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Game 98: Tampa Bay at Toronto pregame
Let's take a break from all this Roy Halladay stuff for a minute, ok? No? Fine. A report indicates that the Phils rejected an offer from the Jays that would've swapped Halladay for Kyle Drabek, J.A. Happ and Dominic Brown.
Moving on…
Let's turn to the fans' favorite punching bag this season: center fielder Vernon Wells. More to the point, have you seen his home-road splits this season? Take a look:
As I've written numerous times this season, no one is more frustrated with Wells' showing this year than Wells himself. He finally put together a nice little 10-game run before the All-Star break, but then came down with a bad flu bug and missed three games. Since then, he has gone 2-for-16 at the plate, entering Saturday's game.
Manager Cito Gaston was asked if there was any way to explain the drastic difference in Wells' numbers at home versus on the road. If you were at Rogers Centre on Friday night, you might have heard the loud boos directed Wells' way all evening. Gaston said that could have a little something to do with it.
"I can hear the fans starting to boo him," Gaston aid. "Whether you believe it or not, you hear that. You hear that. When they boo you on the road, you just try to kick their butts even more. But when it's your own fans, it certainly gets to you a little bit more. But that hasn't always happened — this has just happened lately. So, I'm not sure."
Gaston also talked some about right-hander Casey Janssen, who was activated from the DL on Thursday and optioned to Triple-A Las Vegas rather than being called up to rejoin the Jays. The manager said Janssen isn't quite ready to come back, but when he does, the pitcher will likely be a reliever again.
Asked if Janssen was being viewed long-term as a reliever again, Gaston said he wasn't completely sure.
"I have different thoughts about guys in bullpens and guys that start that have bad arms," said Gaston, referring to Janssen's recent shoulder woes. "To me, I've always thought that maybe the bullpen was the worst thing for you, but everybody seems to think — and maybe he's proved that, too — that he's better off in the bullpen. I don't know.
"You start, you rest for a couple of days, and then you throw again, and then you pitch again. But in the bullpen, you can be up and down, two or three days. I haven't quite figured that one out yet, but maybe he's different. I haven't had him in the bullpen, so we'll see what happens."
Today's lineups:
Third place AL East, 6.5 GB
1. B.J. Upton, CF
2. Carl Crawford, LF
3. Evan Longoria, 3B
4. Ben Zobrist, SS
5. Pat Burrell, DH
6. Carlos Pena, 1B
7. Gabe Kapler, RF
8. Willy Aybar, 2B
9. Dioner Navarro, C
Starter: LHP David Price (3-4, 4.86)
Fourth place AL East, 12.5 GB
1. Marco Scutaro, SS
2. Aaron Hill, 2B
3. Adam Lind, DH
4. Scott Rolen, 3B
5. Kevin Millar, 1B
6. Vernon Wells, CF
7. Alex Rios, RF
8. Jose Bautista, LF
9. Raul Chavez, C
Starter: LHP Brian Tallet (5-6, 4.95)
Don't forget, you can follow me on Twitter: @MLBastian
26 Comments
Cito took a gamble on sending Tallet back out there for the 7th inning and lost the gamble along with the game. Although Tallet's pitch count was only in the high 80's, he has also thrown almost double the innings, he's ever thrown in a year already. We risk injury with him every time out and he should have been pulled after 6.
TB got to Tallet, got momentum and Downs blew his third save in a row which is something I don't think he's ever done in his Blue Jays career (hope nothing is wrong with him).
We've now lost a number of games in this home stand with errors, miscues, missed signals, missed opportunities and just over all really sloppy play. It's painful watching the lack of hitting fundamentals on moving runners from second to 3rd. It appears, the Halladay circus might be affecting the team more than it is Halladay.
On the good side, Hill, for a brief moment was tied for the AL league in home runs, and Scott Richmond went 5.1 innings in Vegas last night, threw about 80 pitches, gave up 2 hits, 1 earned run, 1 walked and struck out 5, so I think he's about ready to return.
Regarding any potential Halladay trade to the Phillies, why not sweeten the pot by adding League to the mix. Make it a four for two or five for two deal? The bottom line is obtaining the players that you covet.
Personally, I don't know why we want Happ in the first place. He's a soft throwing left hander who doesn't measure up to either Romero, Cecil or Rzep. Most of our pitching prospects are left handers-we're loaded with them, so why press for another one who isn't as good as the ones we already have. I'd prefer we got Drabek, Taylor and Brown with Donald thrown in. Drabek is a power right hander who can bring it at mid to higher 90's who could very quickly become our ace. Both Taylor and Brown are A hitting prospects-albeit them outfielders.
I think I like the deal with LA if we get what we asked for which apparently is pitchers Joe Saunders and Sean O?Sullivan and infielders Erick Aybar and Brandon Wood. To me the two guys that make this deal are Wood and Aybar-a 3rd baseman and shortstop.
I wouldn't trade League, I would package Downs, Tallet and or Fraser though. I still think League is our closer in the future.
Glad to see the Jays turned down The Phillies offer of Happ Michael Taylor, pitcher Carlos Carrasco and shortstop Jason Donald.
Lets get Drabek and Brown instead of Happ. The key guys, (IMO) are Drabek, Taylor and Donald.
I agree with you gsjays. However, I doubt the Jays are really after Happ. His name is mentioned in every trade combination/permutation, but there must be someone else the Jays' really want whose name is not being mentioned. Hopefully, something can get done. As for League, his ability to strike out the side is definitely appealing, but I think that we might be able to fashion Purcey into a closing role. We already have 3 other good left handers. Moving League now may provide us with the opportunity to pick up a tier 1 prospect who can hit. Anyway, I just hope that they move Halladay and soon. I am so tired of reading about all this stuff in the media with no results. The whole thing reminds me of Burke, Kaberle and Kessel — a lot of talk, followed by a lot of spin doctoring as to why we need to keep the player once they failed to trade him!!!!
Here is another thought. Remember, JP knows that he is either going to be fired or let go after his contract expires. The trade for Halladay has as much to do with JP's future as it does the Jays. If he robs some poor fool, blind, he will look like a star (at least in his own eyes) and may find a job as a scout with some other organization. If the perception is that he got less than fair value for Halladay, it will reinforce the perception that he is a dummy and his time in baseball will be over. I would prefer to have Beeston handling the negotiations directly.
I think the biggest risk is JP screws up the deal from incompetence, gets a marginal offer like what he's got from the Phillies, nothing is done and we go into an era of 5th or 4th place finishes with limited chance of improving until Wells contract is up.
Not sure about Purcey. I really thought he would straighten out his mechanical and control issues in AAA this year, but so far it doesn't appear like he has.
One game he's great, then the next one he explodes. In the last 3 games he's given up 9,4,2 earned runs and walked 6,3,2 in 5-6.2 innings.
I cannot imagine Purcey as a closer. On the days he struggles with control his worst inning seems to always be the first. Even on days he's great, he still seems to struggle in the first.
One guy who potentially might become The Jays closer is Daniel Farquhar who is the closer with New Hampshire. In his last 9 games (9.2 innings), he's saved 7, halted two, given up 2 hits, walked 4, struck out 13 and given up 0 earned runs. He's from the 2008 draft class and has been a pro just a little over a year, so he's rising fast-as he should be.
He has, without question, the best record or any reliever the Jays have in the upper minors, so I'd be disappointed if he wasn't either promoted to Vegas soon or called up in September and if he keeps up doing what he's doing I'd expect he's a Jay next spring. Here's a scout report on him.
Remember the name Daniel Farquhar, a side-winding reliever.
"I saw him last week at class-A Dunedin. He'll be at double-A in 10 days and in the majors by September," said another scout last weekend in Atlanta. "Most guys down there don't throw hard. He was 89-95 m.p.h. with a plus-slider. Hitters didn't have a chance — right or left-handed."
For his sake, Ricciardi better be bluffing
by Michael Rosenberg as posted on foxsports.com
J.P. Ricciardi, the general manager of the Toronto Blue Jays, is known mostly for talking too much. Actually, that's not fair. He is also known for saying the wrong things. And for saying them at inappropriate times. There are better things to be known for ? like, just for example, winning ? but we take what we can get in this world.
We can only hope that Ricciardi is taking one of his own (in)famous quotes to heart this week. After lying about a player's injury, Ricciardi explained, "They're not lies if we know the truth."
Please, J.P., tell me you're lying. Tell me you really ARE going to trade ace Roy Halladay, despite what you told FOXSports.com's Ken Rosenthal Sunday. Tell me you have thought this through, and you know the best move is to deal Halladay now, while he is as valuable as he'll ever be, and while it can help the Blue Jays the most.
I can only hope, for his sake, that Ricciardi is bluffing. I hope he is smoking out offers with the full intention of taking the best one. In fact, by this point, I hope he already has an offer that he is willing to take, and is simply trying to get an even better one.
And I really hope he has asked this question: What happens if the trade deadline passes and Roy Halladay is still a Blue Jay?
If that happens, then Ricciardi will have announced to the world that he might trade Halladay, then turned down several very nice offers in the hope that the stars align for Toronto in 2010. He will have surrendered his chips.
Balance of article here: http://msn.foxsports.com/mlb/story/9858348/For-his-sake,-Ricciardi-better-be-bluffing
Ultimatley, if Purcey cannot throw strikes he will be nothing more than a good AAA pitcher; especially with all the pitchers that have passed by him this year. I wouldn't mind him being at least tried in the bullpen because other than a couple years starting has been a failure. At this point the Jay have nothing to lose.
Purcey has absolutely electric stuff, and I believe there is a no-hitter in that arm somewhere. From watching him pitch, I believe the problem is mental, rather than mechanical, and he seems to lose concentration at some point and loses it. Maybe they should give him Halladay's book "The Mental Aspect of Pitching", and turn him over to Mel Queen for a while.
"Will the real Kelvim Escobar please stand up?" When Escobar pitched for us, I got pretty good at predicting how he would do by the way he wore his hat. If it was square and down over his eyes, he was in for a good outing. High and back on his forehead a bit, and I could turn off the TV and spare myself the pain.
Another thing that happens to power pitchers like Purcey is that throughout their high school and minor league careers, they never have to face more than 2 or 3 good hitters in a lineup, and get used to just blowing the fasttball past them when they get in trouble. In the majors, you face a whole lot of guys that will turn on a fastball, so there is a big adjustment. They try to compensate by overthrowing, and as a consequence, lose their control. Lets hope Purcey can make the adjustment, because it would be really fun to see him and Romero fighting it out for #1 spot for a few years.
Arnsberg did identify Purcey's mechanical problem when Purcey was here. He also identified how Purcey could fix it, so either Arnsberg was wrong (which I doubt) or Purcey is having difficulty making the adjustment and it might be he never can do it-who knows at this point.
I doubt if it has anything to do with adjusting from college to pro ball since Purcey has been a pro for 5 years.
It could also be that weather has something to do with Purcey's erratic performance as well. There were a couple of games he really blew up in, and the game time temperature was about 107. I'm not sure Vegas is where our AAA affiliate should be. I think the next two or three starts will tell the tale with Purcey and it could be sink or swim.
Looks like Snider might be warming up in AAA. In his last two games Travis has gone 5 for 9 with 2 home runs and 4 rbi.'s.
Here is an idea. Trade Purcey. A huge, young, left-handed starter. There is not a pitching coach in either league who does not think that he can fix Purcey and get him on the right track. Package him with DOC, then ask for the farm. Make it a 5 or 6 for 2 deal. Let's get this thing done, already.
TORONTO — The company that owns the Toronto Blue Jays says it needs to control costs.
Rogers Communications remains committed to the Blue Jays, CEO Nadir Mohamed said Tuesday on a conference call discussing the company's quarterly earnings. The team has put ace Roy Halladay on the trading block.
Rogers bought the Blue Jays in 2000. The company also owns the team's stadium and its flagship radio and television stations, the FAN 590 and Rogers Sportsnet.
"We believe that the financial performance of the Blue Jays can improve," said Tony Viner, president of Rogers Media, the corporate arm responsible for the team, stadium and broadcasting. "In fact, it's the one division of the media company this year, year over year performance is better than it was. We think that we can bring costs reasonably under control and more in line with revenues.
Burt-I like that idea
I think trading Purcey would be a good move. Not that I don't like the guy but the team seems to have quite a few better pitching options at this point; a lot of them younger than Purcey.
I could see Purcey less being traded with Halladay and more being traded with a position player like Rolen.
So Boston have offered Buckholtz and 2 unannounced AAA players. Let's include their choice of Barajas and Scutaro, get Lowrie, Buckholtz and our choice of 2 minor leaguers.
"I doubt if it has anything to do with adjusting from college to pro ball since Purcey has been a pro for 5 years."
gsjays, there is a BIG difference between minor league ball and Major league ball. Even in AAA, you will only face 2-3 really good hitters in a lineup, and you can mostly get a fastball past most of them if you can't think of anything else to do. Most MAJOR league teams have 6-7 hitters that can turn on a fastball. This puts a LOT more pressure on the pitcher, they have to throw more breaking balls for strikes, work their fastball to both sides of the plate, mix up the pitches, and so on.
Purcey has great stuff, and he threw some really good games with the Jays, so the mechanics are there. The mechanical problem is that he is trying to overthrow the ball, and loses command. This is the mental part. He has to learn to take a bit off, thereby getting better control and more movement. That's what Arnsberg told AJ Burnett and it worked just fine, and that is likely what he told Purcey. It took AJ 2 years to buy into it, and it may take Purcey that long or longer.
What you're forgetting is Purcey is failing in AAA. That isn't the mechanical problem Arnsberg described, it's his delivery mechanics-they've always been poor.
I liked your Toronto article, gsjays:
I have only one word for how to put the team back on a paying basis: WIN!!! In 1992-93, there were 50,000 fans out to every game, instead of the 20,000 die hards that show up now.
Actually, I don't think it helped. Other's are taking Tony Viner's remarks in a context of the Jays needing to lower payroll-a pretty dumb thing to say during trading season.
Boston is denying the proposed deal up-and-down. The outfielder apparently signed a no-trade contract, which he would have to wave. That said, the Yanks will pick up Washburn or Arroyo. This puts some pressure on the Sox to keep pace. In turn, any improvement in pitching on the Sox, Yanks, or even Dodgers (e.g., Lee) puts pressure on the Indians to do something. It looks like the Rays will be a non issue, if they don't turn things around in a hurry. Interestingly, perhaps the most pressure will be on the Angels. I think that they have a team that could emerge from the American league. However, if the Yanks and Sox strengthen themselves — and they will — things could be hard for the Angels. All of this could help the Jays move Halladay. However, as I stated before, no general manager wants to appear to be over-paying, so why not expand the Halladay deal to include some sort of young pitching. We need to make this move now while we still have some leverege (sp mistake). The best thing that cold happen is for Lee, Arroyo, Washburn, or someone else to be moved to a contender. Once the first domino falls, others will follow.
Any reason why Johnny Mac is not Starting tonight. He has great numbers against Washburn not to mention 2 homers.


