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Saturday, June 25
Minute Maid Park
Attendance: 27,208
Houston, TX (Sports Network) - B.J. Upton, Casey Kotchman and Evan Longoria each drove in two runs, as the Tampa Bay Rays defeated the Houston Astros, 7-2, in the middle portion of a three-game interleague series.
Wade Davis (7-5), making the 50th start of his career, gave up one run on five hits over seven innings for the Rays, who have won three in a row and seven of eight overall. Davis also struck out three and walked one en route to winning his third straight start.
Hunter Pence and Carlos Lee had an RBI apiece for the Astros, who lost 5-1 in the opener of this series on Friday.
Bud Norris (4-6) allowed three runs on six hits over five full frames to suffer the loss. He also struck out five and walked three.
"He kept working to find his stuff, and his command kind of got him in trouble there with those walks," Astros manager Brad Mills said. "He kept battling through it. It was -- what? -- 95 pitches though five innings, and he wanted to go back out there, but it was a situation [in which] we were down and trying to get some baserunners as well."
The Rays scored one run in each of the first three innings to take an early lead. In the first inning, Ben Zobrist worked a one-out walk and came around to score on Longoria's double down the left-field line.
Reid Brignac hit a one-out single during the Rays' next at-bat. Brignac moved up to second on Davis' sacrifice bunt and scored on Johnny Damon's base hit to right. Brignac slid under the tag at home plate to make it a 2-0 game.
Longoria started the third with a walk and Kotchman followed with a single to put men on first and second. Two batters later, Upton hit an RBI single to left for a 3-0 edge.
Houston finally got to Davis in the fourth. Pence worked a two-out walk and crossed the plate on Lee's double to right-center field to make it 3-1.
Upton's solo homer to left off Fernando Abad in the sixth made it a 4-1 contest.
The Astros had a chance to get some runs back in the home sixth, but they left the bases loaded.
"I think I stayed under control better than I have all year throughout the whole game," Davis said.
Houston scored a run in the eighth to make it a two-run game. Joel Peralta gave up a one-out single to Jeff Keppinger, who scored on Pence's double off the wall in left. Kyle Farnsworth took over on the mound and Lee smacked the ball to the warning track in left field. Sam Fuld dropped the ball to allow Lee to reach base. Matt Downs grounded into a double play to keep it a 4-2 contest.
The Rays tacked on three runs in the ninth to pull away. Fuld doubled Zobrist walked to begin the frame. Longoria followed with an RBI double to left. Sergio Escalona took over on the mound for Enerio Del Rosario and gave up a two-run single to Kotchman.
Farnsworth pitched 1 2/3 scoreless innings to record his 16th save of the season.
Jim Wolf
Tony Randazzo
Larry Vanover
Brian Gorman


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Hello everyone, happy St. Patty's Day. Most of all welcome to spring!! Almost spring...here in Al. we're having warm days and cool nights.
Now about the emu, I've had a pair for 3 years. Every time the eggs hatch, the male kills the babies. What do I do? He had one that had hatched out and we took it from him today, I have it in a box with a heat lamp. I've read different links and they all talk about incubating. My incubator is for chickens, not large enough for emu eggs. Right now the baby is sitting not standing... do I need to do something to make him stand? My son gave me the emu for my birthday one year....I'm not into killing for oil or meat.... I simply like them, as well as my guineas, chickens, ducks, turkeys, pecock and llama. I like babies and watching them grow.....If you have any info, please pass it alone. I don't want to lose this little fellow. |
Follow-Up Postings:
- Posted by velvet_sparrow z10 So. Calif. (My Page) on Fri, Mar 17, 06 at 20:45
Not quite emus, but the United Peafowl Association's website may be of help: http://www.peafowl.org/ARTICLES/index.htm#peachick Also, I googled "raising emus" and got a bunch of results. Another good site on hatching & chicks here, also on what to feed--make sure you are feeding ratite feed: I couldn't find any info on weather the not standing thing is a problem or a normal occurance....how old is the chick? Good luck, and post a pic if you get one! :) Velvet ~:> |
- Posted by joanne_al 7 (firstname.lastname@example.com) on Sat, Mar 18, 06 at 1:09
Thanks Velvet for those links...as for the age, the baby was dry and has all feathers, but still isn't drinking and eating. So we're guessing less than 2 or 3 days old. I did find some info that help alot....thanks again and wish me luck....(-: |
i just hatched a baby emu egg. i have no idea how to care for it!i hahve been searching everywhere online to find what i should feed it and how to feed it but cant find anything helpful and i could not connect to the above site. any info will help me please! thank you!! |
- Posted by vancleaveterry (My Page) on Mon, Mar 10, 08 at 22:44
I found this: "Once an Emu chick absorbs the yolk sac at about 10 days after hatch, these birds are very hardy and only require normal livestock hygiene and maintenance.... "We feed our emu chicks a special feed that has been prepared specially for us by Lanark Leeds Distributor. It consists of 18-20% protein pellet mixed with crushed corn, wheat and soya bean." I would dip his beak in some water and give him fresh water every day. Go to your feed store and see if they have anything that resembles the above formula and mix in some chopped greens. Sit with the bird and simulate picking at the food and greens. Show him how it's done. Show him every day until he gets it. Don't wait for the yolk to be absorbed. "Newly hatched chicks cannot regulate their body heat and need a source of warmth until 3 months old if the outside temperature is cold. Maintain temperature at 90 to 95 degrees F for the first 3 days after hatch. Decrease temperature 5 degrees every 2 weeks. In warm weather, use supplemental heat only at night. The heat source should be of adequate size for all chicks to get around it, and the pen area should be large enough so the chicks can get away from the heat to avoid overheating. Brooder boxes for chicks 1 to 3 days old are typically about 1 foot high and 2 x 3 or 3 x 4 feet in area per 10 chicks. Chicks may pile and smother one another. Avoid overcrowding, extremes of heat or cold and sudden frightening of the chicks. Piling generally becomes less of a problem after the first few weeks. The floor of the brooding area must be easy to clean and have good traction. Chicks can be moved to an 8 x 8-foot nursery pen at approximately 70 to 85 degrees F on day four and then into progressively larger pens. Encourage outside exercise periods and sunbathing starting at 5 to 7 days of age, depending on the weather. Separate juvenile groups by age and/or size into large communal pens (50 x 100 feet) or pastures. Grass usually survives well in emu pens except along the fence, where the birds' tendency to fencewalk kills it. Many farmers feed newly hatched chicks a mixture of chopped greens, a commercial starter crumble and a vitamin/mineral supplement. The greens are thought to attract the birds to the feeder and stimulate feed consumption. Water may be offered before food by about 12 hours. Grit is offered with the food although it is not necessary if feeding a processed commercial diet. Chicks are usually fed twice a day for about an hour. Diets are usually in a small pellet or large crumble form for chicks. Fiber content varies between 7 and 15 percent. Some nutritionists recommend fiber content between 5 and 10 percent. Diets with more than 25 percent protein (such as dog food and catfish chow) have been associated with growth problems in young emu. Breeder diets contain additional calcium, or calcium can be offered "free choice" in the form of oyster shell. Breeders that are too fat do not appear to reproduce as well as those in normal condition. Some emu producers prefer free choice feeding systems, while others prefer one to three daily feedings. However, multiple daily feedings provide a time for interaction with the birds, making it easier to detect illness and control an individual bird's weight." Good luck |
- Posted by backlanelady 6oh (My Page) on Tue, Mar 11, 08 at 0:48
I'm suprised your male is killing the babies. Usually it is the emu male that raises the babies. Are you sure he was trying to kill it? You got good information above. You have to teach the chick how to eat. Sounds strange, but it's true. A feed store should be able to order emu feed for your chick. |
- Posted by vancleaveterry (My Page) on Tue, Mar 18, 08 at 7:56
up date? |
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subset: commoncrawl


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Estonia is home to one of the finest karting tracks we've ever had the pleasure to race on! Indoor karting is a Tallinn hen weekend essential! If you're got a group of speed queens on your hands, grand prix-style racing will keep them happy.
10 cars can race at once on this challenging 400-metre track. In the summer months, it's extended by a further 200 metres outside!
Rev your engines and get the competitive spirit pumping! Jockey for pole position, put your foot right down for the long stretches and be the first past the chequered flag.
Tallinn hen weekend indoor karting includes:


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Recipies to try :)
(13 Recipes) Created by IWUVEGETARIAN
Recipes in this Collection
Very Good 4.8/5
(5 ratings)
Submitted by ALIRA54 Carbs: 12.6g | Fat: 2g | Fiber: 4g | Protein: 10.3g | Calories: 109.6
(no ratings)
Cookbook creator says: try with plain stuffing mix because chicken stuffing mix will have chicken powder from chicken fat in it. Submitted by MRSSARAHPHALEN Carbs: 1.3g | Fat: 7.2g | Fiber: 0.3g | Protein: 2g | Calories: 77.5
Good 3.9/5
(28 ratings)
Cookbook creator says: leave out onion, try with pita bread/chips Submitted by BARBYCHICAGO Carbs: 19.8g | Fat: 2.8g | Fiber: 3.9g | Protein: 11.2g | Calories: 144.6
This recipe has been marked private.
