection of allergen-sensitized and -challenged mice induces eotaxin release from functionally polarized macrophages
Nagarkar, Deepti R.
Bowman, Emily R.
Schneider, Dina
Wang, Qiong
Shim, Jee
Zhao, Ying
Linn, Marisa J.
McHenry, Christina L.
Gosangi, Babina
Bentley, J. Kelley
Tsai, Wan C.
Sajjan, Umadevi S.
Lukacs, Nicholas W.
Hershenson, Marc B.
Journal of immunology (Baltimore, Md. : 1950)
Human rhinovirus is responsible for the majority of virus-induced asthma exacerbations. To determine the immunologic mechanisms underlying rhinovirus-induced asthma exacerbations, we combined mouse models of allergic airways disease and human rhinovirus infection. We inoculated ovalbumin-sensitized and challenged BALB/c mice with rhinovirus serotype 1B, a minor group strain capable of infecting mouse cells. Compared to sham-infected, ovalbumin-treated mice, virus-infected mice showed increased lung infiltration with neutrophils, eosinophils and macrophages, airway cholinergic hyperresponsiveness, and increased lung expression of cytokines including eotaxin-1/CCL11, IL-4, IL-13 and IFN-γ. Administration of anti-eotaxin-1 attenuated rhinovirus-induced airway eosinophilia and responsiveness. Immunohistochemistry showed eotaxin-1 in the lung macrophages of virus-infected, ovalbumin-treated mice, and confocal fluorescence microscopy revealed co-localization of rhinovirus, eotaxin-1 and IL-4 in CD68-positive cells. RV inoculation of lung macrophages from ovalbumin-treated, but not PBS-treated, mice induced expression of eotaxin-1, IL-4, and IL-13 ex vivo. Macrophages from ovalbumin-treated mice showed increased expression of arginase-1, Ym-1, Mgl-2 and IL-10, indicating a shift in macrophage activation status. Depletion of macrophages from ovalbumin-sensitized and -challenged mice reduced eosinophilic inflammation and airway hyperreactivity following RV infection. We conclude that augmented airway eosinophilic inflammation and hyperresponsiveness in RV-infected mice with allergic airways disease is directed in part by eotaxin-1. Airway macrophages from mice with allergic airways disease demonstrate a change in activation state characterized in part by altered eotaxin and IL-4 production in response to RV infection. These data provide a new paradigm to explain RV-induced asthma exacerbations.
Related Articles
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Mission College Computer Applications
Dept. Chair: Curtis Pembrook
Email: firstname.lastname@example.com
Tel: 408-855-5275
Counseling: 408-855-5030
Division: Business and Technology
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The Computer Applications program at Mission is designed to provide skills necessary for success in the 21st century workplace. This includes a focus on
- Office Productivity
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The Office Productivity area is designed to provide skills necessary for success in an ever evolving workplace setting.
The Mobile/Web applications and Cloud Technologies area provides skills necessary to effectively extend workplace collaboration, communication, and knowledge.
The Web markup and Client-side scripting languages area prepares students to develop websites and client-side web/mobile applications.
- Students can take classes on a wide range of application packages offered for the whole semester, online, and for short time periods (five to six weeks).
- Students can earn a variety of certificates and degrees.
- Instructors have strong computer backgrounds who care about your success.
- Classes are offered at beginning, intermediate and advanced levels.
- There are opportunities to apply your knowledge and skills through internships.
Career Options:
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Some career options may require more than two years of college study.
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The Summer/Fall 2016 Schedule of Classes is out. Enroll in the following courses today.
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