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What is it?
A gherkin-shaped native Australian fruit from the subtropics with hundreds of tiny vesicles or pearl-like cells full of sharp, lemony-lime juice that explode in the mouth. The colours of the pearls differ from lime-green to scarlet-red depending on the varietal or hybrid. ''This is the start of Australia's wonderful native foods becoming merged into mainstream society,'' says NSW Northern Rivers grower Fred Durham, of Australian Finger Lime Company.
Where is it?
Chef Shannon Bennett of Vue du Monde sends out freshly shucked Clair de Lune oysters with finger limes as part of his opening barrage of small courses. ''Very simple, very fresh,'' he says. At Attica, chef Ben Shewry has used finger limes in such dishes as ''meat from the pearl oyster pinctada maxima'', with lime butter, shaved radish, finger lime and leek ash. At the Hive Kitchen and Bar, chef John Lawson has fun with finger lime pearls, scattering them over kingfish and bonito ceviche, along with candied lime, candied chilli, and fennel and rocket salad. ''They're beautiful … you've got acidity, texture, a little sweetness - everything you could want in a fruit,'' he says.
Both Sydney Direct and Murdoch Produce wholesalers say finger limes were "huge" about 10 years ago, but are now having a moment in the sun as part of the gradual rediscovery of Australian indigenous produce. For Chris Manfield of Universal, they never went away. She uses them in a dish of Hiramasa kingfish sashimi, sweet grilled eel, pickled seaweed, shiso and finger lime salad with yuzu jelly. "They're really cool to mix with flying fish roe," she says. "We also use them in cocktails and desserts". At Sake Restaurant and Bar, finger limes are the secret ingredient of Shaun Presland's tuna ceviche with coriander, jalapeno, tomato and crunchy fried onions. "It's one of those "what-was-that" ingredients" he says. "People take one bite and get the texture of caviar and the taste of lime, and go "what was that?"'
Why do I care?
They're in season right now (until May and beyond); and they are utterly awesome.
Can I do it at home?
Yes. They cost about $1 each (and the colour of the pearls is a bit of a lottery).
Sourcing it
■ Mr Hive Kitchen & Bar, Crown Metropol, 8 Whiteman St, Southbank, 9292 8300
■ Attica, 74 Glen Eira Road, Ripponlea, 9530 0111
■ Vue du Monde, Level 55, Rialto, 525 Collins St, city, 9691 3888
■ Ritchies Supa IGA stores throughout Victoria.
■ Thomas Dux stores
■ Fresh Generation, Footscray (03) 9687 9225 (Wholesale)
■ Ritchies Supa IGA supermarkets throughout Victoria, NSW and Queensland
■ Universal Restaurant, Republic, Palmer St, Darlinghurst, 9331 0709.
■ Sake Restaurant and Bar, 12 Argyle St, The Rocks, 9259 5656.
■ The Milk Bar by Cafe Ish, 105 Regent St, Redfern. No phone.
■ Richies Supa IGA supermarkets throughout NSW.
■ Waterside Fruit Connection, Pyrmont Fish Market, 9552 2104.
Oysters with cucumber and finger limes
Half Lebanese cucumber, peeled
1 tbsp white sugar
1 tsp salt
2 tbsp rice vinegar
1 tbsp extra-virgin olive oil
2 finger limes
1 tbsp mirin
12 oysters (Pacific or Sydney rock)
1. Cut the cucumber in half lengthwise and scoop out and discard the seeds, then finely slice.
2. Mix the sugar, salt and rice vinegar in a bowl, add the cucumber and leave for 30 minutes, then drain and squeeze out excess moisture.
3.Whiz the pickled cucumber in a blender with olive oil until light and creamy, and chill until needed.
4. Roll each finger lime on a bench to loosen the vesicles, then cut in half crosswise, and gently squeeze the little pearls out onto a teaspoon.
5. Add a drop or two of mirin to each oyster, then top with cucumber and finger lime pearls and serve over ice.
Serves 4 as first course
Photos: Edwina Pickles
Styling: Jill Dupleix
Merchandise: Vicino, Waterloo, NSW