Very Good 4.7/5
(9 ratings)
Cookbook creator says: make in mini muffin pan Submitted by VANDEMON Carbs: 9.8g | Fat: 4.9g | Fiber: 1.5g | Protein: 11.7g | Calories: 128
Cookbook creator says: 220c=425 degrees. work good on grill Submitted by TREEHUGGER73 Carbs: 15.7g | Fat: 4.3g | Fiber: 6.1g | Protein: 10.1g | Calories: 134.2
This is a fabulous recipe for tofu. Easy and fast. It needs no marinating. Just mix the sauce pour it on and bake for half an hour. Submitted by DARUMA Carbs: 8.4g | Fat: 7.1g | Fiber: 0.7g | Protein: 13.3g | Calories: 138.7
(no ratings)
Submitted by CORRIEWILSON Carbs: 28.7g | Fat: 9.9g | Fiber: 1.5g | Protein: 17.3g | Calories: 238
(no ratings)
Submitted by INGMARIE Carbs: 11.2g | Fat: 7.3g | Fiber: 0.6g | Protein: 9.5g | Calories: 132.3
Very Good 4.0/5
(48 ratings)
These burritos can be made ahead of time, individually frozen, then heated for a fast meal. Submitted by MINDCRUSHER1376 Carbs: 68.6g | Fat: 6.6g | Fiber: 31.6g | Protein: 20.5g | Calories: 412
Incredible! 5.0/5
(1 rating)
This is wonderful compared to McDonalds or Tim hortons mix, I have substituded splenda inplace of suger to lower calories, could be done with suger This is the base recipie I use..I plan on increasing the coffee& Cocoa & splenda to have a richer drink..( I am used to black coffee:) but is very awsome! This is a good start of a base that you could do with many other options( using flavored dry creamer, sugar instead of splenda, adding whipcream & drizzling chocolate like the high end coffee shops..) I hope you enjoy this as much as I have! Submitted by HARDESTY1 Carbs: 24g | Fat: 6.4g | Fiber: 1.4g | Protein: 8.3g | Calories: 173.3
Technically this is a crustless quiche, but the addition of flour makes for a delicious crusty bottom and sides. Submitted by JENNLOVE Carbs: 13.7g | Fat: 4.6g | Fiber: 2.2g | Protein: 10.3g | Calories: 134.1
(no ratings)
Submitted by MANDAHOP Carbs: 9.1g | Fat: 3.4g | Fiber: 2.9g | Protein: 7.1g | Calories: 65.5


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What a great day in the garden! 2014 is shaping up to be the best year yet, and who would have thought that would happen after our horrible winter? The daylilies must have loved their two feet of snow cover! ARCTIC LACE -- Yes, I've posted it before, but how could I resist posting again when it posed so prettily? CLOWN PARADE also gets another post for parading so well: Another group shot, this one of RIBBIT RIBBIT: A duo from BACHELOR PARTY: Another repeat, this one from DREAMCICLE SUPREME. The color and substance on this plant are amazing: TRUE TO WHIM, an oldie that earned a new spot in the garden: CONCRETE BLONDE just started its long bloom season: CHILLED EUPHORIA joined the party today: LADY PHARAOH is blooming happily: VANILLA GORILLA is new this year: And finally, RASPBERRY FLAMBE debuted with a perfect bloom that was waist-high. What a great Monday surprise: Chris |
This post was edited by maximus7116 on Mon, Jul 14, 14 at 16:38
Follow-Up Postings:
I love that ARCTIC LACE. Perfect. Makes me wish I had gotten that instead of Victorian Lace which is still being wished away on the junk pile. Ribbit Ribbit does great here too. What a blooming machine. Clown Parade is another great one. Are you seeing any significant increase with it? I ask because here it is slow but the scapes are tall, well budded and opens perfectly. Nice group Chris. Julia |
So many great ones today. Arctic Lace and Clown Parade were both posting perfectly. Chilled Euphoria, Vanilla Gorilla, and Raspberry Flambe are my favorites among the singles. I like the vibrant color of Raspberry Flambe and the white edges on the sepals as well as the petals. It's good to see your photo of True to Whim. I have a seedling from seeds bought on the Lily Auction with that one as a parent, and photos of TTW vary greatly from light lavender to the color yours has. I can see the resemblance of my seedling to True to Whim in your photo. My seedling is much taller than TTW, but has its white midribs. The sepals always quill and the petals usually cascade. Debra |
I've vanilla gorilla as well and just had its first blooms... What a beauty.... |
Stunning combination in the Clown Parade photo. This year I planted some violet-colored monarda with my violet-eyed daylilies but managed to get the heights wrong - the only way I can get both flowers in the same picture is with an aerial shot. :-P Thanks for sharing your fantastic pictures. |
- Posted by twixanddud z5/6 SE Mich (My Page) on Mon, Jul 14, 14 at 18:07
Marvelous is an understatement! Arctic Lace, Clown Parade, Bachelor Party, Vanilla Gorilla. and Raspberry Flambe are my picks. Vanilla Gorilla is one I've thought about getting, your picture of it is great! |
Clown Parade and Arctic Lace are my favorites today but all of them are nice. |
- Posted by maximus7116 MI (My Page) on Mon, Jul 14, 14 at 20:29
Thanks, everyone. Julia, I've had good increase from Clown Parade but am most impressed with the number of blooms it's had since I first planted it. Victorian Lace does well here, but I prefer the whiter blooms of Arctic Lace. Debra, I remember the beautiful seedling you posted from True to Whim, but I assumed you grew TTW. It's probably 30" here and is always a dark purple. I had a feeling you'd like Raspberry Flambe with that white edge. The photos I've seen of Vanilla Gorilla on line look great, so I'm excited to see how it looks once it's settled in. Statmam, I grow about six different varieties of monarda and it's scattered all over the garden. It's hard to get a daylily shot without the bee balm sneaking into the photo! |
- Posted by mantis__oh z6 OH (My Page) on Mon, Jul 14, 14 at 21:12
Raspberry Flambe is sumptuously flamboyant. Has it survived a few winters? I really like Bachelor Party too. |
- Posted by organic_kitten 8 (My Page) on Mon, Jul 14, 14 at 21:25
Well Chris, that shot of Clown Parade with the red Bee Balm is outstanding. Yo should consider entering that one in the contest. Arctoc Lace is lovely, and Ribit Ribit is an eye catcher. I really like Raspberry Flambe too. kay |
- Posted by maximus7116 MI (My Page) on Mon, Jul 14, 14 at 21:43
Well, thanks, Kay! Mantis, Raspberry Flambe was added in 2012, so it's had a couple winters in Michigan. I didn't even notice the scapes, so I was so surprised to walk around the garden and have that one almost staring me in the face. It's not registered as very tall, so the height really surprised me. |
- Posted by jean_ar z8 Ar (email@example.com) on Mon, Jul 14, 14 at 22:29
beautiful. don't matter if you post them over and over.They are not the same bloom each time,since the bloom only lasts one day.ARTIC LACE is a beauty,and I love BACHELOR PARTY, too, and CLOWN PARADE is always a beauty. all your daylilies must have really injoyed that very cold winter and piles of snow.They are all gorgeous. jean |
- Posted by edward_kimball Zone 5b (My Page) on Tue, Jul 15, 14 at 9:16
Arctic Lace was pretty amazing. Feel free to post it every day. |
- Posted by maximus7116 MI (My Page) on Tue, Jul 15, 14 at 10:29
Thanks, Jean. Edward, you must be blooming up there by now, right? We need pics! |
Wow! So gorgeous! I'm adding Raspberry Flambe to my wish list. They are beautifully done pictures as well as beautiful blooms. Thanks for posting them! |
All of your daylily pics are wonderful, but Raspberry Flambe has that " you really have to have me" effect. It's going on my got to get list. Oh the crosses I could dream of making with that one. lol Linda |
This post was edited by opnjmprs on Wed, Jul 16, 14 at 17:13
- Posted by gonegardening 7 VA (My Page) on Wed, Jul 16, 14 at 15:43
Be still my heart, Arctic Lace. When it's good, it's verrry good. Dreamcicle Supreme looks...haha...dreamy. A FL flower liking Michigan! Good to see. Vanilla Gorilla...the name alone makes that a must have. (That was the old me that popped out for a minute!) A Magic of Oz kid...it should have great habits from that one as MoO is a long bloomer here (still going). Very interesting. A very nice day in your garden! Okay...where's today's? |
- Posted by timhensley 5VT (My Page) on Wed, Jul 16, 14 at 18:16
Love Dreamcicle Supreme and Arctic Lace. |
All beautiful. Artic Lace is one of my favorites, but mine didn't do well this year. Maybe because I tried dividing it in the fall. I love the color of your Clown Parade. Mine is new this year and has more yellow in it. |
Rasberry Flambe really grabbed my attention and the shot of Arctic Lace is wonderful. Dreamcicle Surpreme, although listed as a "creamy orange" looks golden yellow to me in your picture, but whatever it's called I like it.........Maryl |
- Posted by maximus7116 MI (My Page) on Wed, Jul 16, 14 at 20:06
Thanks! I was hesitant to add Dreamcicle Supreme this far north, but it has surprised me and done well. Maryl, it is more orange than my photo shows, but a difficult color for my camera to capture. |
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Put the needle to the groove I gets rude and I'm forced
from Wu-Tang Clan – Wu-Tang Clan Ain't Nuthing ta Fuck Wit Lyrics on Genius
"Needle to the groove" as in turntable needle to vinyl groove. Once the beat starts playing, Deck has no choice but to rip it up with his rhymes — He can't help it!