subset: commoncrawl


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MALVERN, Pa., Dec. 7, 2012 /PRNewswire/ -- Auxilium Pharmaceuticals, Inc. (Nasdaq: AUXL) today announced that executive management will participate in the Oppenheimer Annual Growth Conference to be held December 12-13, 2012 at the Waldorf Astoria Hotel in New York City. Mr. Adrian Adams, Chief Executive Officer and President, is scheduled to present an overview of the Company and its product pipeline at 2:10 p.m. ET on Thursday, December 13, 2012.
(Photo: http://photos.prnewswire.com/prnh/20101202/MM10881LOGO)
The presentation will also be webcast on the "For Investors" section of the Auxilium website under the "Events" tab on December 13, 2012. The presentation slides to be used will be available on the "For Investors" section of the Auxilium website under the "Presentations" tab on December 13, 2012.
To access the live webcast, please log on to Auxilium's website approximately fifteen minutes prior to the presentation to register and download any necessary audio software. The presentation replay will be available for ninety days after the event.About Auxilium
Auxilium Pharmaceuticals, Inc. is a specialty biopharmaceutical company with a focus on developing and marketing products to predominantly specialist audiences. Auxilium markets Testim® 1% (testosterone gel) for the topical treatment of hypogonadism and XIAFLEX® (collagenase clostridium histolyticum) for the treatment of adult Dupuytren's contracture patients with a palpable cord in the U.S. GSK co-promotes Testim with Auxilium in the U.S. Ferring International Center S.A. markets Testim in certain countries of the EU and Paladin Labs Inc. markets Testim in Canada. Pfizer has marketing rights for XIAPEX® (the EU tradename for collagenase clostridium histolyticum) in 46 countries in Eurasia through April 24, 2013; Asahi Kasei Pharma Corporation has development and commercial rights for XIAFLEX in Japan; and Actelion Pharmaceuticals Ltd has development and commercial rights for XIAFLEX in Canada, Australia, Brazil and Mexico. The sBLA for XIAFLEX for the treatment of Peyronie's disease was submitted to the FDA in November 2012. Additionally, collagenase clostridium histolyticum ("CCH") is in phase IIa of development for the treatment of Frozen Shoulder syndrome (adhesive capsulitis) and phase Ib of development for the treatment of cellulite (edematous fibrosclerotic panniculopathy). Auxilium also has rights to pursue additional indications for CCH. For additional information, visit http://www.auxilium.com
SAFE HARBOR STATEMENT UNDER THE PRIVATE SECURITIES LITIGATION REFORM ACT OF 1995This release contains "forward-looking-statements" within the meaning of The Private Securities Litigation Reform Act of 1995, including statements regarding the Company's intention to present at the Oppenheimer Annual Growth Conference; and products in development for Peyronie's disease, Frozen Shoulder syndrome and cellulite; and all other statements containing projections, statements of future performance or expectations, our beliefs or statements of plans or objectives for future operations (including statements of assumption underlying or relating to any of the foregoing). Forward-looking statements can generally be identified by words such as "believe," "appears," "may," "could," "will," "estimate," "continue," "anticipate," "intend," "should," "plan," "expect," and other words and terms of similar meaning in connection with any discussion of projections, future performance or expectations, beliefs, plans or objectives for future operations (including statements of assumption underlying or relating to any of the foregoing). Actual results may differ materially from those reflected in these forward-looking statements due to various factors, including further evaluation of clinical data, results of clinical trials, decisions by regulatory authorities as to whether and when to approve drug applications, and general financial, economic, regulatory and political conditions affecting the biotechnology and pharmaceutical industries and those discussed in Auxilium's Annual Report under the heading "Risk Factors" on Form 10-K for the year ended December 31, 2011, and Form 10-Q for the quarter ended September 30, 2012, which are on file with the Securities and Exchange Commission (the "SEC") and may be accessed electronically by means of the SEC's home page on the Internet at http://www.sec.gov or by means of Auxilium's home page on the Internet at http://www.Auxilium.com under the heading "For Investors -- SEC Filings." There may be additional risks that Auxilium does not presently know or that Auxilium currently believes are immaterial which could also cause actual results to differ from those contained in the forward-looking statements. Given these risks and uncertainties, any or all of these forward-looking statements may prove to be incorrect. Therefore, you should not rely on any such factors or forward-looking statements.
In addition, forward-looking statements provide Auxilium's expectations, plans or forecasts of future events and views as of the date of this release. Auxilium anticipates that subsequent events and developments will cause Auxilium's assessments to change. However, while Auxilium may elect to update these forward-looking statements at some point in the future, Auxilium specifically disclaims any obligation to do so. These forward-looking statements should not be relied upon as representing Auxilium's assessments as of any date subsequent to the date of this release.For More Information, Contact:James E. Fickenscher / CFO
William Q. Sargent, Jr. / V.P., IR Auxilium Pharmaceuticals, Inc.
Auxilium Pharmaceuticals, Inc.(484) 321-5900
(484) email@example.com
|SOURCE Auxilium Pharmaceuticals, Inc.
Copyright©2012 PR Newswire.
All rights reserved