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text:
10 Companies Hot Enough to Get Google's Attention
Google's venture fund has invested in 10 companies in a wide range of fields such as antibody research, "green" utility networks, and cars.
Google, YouTube Received 10,000 Government Requests for User Data
Google and the YouTube received more than 10,000 requests for user data from government agencies in the six months ending Dec. 31, 2009, according to newly released data.
100 iPads Set for Deployment at Californian Hospital
The business case for the iPad may be nowhere as clear as it is in healthcare, a multi-billion dollar industry and one of the world's largest consumers of...
HP: No Plans to Kill off 3Com Products
HP says it has no plans to kill off any existing HP or 3Com networking products, but did not rule out such a move in the future.
Tech Icons Get the South Park Treatment
Facebook is just the latest high-tech South Park skewering; the iPhone, Bill Gates, Star Trek, and the Internet all have been lampooned.
10 Head-Turning Tech Products from DEMO
Internet TV, smartphone apps, cloud services and more on display at DEMO Spring 2010.
Social Network Manager Designed
Startup Pip.io develops a layer to interact with a variety of social networks, managing contacts, communication, and privacy.
Google to Appeal Italian Convictions of Three Execs
Google did not give a timeline for legal action, but it denounced the conviction adding, "We and our employees will vigorously appeal this decision."
Facebook Outpaces Yahoo to Become No. 2 Site on Web
According to new research, Facebook had 133 million unique visitors in January and beat out Yahoo as the second most popular Web site in the United States.
Be My Valentine: Tech Titans Mix Work and Marriage
The heartwarming tale of 10 tech companies founded by husbands and wives.
Google Eyes Social Net Role for Gmail
Google Tries to Make Gmail More Like Facebook, Twitter
Twitter Phishing Attack Forces Users to Reset Passwords
Describing it as a "precautionary step," Twitter urges some users to come up with hard-to-guess passwords after a phishing attack.
Articles by Jon Brodkin


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Ballots have been mailed to area residents and for the first time in several years some Billings voters will have a choice in who they vote onto the Billings School District 2 board.
Running to represent Zone 4 -- the neighborhoods immediately north and west of downtown -- is incumbent Kathy Aragon, who has served on the board since 2007, and Dennis Johnson, retired Billings Senior High track and field coach and math teacher.
Trustee Allen Halter is seeking election for his seat representing Zone 6, the northwest corner of Billings. Halter, one of six candidates to apply, was appointed to the board in December after Trustee Barbara Bryan resigned in late October.
He'll face Mary Jo Fox, another of the six candidates to apply for Bryan's seat. Fox, a former trustee who served from 2005-2010, was forced to resign from the board in 2010 when she moved from her home in the Heights to the Indian Cliffs development, which sits just inside Zone 6.
Two contested races out of the three is a shift for SD2. Last year, four seats were up for election and each of them ran uncontested.
Johnson retired from the school district last year and decided to run for the board shortly thereafter. A growing sense of frustration over board infighting and politicking pushed him to the decision, he said.
He likened watching a board meeting to viewing a reality show on television and said the culture there must change.
"They've accomplished absolutely nothing," he said. "I would push hard to try and get a code of behavior adopted."
He and Aragon have a lot of mutual respect. Johnson taught Aragon's daughter in Advanced Placement calculus and coached her on the track.
Aragon was happy to see someone like Johnson volunteer to run for the board. But she said new trustees face a steep learning curve, something she's already accomplished over the last five years.
Where Johnson sees many of the district's issues as board-based, Aragon sees district troubles as a result of poor planning.
"Long-term planning is vital for this district," she said. "And it's something we struggle with."
Along with planning, she said it's necessary for the district to collaborate with the city and other government entities as it plans for the future.
To that end, she and city Planner Candi Beaudry spent the last three years securing a planning grant from the Environmental Protection Agency.
Just last month the agency announced the city and SD2 would receive its Small Growth Technical Assistance Program grant. With it, the EPA will come to Billings, work with the community and create a model plan that could be applied to the various planning needs of the city and school district.
Johnson applauds Aragon's efforts. But, he wants to see the board learn to be more formal, respectful and goal-driven.
"They need to change the way they do business," he said.
Fox decided to run again after watching much of the district's turmoil over the last year. She works for the Yellowstone Boys & Girls Ranch Foundation and with her previous board experience, she said she's got skills to offer.
"I have a track record of serving and caring about kids," she said.
Halter admitted his first few months on the board were more intense than he'd anticipated.
"It's been a huge learning experience," he said.
Still, he's enjoyed it and believes he has skills to offer the district. Halter is general manager and salesman for Allegra Marketing Print and Mail and has served as West High's booster club president.
"I want to know the facts and vote for the kids," he said.
Both Fox and Halter agree that at some point -- likely in the near future -- the district will need a school on the West End. Both agree overcrowded classrooms in the district are one of SD2's biggest issues.
Ballots are due by May 8 and as the newly elected board moves into the summer and into the next school year, trustees will face some weighty issues, including budget shortfalls, adopting and implementing a new national curriculum and changing leadership.
The board is in the process of hiring a new superintendent.
The Omaha, Neb.-based search firm McPherson & Jacobson just submitted to the board a list of 18 applicants; the top picks will fly to Billings to interview the week of the election.
So it will be the new board that hires SD2's next superintendent.
The board deliberately chose to leave the selection process until after elections to give the new board ownership in the superintendent pick.
Running uncontested for the high school District A seat is board Chairwoman Teresa Stroebe. Her name will not appear on the ballot.


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been thinking of getting some to load into a .243 rifle for smaller critter . i did read on the net they dont stabilize in all guns . i'll be shooting them out of a howa 1500 .
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on March 11, 2014I watched The Girl With The Faraway Eyes work radio row at CPAC -- and, if you want to see the saddest gathering of humans this side of the knots of smokers on the sidewalks of New York, hang out with the people grooving at the sight of their favorite radio wingnuts broadcasting LIVE! -- but I did not realize that she was expanding the frontiers of the crazee while she was there.
"I just thank God that there's a billionaire or two on our side," Bachmann told conservative radio host Lars Larson during an interview at the 2014 Conservative Political Action Conference. "All the billionaires seem to be on the radical left, so I'm glad that we have a couple on ours."..."I'm sure that the donors on our side don't like to have their names vilified and that's what this is about, intimidating people from giving money to our cause, that's it," she opined, adding that Democrats should be prosecuted under the Racketeer Influenced and Corrupt Organizations Act (RICO) for their intimidation of billionaires.
Being mean to the Kochs is now to be considered racketeering. I am going to have to spring for a pinstriped suit and a fedora if I'm going to keep up here.
I am going to miss her so.
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HOSPITALITY: THE PELICAN MOTEL is seeking a housekeeping supervisor. Must have prior housekeeping exp. & be bilingual & fluent in English. Apply in person at 99340 Overseas Hwy., Key Largo More info Email a friend |
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In between mouthfuls of White Berry's original yogurt topped with Oreo cookies, 6-year-old Kyle Upman tells The Observer, "It's good!"
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- Jan
28 SILL Global Issues Lecture
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28 Is the American Constitution the One We Deserve or Has it Gone off the Rails? An Einstein�s Circle Forum
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28 Meet The Sky
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Making headlines
Did you notice a familiar name in the February issue of Southern Living magazine? -
Packing on team spirit
No one can accuse of Diane Chechik of not representing her team, the Green Bay Packers. -
Sarasota on the social map
… Well, we already knew that, right? Now apparently all of New York knows how wonderful our slice of paradise is, too.


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I've recently migrated a machine to Windows 8.1. Before I did so I created a system backup of my old Windows 7 configuration.
My question is, can I restore this to a hyper-v VM in Windows 8? Having installed Win 7 on the hyper-v and selected restore, I get the message:
Windows was not able to find any backup sets on
\\mymachine\c$\WindowsImageBackup\username\backup date-stamp.
Please select a different location.
In that directory, there is a vhd file. I then wondered if it would be possible to simply create a new VM and just tell it that this was the VHD; it is apparently not.
So, is what I'm doing not possible? Should I be able to restore to a VM in this way (or in any other)?
For information; the VM I'm trying to restore to has a full Win 7 install.


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Oh, Boraa,b; Kim, Tae Y.a,b; Min, Hyun J.b; Kim, Miyoungc; Kang, Myung S.e; Huh, Ji Y.f; Kim, Youngsood; Lee, Dong S.b,c
aDepartment of Molecular and Clinical Oncology
bCancer Research Institute
cDepartment of Laboratory Medicine
dDepartment of Molecular Genomic Medicine, Seoul National University College of Medicine
eDepartment of Laboratory Medicine, CHA Gangnam Medical Center, Seoul
fDepartment of Laboratory Medicine, CHA Bundang Medical Center, Sungnam, Republic of Korea
All supplementary digital content is available directly from the corresponding author.
Correspondence to Dong S. Lee, MD, Department of Laboratory Medicine, Seoul National University College of Medicine, 28 Yongon-dong Chongno-gu, 110 744 Seoul, Republic of Korea Tel: +82 2 2072 3986; fax: +82 2 766 0827; e-mail: email@example.com
Received April 18, 2012
Accepted September 4, 2012
The antiproliferative effect of simvastatin on tumor cells has been speculated to be by intracellular signal inhibition through 3-hydroxy-3-methylglutaryl acetyl coenzyme A reductase. We examined the killing effect of simvastatin on imatinib-sensitive and resistant chronic myelogenous leukemia (CML) cells (three kinds of CML cell lines representative of each hematopoietic lineage: K562, KCL22, and LAMA84) and T315I and E255K site-directed mutant cells (Ba/F3). The in-vivo effect of simvastatin was determined in K562-xenografted nude mice. Cotreatment with imatinib and simvastatin in imatinib-resistant CML cells showed a synergistic killing effect in K562-R, KCL22-R, LAMA84-R, and E255K mutant cells, but only an additive effect in the T315I mutant cell, although a single treatment of simvastatin strongly inhibited T315I mutant cells. Mechanisms of killing were an induction of apoptosis and cell cycle arrest, through inhibition of tyrosine phosphorylation, and activated STAT5 and STAT3. Simvastatin suppressed the growth of K562-transplanted tumors, and cotreatment with imatinib was more effective in reducing tumor size. Simvastatin also killed primary CD34+ cells from patients with CML more efficiently, compared with CD34− CML cells. Our study shows a synergic effect of imatinib and simvastatin both in imatinib-sensitive and imatinib-resistant cells, but more effective synergism in resistant cells. On the basis of these findings, we suggest that a combination of simvastatin and imatinib may be a potential candidate for the treatment of imatinib-resistant CML.
Chronic myelogenous leukemia (CML) is a stem cell proliferative disorder whose hallmark is a BCR–ABL fusion gene encoding abnormal tyrosine kinase 1. The constitutively active kinase activity of Bcr–Abl in the cytosol contributes towards its transforming function 2 and towards drug resistance through the activation of several key survival pathways, including the mitogen-activated protein kinase (MEK)/extracellular signal-regulating kinase (ERK) cascade, Akt, signal transducers and activators of transcription (STATs), and nuclear factor κB 3–5. These pathways promote cellular proliferation, survival, and resistance to apoptotic stimuli induced by conventional cytotoxic drugs. It is proposed that CML, similar to many other neoplasms, may be the result of a multistep pathogenetic process 6. As the disease progresses through the accelerated phase and into the blast crisis, additional cytogenetic abnormalities become evident 7.
The introduction of imatinib mesylate has revolutionized the treatment of CML because it is a selective inhibitor of the Bcr–Abl tyrosine kinase. Imatinib mesylate has been proven to be highly active in patients with chronic-phase CML and, to a lesser extent, in patients with accelerated and blastic-phase disease 8. Despite its effectiveness against chronic-phase disease, patients with CML eventually become refractory to imatinib through various mechanisms, including reduced drug uptake, mutation of the ATP-binding site, amplification of BCR–ABL, activation of Lyn 9, binding of imatinib to serum α-1 acid glycoprotein 10, or MDR overexpression 11. The development/pre-existence of kinase domain mutants that prevent drug binding is most commonly encountered in imatinib-refractory leukemia 12.
Various strategies to overcome this resistance have been adopted: developing novel drugs that can act on the mutated ATP-binding sites of the Bcr–Abl fusion protein, increasing the dose of imatinib, and combining imatinib with other drugs to block the downstream signal of the Bcr–Abl protein 13. Recently, second-generation compounds with a higher affinity for Abl, such as nilotinib (AMN107), or a high affinity for both Abl and Src kinases, such as dasatinib (BMS-354825), have been tested. However, these agents do not affect the kinase activity of the T315I mutants, which have a sterically reduced drug/kinase affinity that prevents the direct contact of these agents with the Bcr–Abl protein. Thus, the development of new strategies to eradicate such cells that are not affected by mutations in the kinase domain represents a high priority.
Statins, widely used as a cholesterol lowering agents, are competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase 14. HMG-CoA reductase is involved in the synthesis of various molecules such as ubiquinone, dolichol, farnesyl isoprenoid, and geranylgeranyl isoprenoid. These intermediates are essential for the post-translational modification of intracellular G-proteins, such as Rho, Rac, and Ras, which regulate endothelial, platelet, and leukocyte function 15–17. Inhibition of this hydrophobic modification of signaling proteins by statins has significant effects on cell growth in vitro. Furthermore, statins have pleiotropic, or seemingly unrelated, distinct effect on processes such as angiogenesis and inflammation, and also affect a number of novel molecular targets and complex signaling pathways 18. Because of these pleiotropic effects, statins potentially have activity in a number of chronic human diseases. Statins are believed to inhibit downstream signals of Bcr–Abl, contributing toward the growth of CML cells, through inhibition of Ras, Rho, and JAK/STAT.
In this study, we used simvastatin, one of the most pharmacologically potent inhibitors of HMG-CoA reductase. Simvastatin is similar to other relatively lipophilic statins: lovastatin, atrovastatin, fluvastatin, and pitavastatin. We found an antiproliferative activity of simvastatin in CML cells and its killing mechanism. Second, we established imatinib-resistant cell lines through mutation or progressive exposure to increasing concentrations of imatinib and examined the effectiveness of simvastatin alone and in combination with imatinib to overcome imatinib resistance. Simvastatin strongly inhibited the growth of cell lines expressing either the T315I or the E255K mutant form of Bcr–Abl as well as the wild type (WT). However, the synergistic killing interactions between simvastatin and imatinib were not observed in Ba/F3 cells expressing T315I mutant Bcr–Abl. However, cotreatment of both drugs showed synergistic killing interactions in imatinib-resistant K562, KCL22, LAMA84, and in primary CD34+ CML cells. Finally, simvastatin also enhanced imatinib-induced growth arrest in an in-vivo mouse model. Together, these results indicate that simvastatin may be useful in the treatment of imatinib-resistant CML.
K562 cells were obtained from the KCLB (Seoul, Korea). KCL22 and LAMA84 cells were obtained from DSMZ (Braunschweig, Germany). All CML cell lines used in this study were grown in RPMI-1640 supplemented with 10% FBS, 2 mmol/l L-glutamine, 100 μg/ml streptomycin sulfate, and 100 U/ml penicillin G (all from GIBCO, Carlsbad, California, USA). Imatinib-resistant CML cell lines (K562-R, KCL22-R, and LAMA84-R) were derived from the parental K562, KCL22, and LAMA84 cell line after exposure to progressively higher concentrations of imatinib mesylate. K562, KCL22, and LAMA84 cells were cultured with continuous exposure to imatinib mesylate in stepwise increments of 100 nmol/l from 0.1 to 1 μmol/l after every 10 days of culture. Viable imatinib-resistant CML cells were maintained under a selected pressure in a medium containing 1 μmol/l imatinib mesylate. Mouse pro-B Ba/F3 and WEHI3 cell line were obtained from RIKEN (Tokyo, Japan). Ba/F3 cells and variants of Ba/F3 stably expressing Bcr–Abl or the T315I or the E255K mutation of Bcr–Abl were cultured in complete RPMI-1640 medium with or without filtered 10% WEHI medium supplementation as the source of IL-3. They were maintained in a 37°C, 5% CO2, fully humidified incubator and prepared for experimental procedures when in log-phase growth.
RNA was extracted from K562 cells and used to synthesize cDNA. First, Bcr–Abl fragments were amplified by a PCR with K562 cDNA as a template and Bcr–Abl full genes were amplified by an overlapping extension PCR (OE-PCR) and subcloned into the pGEM-T easy vector (Promega, Madison, Wisconsin, USA). Abl mutants (E255K and T315I) were constructed by site-directed mutagenesis using an OE-PCR. The OE-PCR DNA fragments were ligated into TA easy vectors. The presence of the mutations was confirmed by sequencing. The enhanced green fluorescent protein-expressing retroviral vector, MigR1, was a kind gift from Dr Warren S. Pear. The WT and mutated kinase domains in the TA easy vectors were transferred to the MigR1 by EcoRI digestion. Transient transfection of Mig constructs was carried out using the Neon transfection system (Invitrogen, Carlsbad, California, USA) following the manufacturer's protocol. Cells transfected by electroporation were immediately transferred to Ba/F3 cell cultured medium. Cells were selected by FACS sorting using a FACSVantage equipped with a TurboSort option (Becton Dickinson Immunocytometry Systems, San Jose, California, USA).
Normal peripheral blood mononuclear cells were isolated from four healthy donors using Ficoll-Hypaque (Amersham Pharmacia Biotech, Uppsala, Sweden) density gradient centrifugation. Normal hematopoietic cells were collected from cord blood that had been conserved for research, because of the lack of a lymphocyte subset. Bone marrow specimens were obtained from CML patients under a protocol approved by the Seoul National University Hospital institutional review board for the use of samples for research. Mononuclear cells were prepared using Ficoll-Hypaque and CD34+ or CD34− cells isolated to more than 98% purity using MACS columns (Miltenyi Biotec, Auburn, California, USA) and CD34 microbeads (Miltenyi Biotec) according to the manufacturer's recommendations. They were cultured in RPMI-1640 medium containing 10% FBS, 100 U/l of an antibiotic–antimycotic agent, 10 mmol/l HEPES, 1 mmol/l sodium pyruvate, 4.5 g/l glucose, and 0.05 mmol/l 2-mercaptoethanol.