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Edith Chong Pei See: A Thief?
Tuesday, 12 May 2015
Some readers share my recipes on their blogs, such as here, here and here. The bloggers in these examples rewrite the instructions, in their own words. I am flattered and happy that they share my recipes with their readers.
Sadly, not all bloggers are honest. Some people just copy and paste from my blog.
Copying word for word, or almost word for word, is an infringement of copyright, even when the original author is credited. If it weren't, we can all upload best selling books and make loads of money, right?
Posted by KT at 11:57 pm 48 comments Links to this post
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This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
Incidence and Mortality
Estimated new cases and deaths from chronic lymphocytic leukemia (CLL) in the United States in 2012:[1]
CLL is a disorder of morphologically mature but immunologically less mature lymphocytes and is manifested by progressive accumulation of these cells in the blood, bone marrow, and lymphatic tissues.[2] In this disorder, lymphocyte counts in the blood are usually greater than or equal to 5,000/mm3 with a characteristic immunophenotype (CD5- and CD23-positive B cells).[3,4] As assays have become more sensitive for detecting monoclonal B-CLL–like cells in peripheral blood, researchers have detected a monoclonal B-cell lymphocytosis (MBL) in 3% of adults older than 40 years and 6% in adults older than 60 years.[5] Such early detection and diagnosis may falsely suggest improved survival for the group and may unnecessarily worry or result in therapy for some patients who would have remained undiagnosed in their lifetime, a circumstance known in the literature as overdiagnosis or pseudodisease.[6,7]
In two selected series of more than 900 patients followed prospectively for a median of 5 to 7 years, overt CLL requiring chemotherapy occurred in 7% of patients.[5,8] In a database analysis and for up to 77 months before diagnosis, almost all patients with a diagnosis of CLL had prediagnostic B-cell clones that were identified in peripheral blood when available.[4,9]
For patients with progressing CLL, treatment with conventional doses of chemotherapy is not curative; selected patients treated with allogeneic stem cell transplantation have achieved prolonged disease-free survival.[10,11,12,13,14] Antileukemic therapy is frequently unnecessary in uncomplicated early disease.[15] The median survival for all patients ranges from 8 to 12 years in older trials with data from the 1970s through the 1990s.[15,16] There is, however, a large variation in survival among individual patients, ranging from several months to a normal life expectancy. Treatment must be individualized based on the clinical behavior of the disease.[17]
As found in one report, CLL occurs primarily in middle-aged and elderly adults, with increasing frequency in successive decades of life.[18] The clinical course of this disease progresses from an indolent lymphocytosis without other evident disease to one of generalized lymphatic enlargement with concomitant pancytopenia. Complications of pancytopenia, including hemorrhage and infection, represent a major cause of death in these patients.[19] Immunological aberrations, including Coombs-positive hemolytic anemia, immune thrombocytopenia, and depressed immunoglobulin levels may all complicate the management of CLL.[20] Prognostic factors that may help predict clinical outcome include cytogenetic subgroup, immunoglobulin mutational status, ZAP-70, and CD38 (see Prognostic Factors).[2,21,22,23,24,25,26,27,28,29] Patients who develop an aggressive high-grade non-Hodgkin lymphoma, usually diffuse large B-cell lymphoma and termed a Richter transformation, have a poor prognosis.[30] Patients with CLL are also at increased risk for other malignancies, even before therapy.[31]
Confusion with other diseases may be avoided by determination of cell surface markers. CLL lymphocytes coexpress the B-cell antigens CD19 and CD20 along with the T-cell antigen CD5.[32] This coexpression only occurs in one other disease entity, mantle cell lymphoma. CLL B cells express relatively low levels of surface-membrane immunoglobulin (compared with normal peripheral blood B cells) and a single light chain (kappa or lambda).[15] CLL is diagnosed by an absolute increase in lymphocytosis and/or bone marrow infiltration coupled with the characteristic features of morphology and immunophenotype, which confirm the characteristic clonal population.
The differential diagnosis must exclude hairy cell leukemia (refer to the PDQ summary on Hairy Cell Leukemia Treatment for more information), and Waldenström macroglobulinemia (refer to the PDQ summary on Adult Non-Hodgkin Lymphoma Treatment for more information). Waldenström macroglobulinemia has a natural history and therapeutic options similar to CLL, with the exception of hyperviscosity syndrome associated with macroglobulinemia as a result of elevated immunoglobulin M. Prolymphocytic leukemia (PLL) is a rare entity characterized by excessive prolymphocytes in the blood with a typical phenotype that is positive for CD19, CD20, and surface-membrane immunoglobulin and negative for CD5. These patients demonstrate splenomegaly and poor response to low-dose or high-dose chemotherapy.[15,33]
Cladribine (2-chlorodeoxyadenosine) appears to be an active agent (60% complete remission rate) for patients with de novo B-cell prolymphocytic leukemia.[34][Level of evidence: 3iiiDiv] Alemtuzumab (campath-1H), an anti-CD52 humanized monoclonal antibody, has been used for 76 patients with T-cell prolymphocytic leukemia after failure of prior chemotherapy (usually pentostatin or cladribine) with a 51% response rate (95% confidence interval, 40%–63%) and median time to progression of 4.5 months (range, 0.1–45.4 months).[35][Level of evidence: 3iiiDiv] These response rates have been confirmed by other investigators.[36] Patients with CLL who show prolymphocytoid transformation maintain the classic CLL phenotype and have a worse prognosis than PLL patients.
Large granular lymphocytic leukemia is characterized by lymphocytosis with a natural killer cell immunophenotype (CD2, CD16, and CD56) or a T-cell immunophenotype (CD2, CD3, and CD8).[37,38,39] These patients often have neutropenia and a history of rheumatoid arthritis. The natural history is indolent, often marked by anemia and splenomegaly. This condition appears to fit into the clinical spectrum of Felty syndrome.[40] Therapy includes low doses of oral cyclophosphamide or methotrexate, cyclosporine, and treatment of the bacterial infections acquired during severe neutropenia.[37,39,41,42]
Related Summaries
Other PDQ summaries containing information about CLL include the following:
Staging is useful in chronic lymphocytic leukemia (CLL) to predict prognosis and also to stratify patients to achieve comparisons for interpreting specific treatment results. Anemia and thrombocytopenia are the major adverse prognostic variables.
CLL has no standard staging system. The Rai staging system and the Binet classification are presented below.[1,2] A National Cancer Institute (NCI)-sponsored working group has formulated standardized guidelines for criteria related to eligibility, response, and toxic effects to be used in future clinical trials in CLL.[3]
Rai Staging System
Stage 0
Stage 0 CLL is characterized by absolute lymphocytosis (>15,000/mm3) without adenopathy, hepatosplenomegaly, anemia, or thrombocytopenia.
Stage I
Stage I CLL is characterized by absolute lymphocytosis with lymphadenopathy without hepatosplenomegaly, anemia, or thrombocytopenia.
Stage II
Stage II CLL is characterized by absolute lymphocytosis with either hepatomegaly or splenomegaly with or without lymphadenopathy.
Stage III
Stage III CLL is characterized by absolute lymphocytosis and anemia (hemoglobin <11 g/dL) with or without lymphadenopathy, hepatomegaly, or splenomegaly.
Stage IV
Stage IV CLL is characterized by absolute lymphocytosis and thrombocytopenia (<100,000/mm3) with or without lymphadenopathy, hepatomegaly, splenomegaly, or anemia.
Binet Classification
Clinical stage A*
Clinical stage A CLL is characterized by no anemia or thrombocytopenia and fewer than three areas of lymphoid involvement (Rai stages 0, I, and II).
Clinical stage B*
Clinical stage B CLL is characterized by no anemia or thrombocytopenia with three or more areas of lymphoid involvement (Rai stages I and II).
Clinical stage C
Clinical stage C CLL is characterized by anemia and/or thrombocytopenia regardless of the number of areas of lymphoid enlargement (Rai stages III and IV).
*Lymphoid areas include cervical, axillary, inguinal, and spleen.
The Binet classification integrates the number of nodal groups involved with the disease with bone marrow failure. Its major benefit derives from the recognition of a predominantly splenic form of the disease, which may have a better prognosis than in the Rai staging, and from recognition that the presence of anemia or thrombocytopenia has a similar prognosis and does not merit a separate stage. Neither system separates immune from nonimmune causes of cytopenia. Patients with thrombocytopenia or anemia or both, which is caused by extensive marrow infiltration and impaired production (Rai III/IV, Binet C) have a poorer prognosis than patients with immune cytopenias.[4] The International Workshop on CLL has recommended integrating the Rai and Binet systems as follows: A(0), A(I), A(II); B(I), B(II); and C(III), C(IV).[5] The NCI-sponsored working group has published guidelines for the diagnosis and treatment of CLL in both clinical trial and general practice settings.[3] Use of these systems allows comparison of clinical results and establishment of therapeutic guidelines.
Prognostic factors
New prognostic markers are now available to the clinician and investigator.[6,7] The use of these markers to stratify patients in clinical trials, to help assess the need for therapy, and to help select the type of therapy continues to evolve. Prospective trials to verify and establish the role of these prognostic markers are ongoing. No large multivariable analyses exist as yet to test the relative power of these individual prognostic variables.[8] Prognostic indices are under evaluation and will require prospective validation.[9]
Other prognostic factors include:
Treatment of chronic lymphocytic leukemia (CLL) ranges from periodic observation with treatment of infectious, hemorrhagic, or immunologic complications to a variety of therapeutic options, including steroids, alkylating agents, purine analogs, combination chemotherapy, monoclonal antibodies, and transplant options.[1] Because this disease is generally not curable, occurs in an elderly population, and often progresses slowly, it is most often treated in a conservative fashion.[1] In asymptomatic patients, treatment may be deferred until the patient becomes symptomatic as the disease progresses. Since the rate of progression may vary from patient to patient, with long periods of stability and sometimes spontaneous regressions, frequent and careful observation is required to monitor the clinical course.[2]
A meta-analysis of randomized trials showed no survival benefit for immediate versus delayed therapy for patients with early stage disease, nor for the use of combination regimens incorporating an anthracycline compared with a single-agent alkylator for advanced stage disease.[3][Level of evidence: 1iiA] A variety of clinical factors, including IgVH mutation, chromosomal abnormalities by fluorescent in situ hybridization analysis or cytogenetics, beta-2-microglobulin, and lymphocyte doubling time may be helpful in predicting progression of disease.[1]
Infectious complications in advanced disease are in part a consequence of the hypogammaglobulinemia and the inability to mount a humoral defense against bacterial or viral agents. Herpes zoster represents a frequent viral infection in these patients, but infections with Pneumocystis carinii and Candida albicans may also occur. The early recognition of infections and the institution of appropriate therapy are critical to the long-term survival of these patients. A randomized study of intravenous immunoglobulin (400 mg/kg every 3 weeks for 1 year) in patients with CLL and hypogammaglobulinemia produced significantly fewer bacterial infections and a significant delay in onset of first infection during the study period.[4] There was, however, no effect on survival. Routine chronic administration of intravenous immunoglobulin is expensive, and the long-term benefit (>1 year) is unproven.[5,6]
Second malignancies and treatment-induced acute leukemias may also occur in a small percentage of patients.[7] Transformation of CLL to diffuse large cell lymphoma (Richter syndrome) carries a poor prognosis with a median survival of less than 1 year, though 20% of the patients may live more than 5 years after aggressive combination chemotherapy.[8] (Refer to the PDQ summary on Adult Non-Hodgkin Lymphoma Treatment for more information.)
Autoimmune hemolytic anemia and/or thrombocytopenia can occur in patients with any stage of CLL.[9] Initial therapy involves corticosteroids with or without alkylating agents (fludarabine can worsen the hemolytic anemia). It is frequently advisable to control the autoimmune destruction with corticosteroids, if possible, prior to administering marrow-suppressive chemotherapy because such patients may be difficult to transfuse successfully with either red blood cells or platelets. Alternate therapies include high-dose immune globulin, rituximab, cyclosporine, azathioprine, splenectomy, and low-dose radiation therapy to the spleen.[10,11] Tumor lysis syndrome is an uncommon complication (presenting in 1 out of 300 patients) of chemotherapy for patients with bulky disease.[12]
About 1% of morphologic CLL cases express T-cell markers (CD4 and CD7) and have clonal rearrangements of their T-cell receptor genes. These patients have a higher frequency of skin lesions, more variable lymphocyte shape, and shorter median survival (13 months) with minimal responses to chemotherapy.[13]
Computed tomographic (CT) scans have a very limited role in following patients after completion of treatment; the decision to treat for relapse was determined by CT scan or ultrasound in only 2 of 176 patients in 3 prospective trials for the German CLL Study Group.[14]
Because of the indolent nature of stage 0 chronic lymphocytic leukemia (CLL), treatment is not indicated.[1] The French Cooperative Group on CLL randomly assigned 1,535 patients with previously untreated stage A disease to receive either chlorambucil or no immediate treatment and found no survival advantage for immediate treatment with chlorambucil.[2][Level of evidence: 1iiA] A meta-analysis of six trials of immediate versus deferred therapy with chlorambucil (including the aforementioned trial by the French Cooperative Group) showed no difference in overall survival at 10 years.[3][Level of evidence: 1iiA] Whether immediate therapy with the nucleoside analogs or other newer strategies will be superior to a watchful waiting approach is uncertain.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage 0 chronic lymphocytic leukemia. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Several decades of large, randomized, prospective trials of previously untreated patients have demonstrated statistically significant improvements in response rates, event-free survival (EFS), and progression-free survival (PFS) with comparison of combinations of drugs versus single-agent alkylators,[1,2] but only two trials have shown statistically significant improvement in overall survival (OS).[3,4]
The first trial, a comparison of chlorambucil versus fludarabine, after 15 years of median follow-up, showed improved median OS for patients on the fludarabine regimen at 63 months versus 59 months (P = .04), and an improved percentage of patients were alive at 8 years (31% vs. 19%, P = .04).[3,5][Level of evidence: 1iiA]
The second trial, which had 817 patients, compared FCR (fludarabine + cyclophosphamide + rituximab) versus FC (fludarabine + cyclophosphamide) with a median follow-up of 38 months and showed improved OS at 3 years for the rituximab combination (i.e., 87% vs. 83%, P = .01.[4][Level of evidence: 1iiA] Yet neither fludarabine nor FCR has been compared in a randomized study against watchful waiting in asymptomatic or minimally affected patients.
The improvements in response rates from more intensive regimens have maximized the clearance of minimal residual disease. In one prospective trial of 493 patients, clearance of minimal residual disease was an independent predictor of overall survival by multivariate analysis.[6] The surrogate endpoint of such clearance of residual disease, however, has not been shown to improve survival in a randomized prospective trial; the necessary study would take patients who fail to completely clear the marrow with induction therapy and randomly assign them to further alternative treatment versus the same treatment later at relapse, looking at OS as the primary endpoint.[1,2]
The sequencing of the following treatment options cannot be determined from the current set of completed clinical trials. When patients become symptomatic or require treatment, FCR has become the most frequently chosen option outside of a clinical trial, mostly on the basis of the previously described prospective study.[4]
Treatment options:
Note: Standard options are roughly ordered by level of toxic effects, starting with the least toxic options. More recently discovered options are mentioned at the end of the list.
Several randomized trials have compared the purine analogs with chlorambucil; with cyclophosphamide, doxorubicin, and prednisone; or with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in previously untreated patients.[5,22,23,24,25] All of these trials showed higher or equivalent response rates for the purine analog and most showed an improvement in PFS, with one reaching significance in OS favoring fludarabine.[3,22,23,24,25,26][Level of evidence: 1iiDiii]
A comparison of chlorambucil versus fludarabine, after 15 years' median follow-up, showed patients with improved median OS with fludarabine at 63 versus 59 months (P = .04) and an improved percentage of patients alive at 8 years (31% vs. 19%, P = .04).[3][Level of evidence: 1iiA] All of the trials demonstrated higher toxic effects with the purine analogs, especially granulocytopenic infections, herpes infections, autoimmune hemolytic anemia, and persistent thrombocytopenia.[27] The increased risk of infection may persist for months or years after treatment with a purine analog.[26,28]
Although empiric evidence is lacking, some investigators recommend prophylaxis with trimethoprim-sulfa during therapy and for 6 to 12 months afterwards to prevent pneumocystis infection. In a similar way, other investigators employ prophylaxis (e.g., acyclovir) for the herpes viruses.[28] Purine analogs cause less hair loss or nausea than combination chemotherapy, including alkylators and anthracyclines.[24]
Bendamustine is a cytotoxic agent with bifunctional properties of an alkylator and a purine analogue.[29] In previously treated and untreated patients, bendamustine with rituximab has shown response rates around 70% to 90%.[30,31][Level of evidence: 3iiiDiii]
In a randomized comparison with chlorambucil in 319 previously treated patients, bendamustine showed a better response rate (68% vs. 31%, P < .0001) and PFS (21.6 months vs. 8 months) with a median follow-up of 35 months.[32][Level of evidence: 1iiDiii] The German CLL Study Group is comparing bendamustine plus rituximab versus FCR as first-line therapy in patients with CLL who require therapy.[30]
A trial of 817 patients comparing FCR versus FC with a median follow-up of 38 months showed improved OS at 3 years for the rituximab combination (87% vs. 83%, P = .01).[4][Level of evidence: 1iiA] FCR has never been compared to watchful waiting up front in asymptomatic or minimally affected patients. The improvements in response rates from more intensive regimens have maximized the clearance of minimal residual disease (MRD). However, the surrogate endpoint of MRD clearance has not been proven to be a valid surrogate for improved survival in a randomized prospective trial; the necessary study would take patients who fail to completely clear the marrow with induction therapy and randomly assign them to further alternative treatment versus the same treatment later at relapse looking at OS as the primary endpoint.[1,2] A cumulative incidence of 6% to 8 % for myelodysplasia is seen at 5 to 7 years in patients who received fludarabine plus cyclophosphamide, with or without rituximab.[33,34]
A meta-analysis of ten trials comparing combination chemotherapy (before the availability of rituximab) to chlorambucil alone showed no difference in OS at 5 years.[7][Level of evidence: 1iiA]
In a combination regimen, subcutaneous alemtuzumab plus fludarabine or intravenous alemtuzumab plus alkylating agents have resulted in excess infectious toxicities and death, with no compensatory improvement in efficacy in phase II trials.[54,55][Level of evidence: 3iiiDiv] In a randomized prospective study, 335 previously treated patients received intravenous alemtuzumab plus fludarabine versus fludarabine alone; with a median follow-up of 30 months, the combination of fludarabine plus intravenous alemtuzumab had better PFS, with a median of 23.7 months versus 16.5 months (hazard ratio [HR], 0.61; 95% confidence interval [CI], 0.47–0.80; P = .0003); and better OS, with a median not reached versus 52.9 months (HR, 0.65; 95% CI, 0.45–0.94; P = .021).[56][Level of evidence: 1iiA]Profound and long-lasting immunosuppression has been seen, which mandates monitoring for reactivation of cytomegalovirus and prophylaxis for pneumocystis and herpes virus infections.[57,58]
In a prospective randomized trial, 241 previously untreated patients younger than 66 years with advanced-stage disease received induction therapy with a CHOP-based regimen followed by fludarabine.[65] Complete responders (105 patients) were randomly assigned to undergo autologous stem cell transplantation (ASCT) or observation, while the other 136 patients were randomly assigned to receive dexamethasone, high-dose aracytin, and cisplatin (DHAP) reinduction followed by either ASCT or fludarabine plus cyclophosphamide. Although the 3-year EFS favored ASCT in complete responders, there was no difference in OS in any of the randomized comparisons.[65][Level of evidence: 1iiDi]
Patients with adverse prognostic factors are very likely to die from CLL. These types of patients are candidates for clinical trials that employ high-dose chemotherapy and immunotherapy with myeloablative or nonmyeloablative allogeneic peripheral stem cell transplantation.[59,60,61,62,63,64,66,67,68,69,70,71,72,73] Although most patients who attain complete remission after autologous stem cell transplantation eventually relapse, a survival plateau for allogeneic stem cell support suggests an additional graft-versus-leukemia effect.[73]
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage I chronic lymphocytic leukemia, stage II chronic lymphocytic leukemia, stage III chronic lymphocytic leukemia and stage IV chronic lymphocytic leukemia. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Clinical trials are appropriate and should be considered when possible.[1] In small studies, response rates of more than 40% have been reported for lenalidomide [2,3,4] and flavopiridol.[5,6][Level of evidence: 3iiiDiv] The addition of the Bcl-2 anti-sense oligonucleotide oblimersen to fludarabine/cyclophosphamide improved complete response rates in a randomized study of 241 patients with relapsed disease.[7][Level of evidence: 1iiDiv] Bone marrow and peripheral stem cell transplantations are under clinical evaluation.[8,9,10,11,12,13,14]
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with refractory chronic lymphocytic leukemia. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
General Information About Chronic Lymphocytic Leukemia Treatment
Added Fazi et al. as reference 7.
Stage I, II, III, and IV Chronic Lymphocytic Leukemia
Added text to state that in one prospective trial of 493 patients, clearance of minimal residual disease was an independent predictor of overall survival by multivariate analysis (cited Böttcher et al. as reference 6).
Added Fischer et al. and Iannitto et al. as references 30 and 31, respectively.
Added text to state that a cumulative incidence of 6% to 8% for myelodysplasia is seen at 5 to 7 years in patients who received fludarabine plus cyclophosphamide, with or without rituximab (cited Smith et al. and Carney et al. as references 33 and 34, respectively).
Added Badoux et al. and Woyach et al. as references 38 and 39, respectively.
Added text about the chemotherapy combination of ofatumumab plus fludarabine plus cyclophosphamide as an additional treatment option (cited Wierda et al. as reference 43).
Added text to state that a combination regimen of subcutaneous alemtuzumab plus fludarabine or intravenous alemtuzumab plus alkylating agent has resulted in excess infectious toxicities and death with no compensatory improvement in efficacy in phase II trials; however in a randomized prospective study, the combination of fludarabine plus intravenous alemtuzumab had better progression-free survival (cited Elter et al. as reference 56 and level of evidence 1iiA).
Added text about a prospective randomized trial of 241 previously untreated patients with advance stage chronic lymphocytic leukemia (CLL) who were randomly assigned to undergo autologous stem cell transplantation (ASCT) or observation, or receive DHAP followed by ASCT or fludarabine plus cyclophosphamide; there was no difference in overall survival in any of the randomized comparisons (cited Sutton et al. as reference 65 and level of evidence 1iiDi).
Added text to state that single-agent lenalidomide has shown a 50% to 70% overall response in previously treated and untreated patients and that combination therapy and long-term toxicities from using lenalidomide remain undefined for patients with CLL (cited Ferrajoli et al., Chen et al., and Badoux et al. as references 74, 75, and 76, respectively).
Added text to state that autologous T cells were modified by a lentiviral vector to incorporate antigen receptor specificity for B-cell antigen CD19, and then infused into a previously treated patient (cited Porter et al. as reference 77); ongoing clinical trials are testing this concept.
This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of chronic lymphocytic leukemia. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewers for Chronic Lymphocytic Leukemia Treatment are:
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Levels of Evidence
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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The preferred citation for this PDQ summary is:
National Cancer Institute: PDQ® Chronic Lymphocytic Leukemia Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://www.cancer.gov/cancertopics/pdq/treatment/CLL/healthprofessional. Accessed <MM/DD/YYYY>.
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Recipe: Breakfast paletas (ice pops)
You say summer, I say ice pops for breakfast.
Seriously, why not? Especially if you make them yoursef, with ingredients that you know.
Here's a recipe for a yogurt-based pop, which adds a little protein to party. Add some wheat germ or a handful of crushed whole grain cereal for a hit of fiber, if you like. No shame eating these on the go, either.
Read more…