Simvastatin was obtained as a sodium salt from Merck Chemical Ltd (Rahway, New Jersy, USA) and dissolved in DMSO. Imatinib was provided by Novartis (Seoul, Korea) and dissolved in distilled water. The primary antibodies used were antiphosphotyrosine (clone 4G10) and anti-β-actin (Upstate Biotechnology, Lake Placid, New York, USA); anti-STAT5, anti-pSTAT5 (Tyr694/699), anti-STAT3, anti-pSTAT3 (Ser727), anti-Bcr, anti-pBcr (Tyr177), anti-Bcl-2, anti-cytochrome c, anti-XIAP, anti-Mcl-1, anti-caspase 9, anti-caspase 3, and anti-PARP (Cell Signaling Technologies, Danvers, Massachusetts, USA); anti-p16, anti-p18, anti-p27, anti-Cdk2, and anti-Cdk4 (Santa Cruz Biotechnology, Santa Cruz, California, USA); and anti-Abl (8E-9; PharMingen, San Diego, California, USA). Secondary antibodies were peroxidase-conjugated affiniPure goat anti-mouse and anti-rabbit antibodies (Jackson ImmunoResearch Laboratories, West Grove, Pennsylvania, USA).
For the cell viability assay, a CellTiter-Glo luminescent cell viability assay (Promega, Madison, Wisconsin, USA) was used in accordance with the instruction manual. Briefly, 5×103 cells (CML cell lines) or 1×104 cells (patient primary cells) were plated in triplicate into microtiter-plate wells containing 80 μl of medium. The next day, the cells were incubated with the desired concentrations of simvastatin or/and imatinib to a final volume of 100 μl. After 24, 48, or 72 h, 100 μl of CellTiter-Glo reagent was added and the cells were then incubated for 10 min at room temperature. The luminescence was measured using Wallac 1420 (PerkinElmer, Boston, Massachusetts, USA). The synergistic effect of simvastatin and imatinib was determined by analysis of the combination index (CI) using Calcusyn Software (Biosoft, Ferguson, Missouri, USA and Cambridge, UK).
Two hundred micrograms of proteins were solubilized in the rehydration buffer (9 mol/l urea, 2% Chaps, 60 mmol/l DTT, and 0.5% pharmalyte (pH 3–10). Subsequently, isoelectric focusing was carried out using a pre-cast immobilized pH gradient strips (13 cm, pH 3–10, linear; Amersham Biosciences, Piscataway, New Jersey, USA). After rehydration for 12 h at 20°C, the electrophoretic conditions during isoelectric focusing were as follows: 1 h at 500 V, 1 h at 1000 V, and 3 h at 8000 V. The strips were equilibrated for 15 m in an alkylating solution that was identical to the aforementioned buffer, except that 2.5% (w/v) iodoacetamide replaced DTT. The second gel electrophoresis was carried out according to a standard sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE) protocol, using the Ettan DALT6 System (Amersham Biosciences).
The cells were resuspended in a modified RIPA lysis buffer (150 mmol/l NaCl, 1 mmol/l EDTA, 1% Triton X-100, 1% NP-40, 0.5% sodium deoxycholate, 0.1% SDS, 50 mmol/l Tris-HCl, pH 7.4) with a protease inhibitor cocktail (Roche Applied Science, Mannheim, Germany) and a phosphatase inhibitor (1 mmol/l sodium fluoride and 2 mmol/l sodium orthovanadate) in ice for 30 min and centrifuged at 15 000g for 30 min to collect the whole-cell lysate. The proteins (10–20 μg) were separated on an 8–12% SDS-PAGE and transferred onto a PVDF membrane (Millipore, Bedford, Massachusetts, USA). Western blotting was carried out with specific primary antibodies and peroxidase-conjugated affinipure anti-mouse or anti-rabbit secondary antibodies. Proteins were visualized with ECL plus enhanced chemiluminescence reagents (Amersham Biosciences). Western blotting for antiphosphotyrosine was carried out after two-dimensional polyacrylamide gel electrophoresis (2-DE) using the same method. Subsequently, the pattern of immunoreactive spots was matched to the pattern of spots in the silver-stained gel. The spots on the gel were in gel digested for identification by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS).
Protein spots were excised from the stained gel, and the gel spots were then destained. Enzymatic in-gel digestion with trypsin (Promega, Southhampton, UK), extraction of the peptides from the gel, desalting, and concentration analysis were carried out according to the methods of Thiede et al. 19. The in-gel digested peptides extracted were identified by peptide mass fingerprinting using the matrix-assisted laser desorption/ionization time of flight/time of flight (MALDI-TOF/TOF) 4700 Proteomics Analyzer (Applied Biosystems Inc., Foster City, California, USA) at the Human Genome Research Institute (Seoul, Korea). The peptide mass fingerprinting produced by MALDI-TOF/TOF was searched using the programs MASCOT, developed by Matrix Science Ltd (available at http://www.matrixscience.com/cgi/search_form.pl?FORMVER=2&SEARCH=PMF), and the ExPASy molecular biology server at SWISS-PROT (http://www.expasy.ch).
K562, KCL22, and LAMA84 cells (2×106 cells) were seeded in 60-mm dishes for 12 h before being treated with simvastatin. Cells were harvested at 48 h after treatment and washed twice with PBS. Both the untreated and the treated cells were stained with annexin V and propidium iodide according to the manufacturer's protocol (Roche Applied Science). The percentage of apoptotic cells was determined by FACSCalibur flow cytometry (Becton Dickinson Immunocytometry Systems) using Cell Quest Software (BD Biosciences, San Jose, California, USA).
K562, KCL22, and LAMA84 cells (2×107 cells) were seeded in 100-mm dishes for 12 h before being treated with simvastatin. Cells were harvested at 24 h after treatment and isolated between cytosol and mitochondrial fractions according to the instructions of the mitochondria isolation kit for cultured cells (Pierce, Rockford, Illinois, USA). The protein samples were quantified, separated by 15% SDS-PAGE, and subjected to western blotting.
K562, KCL22, and LAMA84 cells were exposed to 25 or 50 μmol/l simvastatin for 24 h and washed twice with a cold PBS solution. After fixing with cold 75% ethanol overnight, cells were stained with 1 μg/ml propidium iodide and exposed to 5 μg/ml RNase I at room temperature for 1 h. Cell cycle distribution was assessed by FACSCalibur flow cytometry (Becton Dickinson Immunocytometry Systems).
Six-week-old Balb/c-nu/nu female mice were purchased from Central Lab Animal Inc. (Seoul, Korea). K562 cells were suspended at 5×106 cells/ml in Matrigel (Becton Dickinson Immunocytometry Systems). The K562 xenograft was established by a subcutaneous injection of 1×106 cells into the right flanks of mice. Ten days after inoculation, the mice were randomized into groups of five, and imatinib, simvastatin, imatinib, and simvastatin, or vehicle was administered 5 days/week for up to 30 days in total. Tumor sizes were assessed at least three times a week by caliper measurement and their volumes were calculated from the formula, tumor size (mm3)=(d2×D)/2, where d and D are the shortest and the longest diameters of the tumor, respectively. Animal procedures were approved by the institutional review board at Seoul National University Hospital.
Student's t-test was used to calculate the difference between cell line samples; Friedman's and Mann–Whitney's nonparametric tests were carried out to calculate significant differences. Nonparametric tests were carried out to calculate significant differences between CML samples. Significant differences versus the control group in animal study were determined by analysis of variance.
To examine the effects of simvastatin on three different CML cell lines (K562, KCL22, and LAMA84), cells were treated for 48 h with several simvastatin concentrations (5, 10, 20, 25, 40, and 50 μmol/l). Incubation of the CML cells with simvastatin or imatinib induced a dose-dependent inhibition of proliferation (Fig. 1a and b). Notably, LAMA84 cells were rather resistant to simvastatin, but more sensitive to imatinib, compared with K562 and KCL22 cells (Fig. 1a and b). The viability of K562, KCL22, and LAMA84 cells after exposure to 20 μmol/l simvastatin was significantly reduced to 49, 56, and 67%, respectively (P<0.001, K562, KCL; P<0.01, LAMA84), compared with 80% for normal human peripheral blood mononuclear cells (Fig. 1b).
To determine whether simvastatin was effective against mutation-induced imatinib-resistant cells, we treated Ba/F3 cells expressing either WT Bcr–Abl or the T315I or E255K kinase mutants with simvastatin for 48 h. Ba/F3 cells expressing WT Bcr–Abl were sensitive to imatinib, but Ba/F3 cells expressing Bcr–Abl kinase mutations were resistant to imatinib mesylate (Fig. 1c). Ba/F3 cells expressing either WT or mutated Bcr–Abl were equally sensitive to simvastatin, including cells harboring the T315I mutation (Fig. 1d).
The cotreatment of imatinib and simvastatin induced synergistically enhanced antiproliferative activity in the imatinib-sensitive cell line K562 (CI<1) compared with single-agent treatment (Table 1). In KCL22 and LAMA84 cells, combination treatment showed slightly synergistic or additive effects, as indicated by CI values (Table 1). In contrast, cotreatment of imatinib and simvastatin induced a synergistic effect on antiproliferative activity in all imatinib-resistant cell lines (K562-R, KCL22-R, and LAMA84-R) (Table 1). Combination treatment of K562-R, KCL22-R, and LAMA84-R cells increased sensitivity towards both drugs as combination IC50 values were reduced by a factor of 2 in K562-R, a factor of 3 in KCL22-R, and a factor of 4 in LAMA84-R as compared with imatinib alone (Table 1). The cotreatment of simvastatin and imatinib induced synergistically enhanced antiproliferative activity in Ba/F3 cells expressing WT or E255K mutant Bcr/Abl compared with single-agent treatment (Table 1). In T315I mutant Bcr/Abl cells, combination treatment showed additive or slightly antagonistic effects, as indicated by CI values ranging between 1 and 1.5 at 50–90% growth inhibition levels (Table 1).
Simvastatin was evaluated in CD34+ and CD34− mononuclear cells sorted by immunobead separation of bone marrow aspirates of five patients with CML in the chronic phase. The viability of CD34+ CML cells with 10, 25, and 50 μmol/l simvastatin was reduced to 51, 33, and 17%, respectively (Fig. 1e). CD34+ CML cells appeared to be more susceptible to cell death after treatment with simvastatin compared with CD34− CML cells (P<0.05; Fig. 1e). The results were compared with the effects also observed in normal CD34+ and CD34− (n=5). When the CML CD34+ cells were exposed to 10 or 25 μmol/l simvastatin, a significant enhancement in cell death was observed compared with normal CD34+ cells (P<0.05; Fig. 1f). In contrast, cell viability was not significantly different in normal CD34− and CML CD34− cells (Fig. 1f). Next, we studied whether the suppressive effects of simvastatin on CML CD34+ cells could further be promoted by cotreatment with imatinib. A synergistic effect between simvastatin and imatinib was observed in primary CML cells from patients compared with simvastatin alone (CI<1.0; Table 2).
Thirty Balb/c-nu/nu mice were injected subcutaneously with K562 cells. After 10 days, the tumor mean volume reached 0.13±0.04 cm3. Then, simvastatin (10 or 20 mg/kg), imatinib (5 mg/kg), or cotreatment (10 mg/kg simvastatin+5 mg/kg imatinib) was provided once daily, 5 days, weekly for 4 weeks by an intraperitoneal injection. After 10 days, the tumor volume of the 20 mg/kg simvastatin-treated group (n=5) began to decrease, and the tumor volume decreased by as much as 30% after 30 days after treatment compared with the control group (placebo-treated group, n=5) (Fig. 2a).
In the 10 mg/kg simvastatin-treated group, no significant changes in tumor volume were observed, but in the cotreated group with 5 mg/kg imatinib (n=5), a greater than 50% decrease in tumor volume was observed, indicating that cotreatment combination treatment effectively induced cell death compared with imatinib alone (Fig. 2b).
To determine the differential tyrosine phosphorylation between the 50 μmol/l simvastatin-treated and the simvastatin-untreated K562 cells, the protein samples from these cell lines were separated by 2-DE and immunoblotted with the phosphotyrosine antibody, mAb 4G10. The 39 spots were identified by MALDI-TOF/TOF (Supplementary Fig. 1, http://molecular-cytogenetics.org/). As shown in Table 3, 14 proteins that have scores over 100, including values, were identified in this experiment. These proteins showed a marked decrease in tyrosine phosphorylation in response to treatment with simvastatin. Simvastatin induced a decrease in tyrosine-phosphorylated proteins, including proteases (26S proteasome non-ATPase regulatory subunit 13), DNA/RNA processing proteins (RuvB-like 2, nucleolar RNA helicase 2), oxidoreductase proteins (retinal dehydrogenase 2), chaperones (T-complex protein 1 subunits α, θ, 78 kDa glucose-regulated protein precursor, stress-induced-phosphoprotein 1, T-complex protein 1 subunit γ), glycolysis proteins (α-enolase), cytoskeleton proteins (vimentin, WD repeat-containing protein 1), and microtubule proteins (tubulin α-1B chain) (Table 3).
The annexin V assay showed that 48 h of exposure to 25 μmol/l simvastatin induced apoptotic rates in K562, KCL22, and LAMA84 cells of 21, 16, and 21%, respectively, and 27, 44, and 39%, respectively, after 48 h of exposure to 50 μmol/l simvastatin (Fig. 3a). When exposed to 25 or 50 μmol/l simvastatin for 24 h, western blot analysis of proapoptotic and antiapoptotic proteins showed that 25 μmol/l simvastatin induced the increased expression of proapoptosis proteins [cytochrome c (cytosol), cleaved caspase 9, caspase 3, PARP), and the decreased expression of Bcl-2, Mcl-1, and XIAP (Fig. 3b).
To determine the effect of simvastatin on the cell cycle, the CML cells were incubated for 24 h with 25 and 50 μmol/l simvastatin. Treatment with simvastatin induced a dose-dependent accumulation of cells in the G1 phase and a decrease in the total S-phase population of K562, KCL22, and LAMA84 cells (Table 4). Simvastatin induced upregulation of p27kip, but not of p16Ink4A or p18Ink4c in K562, KCL22, and LAMA84 cells, whereas imatinib induced upregulation of p16Ink4A, p18Ink4c, and p27kip in LAMA84 cells. Both simvastatin and imatinib induced downregulation of Cdk2 and Cdk4 (Fig. 4).
Treatment with simvastatin attenuated the levels of pSTAT5, which was increased in all three imatinib-resistant CML cells (Fig. 5). In imatinib-resistant cell lines, simvastatin markedly reduced the increased pSTAT5 levels. Treatment with simvastatin also inhibited the levels of pSTAT3 (Fig. 5). The expression of phospho-Lyn was also markedly elevated in K562-R and KCL22-R cells but was inhibited following exposure to simvastatin. Moreover, treatment with simvastatin inhibited increased phospho-ERK1/2 in all three imatinib-sensitive and imatinib-resistant CML cells (Fig. 5).
Statins have been shown to inhibit tumor growth and induce apoptosis in a variety of tumor cells, including prostate cancer 20, colon cancer 21,22 breast cancer 23–25, melanoma 26,27, multiple myeloma 28, and leukemia cell lines 29–31. Recently, several clinical trials have assessed the antitumor activity of statins, indicating the potential role of statins in both cancer prevention and treatment 32,33. In this study, we hypothesized that simvastatin would exert anti-CML effects independent of Bcr–Abl and sensitize imatinib-resistant cells to the residual apoptotic effects of imatinib, thereby overcoming drug resistance. To examine this hypothesis, we evaluated the effect of simvastatin on imatinib resistance in two clinically relevant cell lines, Ba/F3p210E255K and Ba/F3p210T315I, in comparison with Ba/F3p210WT and untransfected Ba/F3 cells.
Despite the presence of Bcr–Abl mutations, Ba/F3p210WT, Ba/F3p210E255K, and Ba/F3p210T315I cells were equally susceptible to the antiproliferative effects of simvastatin, yielding IC50 values of 5.0±0.1, 4.6±0.5, and 4.5±0.1 μmol/l, respectively (Table 1). In addition, cotreatment with simvastatin and imatinib exerted synergistic effects on imatinib-resistant K562, KCL22, and LAMA84 cells, as well as on Ba/F3 cells expressing E255K mutant Bcr–Abl. Interestingly, three imatinib-resistant CML cell lines (K562-R, LAMA84-R, and KCLR cells) derived from human erythrocytic (K562), erythroid-megakaryocytic (LAMA84), and myelocytic (KCL22) hematopoietic cells showed different levels of resistance to simvastatin (Fig. 1b), indicating that simvastatin can kill CML cells through a Bcr–Abl independent mechanism. Thus, the combination of simvastatin and imatinib treatment might overcome drug resistance to imatinib caused by point mutation or Bcr–Abl protein overexpression.
The resistance of Bcr–Abl-positive cells to imatinib may occur through multiple mechanisms, including amplification of the Bcr–Abl gene, mutations in the Bcr–Abl kinase ATP-binding site, or a reduction in intracellular drug uptake 34–36. Although gene amplification is not universally encountered in resistant cells, an increase in Bcr–Abl protein expression commonly occurs at least in cultured cell lines 35,36. In our study, three imatinib-resistant cell lines (K562-R, KCLR, and LAMA84-R cells) showed increased Bcr–Abl protein expression. In addition, imatinib-resistant K562-R cells showed an elevated level of Lyn protein and phosphorylation, whereas parental K562 cells suppressed Lyn expression (Supplementary Fig. 2, http://molecular-cytogenetics.org/).
Src kinases are generally considered as important but not crucial downstream targets of Bcr–Abl kinase in chronic-phase CML. However, Lyn kinase, a member of the Src family, may play an important role in certain situations. It has been reported that Lyn kinase is overexpressed in some imatinib-resistant CML cell lines 37 and imatinib-resistant patient specimens 38; moreover, its activation does not depend on Bcr–Abl kinase 9,39–42. Therefore, abnormal regulation of Lyn kinase may interfere in the Bcr–Abl signaling complex, including CrkL, STAT5, and MAPK 39–41,43. We found that simvastatin strongly inhibited Lyn phosphorylation and Bcr–Abl downstream signaling complexes such as STAT5, STAT3, and ERK1/2 phosphorylation (Fig. 5), indicating that simvastatin suppresses protein expression involved in imatinib resistance.