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Okay folks, we are all secure atheists, right? This question is just for fun! What religious themed songs have you caught yourself singing along with, or at least taping your foot to? Here are two songs that get me every time: Three Wooden Crosses sung by Randy Travis & Jesus Take the Wheel sung by Carrie Underwood.
Views: 1484
yeah, i really like that tune "Cassie" even though it's both religious and also based on the fake story about a girl being shot at Columbine because she believed in god.
Folow this link posted by Dustin. Be warned you could suffer long term sanity problems if you watch the whole thing!!!!!
"Awake and Alive" and "Hero" by Skillet. Which I totally pretend are about people rather than God, because it sounds too good to xtian. :P
Johnny Cash's cover of Personal Jesus. He sang it with conviction, and I find his rendition to be a very soulful song.
"I will follow Him" by: Little Peggy March. Everybody thought it was about her boyfriend, but it's about JESUS!
"Crying in the chapel" by: Elvis, everyone thought is was a love song, but he was crying because "I've come to know the lord"
Let it Be - The Beatles.
Prog rock geek that I am, I have to go with Supper's Ready (Genesis) and Awaken (Yes). That's an hour's worth of spiritual goodliness right there,
"Oh Victory in Jesus" - LOL. But the "Jesus Take the Wheel" is nice mockery song, I think.
Spirit in the Sky
3 Wooden Crosses & Jesus Take the Wheel were good songs.
I also enjoy Josh Turner's "Long Black Train".
"Amazing Grace" is nice for tradition. I also like "Eternal Father; Strong to Save" or colloquially known as "The Navy Hymn".
"Hallelujah" by Leonard Cohen
"What if God Was One of Us?" by Joan Osborne
I think the entire soundtrack of "O Brother, Where Art Thout?" would also be in my favorites.
Warren Sapp "He Saw The Best In Me" and "Jesus On The Main Line" (Tell Him What You Want) LOL