To examine the underlying mechanism, we carried out 2-DE protein analysis and immunoblotting with a phosphotyrosine antibody. Simvastatin induced a decrease in the levels of tyrosine-phosphorylated proteins, which play a key role in tumor development by promoting cell growth. These proteins included proteases, DNA/RNA processing proteins, oxidoreductase proteins, and chaperones. Thus, these findings support the antiproliferative and proapoptotic activities of simvastatin.
In chronic-phase CML, the stem/progenitor cells are intrinsically less sensitive to imatinib than the more mature CML cells, which compose the bulk of the leukemic clone. However, van der Weide et al. 44 have reported that simvastatin and tipifarnib exert an enhanced suppressive effect in primary sorted CD34+ acute myeloid leukemia cells. In addition, Chen et al. 45 showed that the combination of imatinib and simvastatin sensitized CD34+ K562 cells to cell death. We examined the effect of simvastatin on CML patient's primitive CD34+ and CD34− cells. The combination of imatinib and simvastatin induced significant cell death of imatinib-resistant CD34+ cells. We also found that simvastatin was more effective in CML CD34+ cells than in CML CD34− or normal CD34+ cells. Although the detailed mechanism of how simvastatin sensitizes imatinib-resistant CD34+ cells to imatinib is still unknown, the data from the present study suggest that simvastatin may block the resistance of imatinib through downregulation of Bcr–Abl transcription, which is regulated by multiple factors in cancer cells.
Collectively, this study showed the synergistic effect of imatinib and simvastatin, as well as the effects of simvastatin alone, on CML cells. Simvastatin induces cell cycle arrest in the G1 phase through p27kip and apoptosis in CML by blocking the downstream signals of the Bcr–Abl pathway, such as STAT5 and STAT3. Simvastatin also reduces tyrosine kinase phosphorylation, which plays a key role in tumor development by promoting cell growth. Thus, simvastatin may be useful in the treatment of imatinib-resistant CML through a Bcr–Abl independent mechanism.
This work was supported in part by the Basic Science Research Program through the National Research Foundation of Korea (NRF) Funded by the Ministry of Education, Science and Technology (2012-0002257), a grant of the SNUH Research Fund (04-2007-082-0), a grant of the Korea Foundation for Cancer Research (KFCR-2009-003), a grant of the Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (A120216), a grant of the Korea Food & Drug Administration in 2012 (10172KFDA993), and Cancer Research Institute, Seoul National University Grant (2009).
There are no conflicts of interest.
chronic myelogenous leukemia; imatinib resistance; simvastatin
© 2013 Lippincott Williams & Wilkins, Inc.
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Woman tells Corpus Christi police son was stabbed by his girlfriend
CORPUS CHRISTI - Looking for a man stabbed late Monday, police instead found a blood covered apartment door.
A woman called police about 10:15 p.m. after she received a call from a relative saying her 27-year-old son had been stabbed by his 34-year-old girlfriend.
Officers went to an apartment in the 3000 block of Antelope Street and found blood, but neither the woman's son nor his girlfriend were there, police said.
The man's mother told police she last saw her son running toward the Hillcrest area with a wounded arm.
About an hour later, the man walked into Christus Spohn Hospital Memorial seeking treatment for a severe laceration on his left arm, police said.
The man told officers that several men stabbed him earlier on Stillman Avenue.
Police at the hospital said the man was uncooperative and would not give more details.


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Just curious as to how many out there are using a revolver as part of their CC amory.
This is a discussion on Revolver v. Semi-Auto within the Concealed Carry Issues & Discussions forums, part of the Defensive Carry Discussions category; Just curious as to how many out there are using a revolver as part of their CC amory....
Just curious as to how many out there are using a revolver as part of their CC amory.
Always Carry, Never Tell
S&W Shield 9mm
Ruger LCP .380
NRA Member
Certified NRA Instructor
...unless I must be in very hazardous circumstances, my SP or my Bodyguard .38 are my BUG always...if I'm in a part of town I'd rather not be in or on the long road, my P97 or P95 may be the BUG to my P90....
I prefer to use the right tool for the job, which includes caliber selection as well.
Not that I'm OCD or anything...
'Clinging to my guns and religion
Why do you need to know? Are you trying to make your decision? Which pistols and revolvers are you trying to decide between for your own personal use?
While I carry a semi auto 95% of the time, I do carry a revolver on occasion.
Freedom doesn't come free. It is bought and paid for by the lives and blood of our men and women in uniform.
USAF Retired
NRA Life Member
Semi auto only..
Don"t let stupid be your skill set....
Never be ashamed of a scar. It simply means, that you were stronger than whatever tried to hurt you......
Semi auto...very few exceptions...
Sometimes in life you have to stand your ground. It's a hard lesson to learn and even most adults don't get it, but in the end only I can be responsible for my life. If faced with any type of adversity, only I can overcome it. Waiting for someone else to take responsibility is a long fruitless wait.
Always Carry, Never Tell
S&W Shield 9mm
Ruger LCP .380
NRA Member
Certified NRA Instructor
I don't carry regularly, but I'm thinking about picking up a S&W j-frame as a ccw. When in bear country, I carry a revolver. I answered 'neither' because I carry so rarely, but I suppose 'revolver' might have worked for me too.
I've never been in a gunfight as a civilian, so it's hard to see where I 'need' more firepower than a model 649. Plus I like the simple reliability of a revolver.
Woops, I probably should have chosen both but I primarily carry an LCR.
"Was there no end to the conspiracy of irrational prejudice against Red Ryder and his peacemaker?"
Revolvers, more elegant weapons for a more civilized age.
Wonder if there's anyone here with a Class III EDC weapon...
Semi-auto only.
Cogito, ergo armatum sum. I think, therefore I am armed. (Don Mann, The Modern Day Gunslinger; the ultimate handgun training manual)
image.jpgRevolvers for cc. Keep a g17 with night sights and glock light on nightstand
EDC is a sp101 3" although if I were going somewhere I felt I needed extra protection fullsize berretta in 40sw
Sent from my SCH-I405 using Tapatalk 2
I carry Semi Auto for the capacity but I wouldn't have a problem carrying a revolver if that was what I had.


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Reviews Written | 1 Review | Average Review Score | |
Community Votes | 3 out of 3 users recommended your reviews | Total Comments on Your Reviews | 1 Comment |
Heroman episode 1 review
Heroman is an anime series made in colaborration with Stan Lee and Studio Bones. Going into it, I didn't expect it to be great. Sure, Stan Lee was great back in the day, but his storytelling has stayed in the past. This episode proved this. Don't get me wrong, this ... |
3 out of 3 found this review helpful. |


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Recipe seems to be missing "beans" in the ingredients. I used Navy beans and added ground beef for my carnivorous family. Used cubes of fresh mozzarella rather than shredded, and that was delightful.
Skillet Gnocchi
Photo: bfogler
Yield: 6 servings
Community Recipe from
Recipe Time
Prep Time:
- 1 tablespoon(s) extra-virgin olive oil
- 16 ounce(s) Gnocchi
- 1 yellow onion
- 4 cloves garlic minced
- 1/2 cup(s) water
- 6 cup(s) Chard Leaves chopped
- 15 ounce(s) can tomatoes with italian seasoning diced
- 1/4 teaspoon(s) freshly ground pepper
- 1/2 cup(s) mozzarella cheese
- 1/4 cup(s) parmesan cheese
- 1. Heat 1 tablespoon oil in a large nonstick skillet over medium heat. Add gnocchi and cook, stirring often, until plumped and starting to brown, 5 to 7 minutes. Transfer to a bowl.
- 2. Add the remaining 1 teaspoon oil and onion to the pan and cook, stirring, over medium heat, for 2 minutes. Stir in garlic and water. Cover and cook until the onion is soft, 4 to 6 minutes. Add chard (or spinach) and cook, stirring, until starting to wilt, 1 to 2 minutes. Stir in tomatoes, beans and pepper and bring to a simmer. Stir in the gnocchi and sprinkle with mozzarella and Parmesan. Cover and cook until the cheese is melted and the sauce is bubbling, about 3 minutes.
March 2013
This recipe is a personal recipe added by bfogler and has not been tested or endorsed by MyRecipes.