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Items where Author is "Leung, Yan-kit Ingrid"
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Book Section
Liszka, Sarah Ann (2009) Associating meaning to form in advanced L2 speakers: An investigation into the acquisition of the English present simple and present progressive. In: Snape, Neal, Leung, Yan-kit Ingrid and Sharwood Smith, Michael, (eds.) Representational Deficits in SLA: Studies in honor of Roger Hawkins. Language Acquisition and Language Disorders (47). John Benjamins Publishing Company, Amsterdam, Netherlands, pp. 229-246. ISBN 9789027253088


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Creating your own signature voice can be very difficult, but creating your own signature sound in a medium where all drum patterns and strings sound the same is highly recognizable. Centric (born Christopher Louray Mandujan, 28) a producer from California is doing just that. His poignant percussions and bass patterns are reminiscent of what some would consider is left of the golden era of hip-hop beat making. His sound is classified as "New Age Soul" with influences such as Pete Rock, Dj Premier, J-Dilla, Kanye West and Alchemist. His instrumental canvas has already been blessed by MC's such as Canibus, Skillz, Kool G Rap, A+, Sean Price, Big Noyd, Rapper Big Pooh, Skyzoo, Sadat X, San Quinn, Mistah F.A.B, Yukmouth, Black Rob, Cashis (Shady Records) and various others.
Skipping a beat in this industry can leave you far behind, an everyday reality for Centric. The accolades and acknowledgment he has received continues to grow as his fans await his new project "The Alter Ego". The singles "Hear the Whispers" featuring Wordsmith, "The Recipe" featuring Kool G Rap and "Tongue Action" featuring Trife has already been considered mainstream hits and gaining impetus for plays on radio stations across the country. With appearances from A+, Big Noyd and G-Unit's DJ Young Cee, Centric is ready to bring the new sound of his generation to the earlobes of the masses.
From compilations to video appearances to album releases and major production credit, Centric has maintained his signature sound. He continues to bring the listener a sound that has a lasting reverberation. For those who have said hip-hop is dead or it has been locked away now can say it is "Free At Last".


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Toner Cartridge Recycling
The Joseph T. Simpson Public Library, in partnership with Staples, collects empty toner cartridges for recycling. For each cartridge donated, we will receive a credit on future purchases at Staples.
Recycling toner cartridges reduces landfill waste and helps the Joseph T. Simpson Public Library, while helping the environment.
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Main Content
Legend has it that Ben Franklin, in an eloquent plea to our Continental Congress, ably related the virtues of one of America's finest birds, the wild turkey (Meleagris gallopavo). The bald eagle, however, was chosen as our national bird because it represented fierce independence. Two centuries later, we are reminded of Mr. Franklin's habitual wisdom. Wild turkeys are increasing in numbers and range annually, while our bald eagle is finding it increasingly difficult to cope with the relentless march of civilization and is in great danger of passing from the American scene.
The Merriman's turkey of the West, Gould's turkey of the Southwest, the Rio Grande turkey, Florida turkey and Eastern turkey are closely related birds which have learned to live in a great variety of climates and land uses. Each has responded well to protection, trapping and transplanting, timber management and other game management practices. Like the deer, once extinct but now inhabiting every county of Indiana, the future of wild turkey traditionally lived in larger tracts of timber, they are already responding well to agricultural ranges especially where unplowed cornfields provide an additional winter food source.
General Characteristics
All domestic turkeys are descendants of those taken from the wild in North America and Central America. Genuine wild turkeys resemble their tame relatives, but generations of escaping meat eaters has resulted in extreme wariness and preference for rapid take off and flights of more than a mile.
The wild turkey's naked head and neck have bluish cast, while the overall appearance is glossy black with a metallic sheen. Hens are smaller than gobblers, less lustrous and do not have the bristly black beard hanging from the center of the breast.
Family Life
Late winter finds flocks dividing into smaller groups with the hens in one flock, young males in another and old gobblers in a different group. These bearded ancestors select and defend against all competitors a territory for their harem. Each morning, they call to and court as many hens as they can lure away from neighboring gobblers. These displays of grand feathers, courtship movement and occasional lusty fights are performed from February through May.
Hens slip off from their companions and throw together a careless but well-screened nest located on the ground and often concealed by brush and low vegetation. Nests may contain seven to 20 eggs, but the average is about 12. The hen seldom leaves the nest after incubation. Pink/brown chicks emerge to live and feed on the ground until they begin awkward flights when about a month old. This family group feeds, roosts and loafs together until large flocks congregate in late autumn.
Food Habits
Insects provide high energy food for fast-growing poult, but the backbone of turkey's diet consists of wild fruits, acorns, green leaves, seeds, and domestic grains. Those of our eastern woodland feed on sumac, wild grapes, dogwood berries, beechnuts, acorns, greenbrier, roots and tubers. Water is taken freely and grit consumed to grind harder foods.
Restoration Efforts
A combination of uncontrolled hunting and nearly absolute destruction of timber completely wiped out turkeys in Indiana and other Midwestern states. As late as 1945, it appeared that they might be a vanishing species in the United States. As marginal farmland returned to timber and conservation practices were applied to our plundered land, the state was set for turkey revival.
Turkeys raised on game farms were released by the thousands, but only those with a high percentage of wild blood could survive. Semi-wild birds sought nearby barnyards and rapidly disappeared. Reservoirs of pure wild stock were trapped in the wild and transplanted into suitable habitats. Between 1956 and 2004, 2,795 wild trapped birds were released at 185 sites around the state. Wild turkeys now exist across the state and now several generations of citizens throughout the state can now see or hunt wild turkeys for the first time in their lives in a state where a little over a generation ago wild turkeys did not exist. Spring density over most of the turkey range in Indiana is one to six birds per square mile with some estimates as high as 25 birds per square mile.
Spring hunting for gobblers only occurs statewide. The bag limit is one bird. Since the early 2000's annual spring harvests have exceeded 10,000 birds with over 50,000 hunters participating. A conservative fall season was implemented in 2005 and annual fall harvests less than 1,000 birds.
Some Hazards
Turkey eggs are especially vulnerable to ground predators during the nesting period and young poults are vulnerable prey to a wide variety of predators. Larger adults are not as susceptible to predation and generally live for several years.
Turkey Management in Indiana
The Division of Fish and Wildlife has followed the management plan listed below:
- Used only wild-trapped birds for restocking in areas of suitable habitat.
- Provided sustainable spring and fall hunting opportunities with the primary emphasis on spring hunting opportunities.
- Provided technical assistance to private land owners on how to better manage their lands for wild turkeys and other wildlife.
- Conducted habitat management on public lands to enhance nesting and brood rearing habitat.
- Monitors turkey population trends to ensure the sound stewardship of this natural resource.
Click here for more information on wild turkeys and managing their habitats


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How to make Calls to an *087 number
From any fixed line or cellular telephone you can dial a Voicesource 087xxxxxxxxx IP number at national call rates. After installation of our direct interconnects (July 2006) with Vodacom and Telkom in SA you will be able to:*Dial the IP phone number directly i.e. 087xxx xxxx.


text: PureAire Odour Eliminator Essence - 100ml Customer Rating 5 1 review £6.74 Was £8.99 saving you 25% 67 reward points UK Delivery £1.95 - Free when you spend £15 In stock -This product will ship today if ordered within the next 15 hours and 31 minutes. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 25 30 35 40 45 50 60 70 80 90 100 110 120 130 140 150 Add to basket 100% Secure Shopping Product code: 4806 Description Contents Usage Reviews Questions Description PureAire Odour Eliminator Essence deodorises, refreshes, neutralises. PureAire Essences All PureAire aromatherapy essences are made from botanical extracts, essential oils and contain Vital Oxide disinfectant which has antibacterial and antifungal properties. They are non-toxic, non-flammable, alcohol free, biodegradable & environmentally safe. PureAire fragrances may encourage relaxation, soothe your mind and enhance your overall state of wellbeing. Ideal for use with PureAire Systems: PureAire Revitaliser Classic - Air Purifying System PureAire Revitaliser LuminAire - Air Purifying System PureAire Revitaliser LuminAire Plus - Air Purifying System PureAire Revitaliser Lite N Aire - Air Purifying System Contents Contains: Odour Eliminator Essence - 100ml. Usage Shake well before use. Add 2.5 - 5ml (2-3 squirts) to approx 1.5 litres of clean water in a PureAire Revitaliser. Store in a cool, dry place, keep away from direct sunlight. In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. Keep out of reach of children. Not for oral consumption. Reviews Below are reviews of PureAire Odour Eliminator Essence - 100ml by bodykind customers. If you have tried this product we'd love to hear what you think so please leave a review. Leave a review Score Comments Name Email Submit review Score 5 Date 30/03/2018 Posted by Dominique Williams Comment Efficient odour eliminator leaving just a very fresh, pleasant, subtle smell Questions & Answers Below are questions that bodykind customers have asked us about this product. If you want to know more about this product please don't hesitate to ask us a question. Ask us a question Question Email Confirm Email Submit question


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Marian (Ind.) Wins First-Ever Football National Championship
ROME, Ga. - (Box Score) No. 5 Marian (Ind.) claimed its first-ever national crown by winning the 57th annual Russell Athletic-NAIA Football National Championship in overtime, 30-27, over No. 3 Morningside (Iowa) Thursday night at Barron Stadium in Rome, Ga. The Knights, who were playing in their first-ever national title game, outscored Morningside 20-7 over the final 15 minutes and overtime period en route to the victory.
"We have guys who don't quit," said Marian head coach Ted Karras, Jr. "They're true believers, and a lot of them were pioneers. We only started football literally six years ago. We recruit guys who are hungry - hungry to play and hungry to get their degree - who have a never-say-die attitude. These are quality guys, who get their business done - on and off the field.
Marian's placekicker Mike Josifovski, who sent the Knights to the championship contest with a 51-yard game-winning field goal in the semifinals on Dec. 3 against Missouri Valley, again played hero by converting a 35-yard field goal attempt as time expired to send the contest into the first overtime period in the 57-year history of the national championship. The Knight defense held strong in Morningside's overtime opportunity, setting up Josifovski for another game-winning attempt. He again did not disappoint, splitting the uprights on a 26-yard game-winning field goal. Josifovski was named Outstanding Offensive Player of the Game for his performance.
The Morningside offense sized control early, marching 70 yards on its opening possession to take a 7-0 lead at the 10:25 mark of the first quarter. The drive was capped by a Fred Jones 10-yard touchdown run, his first of two scores on the evening.
Marian (12-1) capitalized on a Mustang turnover to tie the score 7-7. However, Morningside responded with its second 70-yard scoring drive of the first quarter when Joel Nixon found Joel McCabe on a six-yard touchdown pass.
Josifovski nailed a 36-yard field goal with 3:55 left in the first half to make it a 14-10 Mustang advantage at the break.
Morningside (13-1) again drew first blood with its third 70-plus drive of the contest to open the second half scoring. Jones, who ran for more than100 yards for the first time this season, tallied his second touchdown of the night on a 1-yard dive. After David Galloway missed the PAT, Morningside held a 20-10 advantage.
Marian pulled within three, 20-17, two minutes later when Tevin Lake found the end zone for the second time on a 4-yard run with 7:33 left in regulation. That score capped the Knight's longest drive of the game - 88 yards on 11 plays.
The Knights took their first lead of the contest with 2:46 remaining, 24-20, when Adam Wiese tossed his only touchdown pass of the evening on a 61-yard strike to Nathan Jones. It was Wiese's 29th touchdown pass of the season and 52nd of his career.
Faced with a fourth-and-15 on its own 44 yard-line, the game began to look in doubt for the Mustangs. However, Nixon, who completed 22-of-39 passes for 228 yards, found Kyle Schuck with a 35-yard pass to give Morningside a first down with the ball on the Marian 21. Morningside, aided by a Knight pass interference penalty, scored two plays later when Nixon connect with a wide open Shuck in the end zone. The touchdown gave the Mustang's a 27-24 lead with a 1:04 remaining, which proved not enough to withstand Marian's late-game heroics.
Wiese paced the Marian offense with 242 yards of total offense, including 223 through the air. Lake, who notched his ninth 100-yard performance of the season, finished with 104 yards and two touchdowns on 23 attempts.
Defensively, five Knights finished the game with double-digit tackles, including John Keever's game-high 18 stops. Robert Palmer was named Outstanding Defensive Player of the Game after positing 13 tackles, one tackle-for-loss, one interception and one forced fumble.
2012 Russell Athletic-NAIA Football National Championship Awards
Outstanding Offensive Player of the Game: Mike Josifovski, Marian (Ind.)
Outstanding Defensive Player of the Game: Robert Palmer, Marian (Ind.)
|Marian (Ind.)
|Morningside (Iowa)
Scoring Summary
MC - Fred Jones 10 yd run (David Galloway kick), 10:25, 1st
MU - Tevin Lake 7 yd run (Mike Josifovski kick), 6:19, 1st
MC - Joel McCabe 6 yd pass from Joel Nixon (David Galloway kick), 1:44, 1st
MU - Mike Josifovski 36 yd field goal, 3:55, 2nd
MC - Fred Jones 1 yd run (David Galloway kick no good), 9:34, 3rd
MU - Tevin Lake 4 yd run (Mike Josifovski kick), 7:33, 4th
MU - Nathan Jones 61 yd pass from Adam Wiese (Mike Josifovski kick), 2:46, 4th
MC - Kyle Schuck 7 yd pass from Joel Nixon (Ty Littzen kick), 1:04, 4th
MU - Mike Josifovski 35 yd field goal, 0:00, 4th
MU - Mike Josifvoski 26 yd field goal, 1st OT
National Championship Game Notes
• This marked the first-ever overtime contest in the 57th annual game.
• With the three-point margin of victory, this game has been a nail-biter in recent memory. Since 2009, the average margin of victory has been 3.25 points.
• The official attendance was listed at 5,263.
• This is the fifth-straight year that Rome, Ga., has served as host and the 45th different site for the Russell Athletic-NAIA National Championship.
Team and Individual Notes
• Morningside (Iowa) opened up the scoring in tonight's game at the 10:25 mark of the first quarter. Teams that score first now own a 10-6 record since the NAIA went to one division in 1997 - Saint Francis (Ind.) in 2006 was the last team to score first and lose the national championship.
• Tonight's matchup was the time since 2007 that both teams scored at least one touchdown in the first quarter.
• Fifth-ranked Marian (Ind.) becomes the second-straight team to win the national title with that position in the poll.
• Out of the Mid-States Football Association Mideast League, Marian is the second-consecutive team to win the title from that league. Saint Xavier (Ill.) was the 2011 champion.
• Morningside's (Iowa) Fred Jones scored at the 10:25 in the first quarter, which was the fifth earliest touchdown in a title game since 1998.
• Morningside's 14 first quarter points are tied for the most in the first quarter since the NAIA went to one division in 1997.
• The 21 combined points scored in the first quarter (14 by Morningside, 7 by Marian) was the most since 2006.
• Morningside's Joel Nixon's interception thrown in the second quarter was the first pick thrown in a title game since 2009.
• Marian's Adam Wiese entered the game one yard shy of 3,000 season passing yards. After his 233 yards tonight, he wraps up his 2012 season with 3,232 yards.
• Marian recorded an interception in 23 of its last 25 games, including its current streak of 12-straight to end this year.
• This was the fourth-straight title game with 11-or-more combined penalties - eighth since 1997.
• Morningside lost its bid to become the first unbeaten team to win the championship since Carroll (Mont.) in 2010.
• The lower-ranked team (No. 5 Marian) has now won six of the last seven national championships (No. 3 Morningside).
• After winning the Outstanding Offensive Player of the Game, Marian's Mike Josifovski becomes the second placekicker to win that same award. Braden Wieking of Sioux Falls (S.D.) was honored back in 2009.
• Both programs are appearing in their first-ever national championship, which marked the first time since two rookies went at it since 1998.
• The game was filled with penalties: this marked the first time since 1997 (when tracked) that a team has been penalized more than 100 yards (Marian had 12-for-160; Morningside had 12-for-157).
• This meeting was the first between the two programs in regular season or postseason.
• Marian wins its first-ever NAIA National Championship in any sport - this was only the sixth year for varsity football.
Postgame Press Conference Quotes
Marian (Ind.)
Head Coach Ted Karras, Jr. - Overall Comments
"I'm really proud of our players and their never-say-die mentality. This was a hard-fought game. It came down to a last-second kick again-the second year in-a-row for us. These guys have all believed in us. We've only been around six years. We started football for a lot of reasons, and to get to this point only happens with great coaches and great football players like these."
Mike Josifovski (Kicker) - Overall Comments
"The life of a kicker is a lonely life, all we do all day long is kick. When you sign up for this job, they warn you about these moments. These are the moments you want to hold onto and take advantage of. Fortunately for me, I have a great team and a great coaching staff around me."
Tevin Lake(Running back)-Overall Comments
"Coach preached at half time what he's preached all season. We have to work hard as a team and work together."
Robert Palmer (Linebacker)-When asked about being the MVP
"It's just a name for a player. It's a team effort-offensively, defensively-and it all came together."
Coach Ted Karras, Jr., -- about Josifovski
"I want to be sure you all know that Mike and I came from the same high school-Hobart High School in Indiana"
Coach Ted Karras, Jr. - On the season
"We have guys who don't quit. They're true believers, and a lot of them were pioneers. We only started football literally six years ago. We recruit guys who are hungry-hungry to play and hungry to get their degree-who have a never-say-die attitude. These are quality guys, who get their business done-on and off the field.
You saw it-a lot of people probably counted us out, but we came down the field and got it done. I couldn't be more proud of these guys.
Head coach Steve Ryan - Overall Comments:
"It was a great game. We made some plays down at the end, and I thought we gave ourselves a chance to win-it just didn't happen."
Joel Nixon (quarterback) - Overall Comments:
"I thought we put ourselves in a really good position to win the game. We fought as hard as we could. There wasn't one person who went into that locker room who didn't give it all on the field. I'm really proud of our team and I'm really proud of our coaching staff and the support they've given us all season. With it being so close, you always have the what-ifs. But Marian made the plays they needed to down the stretch, and they are the deserving team-they earned the trophy."
Coach Steve Ryan - Reflecting back on the season
"It was a great year, It was a special year-just the way we came together. I didn't think we thought we'd end up here (in the championship game), but it was a special year. It's a special team and it was a great year. A lot of players really developed. Joel developed into a great quarterback."


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Our Top Ten Blog Posts by Readership in 2011
Originally published on July 20, 2011
Last week, more than 59 governments and 100 civil society groups joined the Government of Brazil and the United States to announce the Open Government Partnership (OGP) in Washington, DC. The initiative brings together nation states, civil society, and the private sector to address problems that Governments are unable to solve alone. Rather than seeing citizens and civil society groups as competitors, governments from the North and South asserted that private actors, commercial and non-profit, are essential partners in solving complex social problems. And this requires a new social contract, a shift from eGov to WeGov.
The OGP start with open data but goes beyond transparency and accountability. As the UK's Director of Transparency, Tim Kelsey, stated, "open data is a necessary precondition for open government" but something broader and deeper than freedom of information is needed. Open Government and ultimately open development is about putting citizens at the center of the development paradigm and creating a new model for engagement. Sometimes a pothole can be a gateway to civic engagement.
Tools like Huduma in Kenya or SeeClickFix in the US enable citizens to use their phones and web browers to log and prioritize public service problems in their own communities. In the US, it's the proverbial pothole that's their most common pain-point. City governments from New York to Bangalore and Nairobi are paying attention and using citizen reporting tools to prioritize public service actions and enlisting neighborhood groups to solve problems. As Tim O'Reilly famously said, the days of 'vending machine government' where citizens pay their taxes and governments solve their problems are gone. We need a new paradigm. Government is a platform and open government is about enlisting large numbers of people to address public service challenges.
To realize this vision, however, Governments must do something that makes many people uncomfortable. Relinquish control and allow communities and non-experts to help manage and moderate development processes. That means shifting the contract between state and citizen.
Latvia gives us one such example in manabalss.lv. The portal allows citizens to propose new legislation to Parliament. If a citizen or group can gather 10,000 signatures from their fellow Latvians, they get an audience with the Latvian Parliament. Policy makers have realized their own people can be partners in governance. In the UK, a government mandate to liberate hospital performance data including doctor performance, resulted in a 20% reduction in mortality in select hospitals.
In Mexico, the International Budget Partnership (IBP) described a program working with citizens and local governments to monitor budgets, contracts, and the use of 'information power to hold the powerful to account'. But challenges abound and political will is crucial in making hard decisions to invigorate participation. While energy from the Arab Spring abounds, many struggle to make sense of what happened and what it means for governments. We know that ignoring citizen voices and squashing meaningful engagement is potentially disastrous but we don't know what works when civil society is weak, citizens are frustrated, and governments are unable to meet the needs of a growing and restive population.
And what is the role of multilaterals and the World Bank Group in all this? That question was asked explicitly to Kenyan officials who recently launched an Open Kenya initiative, freeing for the first time public expenditure data, census data, and household surveys. The answer was clear. Help end knowledge monopolies. Link our experts with expertise elsewhere. Encourage citizen feedback loops. Use technology to enable citizen engagement of a different kind. As we move towards a world of hyper-connected citizens, government has no choice but to embrace transparency and leverage citizens as partners in governance.
These were the words of Dr. Bitange Ndemo, a Permanent Secretary in the Kenyan Government. You can't change what you can't see and that's why open data is a necessary precondition for open government. But it's about more than freeing information. The experience of MKSS in India starts with "the right to know – the right to live" but goes beyond access to information. Social audits are effective precisely because government officials, civil society activists, and the media work together to listen to citizens, end impunity, and mobilize social action. Data is fuel but people are drivers. Both are necessary for social change.
Global mechanisms like the OGP encourage multi-stakeholder engagement. International actors like the World Bank can catalogue these partnerships, connect practitioners to each other, and aggregate demand from government and civil society partners. It's about brokering knowledge, learning, and innovation between governments and other stakeholders. Finance becomes instrumental to lubricate the path of knowledge exchange. While this is not a traditional role for development Banks, helping governments partner with citizens to solve pressing social and economic problems may be the most important role they can play going forward.
Related blog post by Aleem: Let's Move Beyond Open Data to Open Development
Photo: U.S. Secretary of State Hillary Rodham Clinton delivers remarks at the Open Government Partnership High-Level Meeting, at the U.S. Department of State in Washington, D.C., on July 12, 2011. [State Department photo/ Public Domain]


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The International Lacrosse Federation (ILF) World Championship began as a four-team invitational tournament that coincided with Canada's centennial lacrosse celebration in 1967. The Mt. Washington (Md.) Lacrosse Club represented the United States and won the tournament. Seven years later, Australia celebrated its lacrosse centennial, and the U.S. fielded an all-star team to compete in a similar international invitational tournament. It was here that the concept of holding a world championship tournament every four years was born. The U.S. has captured NINE ILF World Championships and finished second twice, including the most recent world Championship this past summer in 2010 in Manchester, England. Prior to losing to Canada in the 2006 championship game, the Americans had not lost a game since the 1978 final, a 17-16 overtime setback to Canada. The winning streak spanned 38 games through seven ILF tournaments.
ILF World Championships History
Manchester, England
* The 1967 team was the Mt. Washington Lacrosse Club from Baltimore, Md.
The 30-man roster by position with professional teams, collegiate alma maters, and previous U.S. team experience noted:
Ned Crotty, New York Lizards, Duke*
Marcus Holman, Ohio Machine, North Carolina
Kevin Leveille, Rochester Rattlers, Massachusetts
Brendan Mundorf, Chesapeake Bayhawks, UMBC*
Rob Pannell, New York Lizards, Cornell
Steele Stanwick, Ohio Machine, Virginia
Garrett Thul, Florida Launch, Army
Kevin Buchanan, Boston Cannons, Ohio State
David Lawson, Rochester Rattlers, Duke
Matt Mackrides, Chesapeake Bayhawks, Penn State
JoJo Marasco, New York Lizards, Syracuse
Paul Rabil, Boston Cannons, Johns Hopkins*
Max Seibald, New York Lizards/Philadelphia Wings, Cornell*
Matt Abbott, Chesapeake Bayhawks, Syracuse
Dan Burns, Chesapeake Bayhawks, Maryland
Kyle Harrison, LXM PRO, Johns Hopkins^
Jeff Reynolds, Chesapeake Bayhawks, Maryland
Chris Eck, Boston Cannons, Colgate
Mitch Belisle, Boston Cannons, Cornell
Jesse Bernhardt, Chesapeake Bayhawks, Maryland
Tucker Durkin, Florida Launch, Johns Hopkins
Michael Evans, Chesapeake Bayhawks, Johns Hopkins
Joe Fletcher, Loyola +
Kyle Hartzell, New York Lizards, Salisbury
Brian Karalunas, New York Lizards, Villanova
Lee Zink, Denver Outlaws, Maryland
Drew Adams, New York Lizards, Penn State
John Galloway, Rochester Rattlers, Syracuse
Jesse Schwartzman, Denver Outlaws, Johns Hopkins
* 2010 U.S. men's national team member
^ 2006 U.S. men's national team member
+ Current college player
For more information on the U.S. men's national team, visit www.uslacrosse.org/usmen. Follow the team on Facebook at fb.com/uslacrosse, on Twitter and Instagram at @uslacrosse and use #USAMLAX.
The World Champion U.S. Men's National Teams train and play using best-in-class products provided by Nike (apparel and footwear), STX (equipment), Cascade (helmets) and Shock Doctor (mouth guards). Nationwide and Marriott International are official sponsors of Team USA.
New Privacy Policy


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DART General Meeting
- Sutter Memorial 5151 F St Sacramento, CA, 95819 United States (map)
Would you like DART to attend your event? Please complete the form below and a DART officer will contact you. Note: DART may have difficulty staffing events submitted with less than 45 days notice.
The Drowning Accident Rescue Team (D.A.R.T.) is a non-profit, all volunteer organization which is funded by donations, grants and fundraising events, such as our annual Crab Feed and our Fireworks Booth.
Our primary mission is to save lives and recover property from the various rivers, lakes and waterways in and around Sacramento County.
We accomplish this mission through numerous rescue, recovery, education and prevention activities.


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Why We Keep Losing Our Keys
Everyday Memory Lapses Hit at Any Age; Train Your Brain to Find Things Faster
You've put your keys somewhere and now they appear to be nowhere, certainly not in the basket by the door they're supposed to go in and now you're 20 minutes late for work. Kitchen counter, night stand, book shelf, work bag: Wait, finally, there they are under the mail you brought in last night.
Losing things is irritating and yet we are a forgetful people. The average person misplaces up to nine items a day, and one-third of respondents in a poll said they spend an average of 15 minutes each day searching for items—cellphones,...


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Supreme Court Clinic
Students work closely with faculty members on cases before the United States Supreme Court. Students assist in representing clients who are seeking review of lower court decisions or who have cases before the Supreme Court following grants of certiorari. Students conduct in-depth research and draft pleadings such as petitions for certiorari, briefs in opposition, reply briefs, and merits briefs. The weekly classroom component introduces students to Supreme Court procedures and practice.


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- The juicy information is rarely included. The information that you really want to find out, such as what went wrong and why it went wrong, is rarely discussed. If problems, oops I mean "challenges", are discussed at all they're typically glossed over in favor of focusing in on the positives. Although many people want to write up the juicy bits this information is invariably edited out through the company's vetting process. In short, my advice is to take case studies with a grain of salt.
- Some case studies are more fiction than fact. Although this isn't a problem with IBM case studies due to the governance efforts of my good friends in IBM's legal department (we love you folks, really) it can be an issue with some case studies.
- The case study may no longer be true today. Stuff happens. Perhaps the case study was mostly true at the time it was written, but now that time has passed problems have appeared that weren't apparent earlier, thus the effort wasn't as nearly as successful as it was written up. For example, a few years ago I ran into the manager of a team that I had read about in one case study, only to find out that once the study was published the key team members left the company to become consultants in that subject area. Having lost these people, who were all very highly skilled, his system proved to be unmaintainable by the rest of his staff who weren't so highly skilled and had to be rewritten. Over time the success story turned into an abject failure.
- Waiting for case studies puts you in the position of follower. For every case study that gets written, dozens, if not hundreds of similar efforts didn't get written up. Writing case studies is hard, takes time, and the writer seldom gets much benefit from doing so. The lag time between the project completing and the case study being published can be many, many months and sometimes years. The implication is that by the time you wait for several case studies that are similar to your situation you've pretty much lost all opportunity for competitive advantage and are now merely trying to catch up to the organizations who are clearly ahead of you (the writers of the case studies).
- What has the requester given back to the community? I often hear people lament that there isn't enough case studies, or isn't something close enough to their situation. Yet, when I ask them how many case studies they've written and the answer is usually none. If you want to get you also need to give. ;-)
Further reading:


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I'd assume that it's safe to say that everyone who reads this blog loves two things: the internet and images. We are all here because we love graphics, love data and are constantly on the internet. Today's infographic is all about what we love most. Images on the internet!
Images have gotten better. Image quality has increased all over the internet. Increased image quality and an increase of images per article increases views and aids in searchability. Various new-ish aps and websites aid in the promenance of images. Pinterest boasts inspiring fashion, food and decor photos, earning swoons across America. Facebook allows users to upload photos of their friends family and fun times. Instagram, which we all know i love, gives even the most novice of photographers an opportnity to publish their own photos.
Images are beautiful and allow inspiration. Horray for the image revolution! [Via]
© chelseykilzer for Daily Infographic, 2012. |
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