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I thought it'd be fun to post what everyone has purchased so far or what they plan to get this year. Today I planted 7 cuttings that I purchased -- Jeannie Moragne an a mystery from MPG, and 5 cuttings from Wendy -- Divine, Rhonda, California Sunset, Desert Sunrise, and Xquisite. I am also waiting to hear from John about a Milan too. |
Follow-Up Postings:
- Posted by disneyhorse 10A (My Page) on Sat, Apr 5, 14 at 0:11
They look snug there. What are the bitty seedlings? |
A few varieties of desert rose seedlings. ;) |
- Posted by disneyhorse 10A (My Page) on Sat, Apr 5, 14 at 0:43
Adeniums are my 2014 plant (every year I pick a new type of plant to learn about... Plumeria were my 2013 plant so I bought a couple, rooted some cuttings and planted some seeds). My sister gave me some imported adenium seeds for Christmas in preparation and I've been patiently waiting for it to warm up. I don't have a cozy box like that for them! Are they kind of like plumeria seedlings? |
This post was edited by disneyhorse on Sat, Apr 5, 14 at 1:21
Since I have more room this year I bought last month 7 rooted plants from Matt. A Puu Kalea, Don angus, fantasy Island, Waimea, Kaneohe Sunrise, J. L. Pink Pansy, and a Kona sunset. I already had a few of them but since the price was right I thought that I would get a few more and see which ones bloom first. LOL I am very happy with them and do have my eye on a couple more but will see what happens. I also have almost a hundred which I am rooting so at this rate I might run out of room. I do sale off the extra ones in the late summer when most are blooming. And it looks like it is going to be a great year. With so many that are going to bloom. I have not counted them lately but most have close to 400 + plants. I can not wait to see all of the first time bloomers this year. Enjoy your weekend, Barb p.s. Here is a picture of some of my backyard from a second story window. |
This post was edited by barb13 on Sat, Apr 5, 14 at 4:09
Wow you got a forest there barb13. ;) Disneyhorse -- I think they are different an a bit more slow going than plumeria seedlings. Their seeds are teeny tiny too, almost like the size if a cooked rice grain. |
Wow Barb! Looks like you have a plumeria farm going! LOL. Hey that what one of my neighbor asked me and I only have around 80! So 400... wow... please share photos when they bloom! Lynn |
I would love to see this same photo when they're all leafed out and in bloom! |
I will keep everyone updated. Only problem with that picture is that it does not get the whole yard. Many more and I even have room for a veg. garden. It is a great year. Barb |
I have no plans to purchase anything new this year. I pretty much have all I want short of one or 2. I may have to have someone stop me from going to Southwood when they get their JJ plants in. Mike |
Kim - WOW!!! Your setup looks excellent and what an AWESOME bunch of new plumies you got!!! So many nice, multi-tip ones! And who's that giant in the back right corner?! So exciting! How is Wendy doing?! Sounds like she's doing great, so happy for her! I miss talking to her - I'm not on FB anymore and she's not on here really anymore but please do tell her I said hello if you talk to her. I love your adenium seedlings too! I have a bunch of adenium arabicum and obesum that I've grown from seed and they are so fun! They grow really fast but don't take up as much space as plumeria. I'll have to post some pics. Barb - I love all of your space back there for your plumies! (Is that a goose or a duck (and babies?!) back there?! I got antsy and bought a few plumies this year, here's what I got. If they say rooting, it's because I CHECKED! haha! I was afraid because Bill started rotting for some reason and I had to check the rest before it got too bad to stop like I think Bill's is. Scentsational - cutting - LOST IT Artistry - cutting - ROOTING! JL Hawaiian Sunset - cutting -ROOTING! Jefferson's Gold - cutting - ROOTING! Lurline - cutting - ROOTING! Mystery - cutting - tried rooting, developed a "walnut" type callus so had to re-cut and currently trying to re-callus. Orange Zest - BOUGHT ROOTED Bill Moragne - cutting - have had to cut it back twice, seeing if it will callus but it's not looking good. I must have not had a good callus to start, I don't know what happened. :( Waimea - BOUGHT ROOTED Cindy Schmidt - cutting - also started to look rotted at the bottom, took it out, re-cut and now callusing. Katie Moragne - bought rooted - broken by the post office but both pieces are looking fine right now. And of course some seedlings heh heh! Too many but you all know how this story goes, LOL!!! |
This post was edited by elucas101 on Mon, Apr 7, 14 at 17:12
Not a real duck and her babies, got from a neighbor when she passed away. I have bought 3 different times a Bill Moragne and have never been able to get them to root. Don't seem to have problems with other ones. I hope that yours does much better. Now that the pool is filled in I have so much room but at the rate I am going I am going to run out of room. Well, I will worry about it when it happens. One of the pictures from last year. |
One more picture from last year. This is the first time that my Duke has bloomed and I was not disappointed. |
Emily - That big baby is the 'Jeannie Moragne' I got from Doug. It's circumference is probably the size of a half dollar or better. It is the beefy-est cutting I have ever received. It formed a nice small callus on it within 1 week of receiving it before I planted it. I believe Wendy is doing swell. Her business is doing really good -- always getting nibbles on cuttings / plants on her Double Peak Plumeria FB page. Also her family is expanding too -- she posted on her personal FB page that she is gonna have twins. ;) I still have my Waimea that I got from her. I hope to see an inflo this time around if not, I am gonna give her plenty to eat. LOL. I also won't be getting Milan from John. He didn't have any available in 2 gallon. A bit of a disappointment but oh well, I have several lovely varieties to look forward to [if] they root for me. But I will admit I have also been eye balling 'butterfly gold'. Love the veining plus its bloom is quiet large. <3 I still have some of my seedlings. They are approaching the 2 year old mark. Queen of Hearts (mother plant was a red australian variety), is 17 inches tall and plumping up -- she has nice dark green leaves with red/orange veins, my VCR seedling is 22 inches tall and plumping up nicely as well. Also my Deep Desire is about a foot tall -- she also has nice dark green leaves with red/orange veining. QOH and VCR are currently in 2 gallon pots. Also I have starting some more seeds as well. So far I have about a 5-6 inch penang peach, mr ambassador, kaneohe sunset, 2 kimos, and 2-3 mary moragnes. I only keep the ones that shows red/orange/pink veining on the leaves b/c I think maybe they'd make interesting plants someday. Barb - Lovin' your Duke, looks real pretty. :) |
This post was edited by kim319 on Mon, Apr 7, 14 at 18:56
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Santana could be part of Twins' exodus
FORT MYERS, Fla. -- The great Johan Santana ignited a major stir in the Twins' universe the other day.
But not the way you'd think.
But The Great Santana is way too professional to spit out any ultimatums like that. So what he actually said was this:
He thinks he can get better.
Better? How, exactly? By striking out 27 some night?
"I don't think that's what he means," laughs catcher Mike Redmond. "But you never know."
"I'm not sure exactly what he has in mind," says GM Terry Ryan. "But whatever it is, I'm all for it."
Better? We remind you that The Great Santana probably should have won the last three AL Cy Young awards (as opposed to "only" two out of three). We also remind you that he crushes all the active pitchers in his league in just about every number on the stat sheet over those last three seasons.
So if he does get any better, it sure isn't going to make him more affordable for this team he works for. This team he loves. This team that loves him. This team that isn't exactly working with the Yankees' budget -- and never will be.
"I would love to stay here," Santana says, "with this team, in this city, because I love everything about this team and what I do here. But at the same time, this is business. And a lot of things are out of my control. You've got to have a team that's willing to negotiate and to keep you. So if it doesn't work out that way, if that means you have to go somewhere else, it's tough. It's bad. But that's the way it is, because it's a business."
ACTIVE PITCHERS (min.: 100 decisions) |
1. Johan Santana | .716 | 78 | 31 |
2. Pedro Martinez | .691 | 206 | 92 |
3. Roy Oswalt | .676 | 98 | 47 |
4. Tim Hudson | .665 | 119 | 60 |
5. Roy Halladay | .664 | 95 | 48 |
6. Roger Clemens | .662 | 348 | 178 |
7. Randy Johnson | .662 | 280 | 147 |
8. Mark Mulder | .644 | 103 | 57 |
9. Andy Pettitte | .641 | 186 | 104 |
10. Mike Mussina | .641 | 239 | 134 |
They have had themselves a tremendous run these last six seasons. A heartwarming run. A run that serves as an inspiration to the Pirates and Royals and all those other downtrodden middle-market franchises that know they, too, will never be the Yankees.
But it is time once again to ask: Are the Twins nearing the end of this era?
Torii Hunter, the last link to the beginning of that era, is a year away from free agency. Santana is two years away. Joe Nathan, a guy who deserves to be right in the middle of the who's-the-best-closer-alive debate, is also two years away.
So as good as they should remain in their next era -- the Joe Mauer/Justin Morneau era -- the window for them to win with this current, special group of characters will stay open for only so long. They know that. They talk about it openly, in fact.
"There's a lot of guys who could be gone," says Hunter. "So that window of opportunity -- it's getting small. And we definitely -- definitely -- want to try to win (a World Series) before we get out of here together."
Hunter has seen every single Twins mainstay who once surrounded him call in the moving vans. Jacque Jones. David Ortiz. Brad Radke. Corey Koskie. A.J. Pierzynski. Gone. All of them.
So no wonder the center fielder makes the assumption we always have seemed to make about the Twins -- that when his time comes, when Santana's time comes, when Nathan's time comes, they all will have a new zip code to call their own.
But maybe we shouldn't be so quick to make that assumption. Suddenly, there is a new ballpark on the Twins' horizon in 2010 (assuming the politicians stop fighting about it).
That should mean, says Ryan, that the financial impact of that park should show up in the Twins' checking account in 2009. But the GM also says we shouldn't make any other assumptions about what else it will mean.
"You know, we've retained (Chuck) Knoblauch, and we've retained (Kirby) Puckett, and we've retained (Kent) Hrbek," says Ryan. "We've retained (Rick) Aguilera. And we've retained Radke. So we've retained people. I don't think (losing all these players) is a given."
So clearly, the Twins have no desire to wave goodbye to everybody. But from the standpoint of sheer irreplaceability, how could there be anyone in their midst they could less afford to wave goodbye to than The Best Pitcher in the Solar System?
Maybe, somewhere down the road, Francisco Liriano will recover from Tommy John surgery and go right back to being the 12-3, 2.16 ERA dominator he was last year. Maybe their next wave of live arms -- Matt Garza and Glen Perkins and Kevin Slowey -- will live up to the hype.
But there is only one Johan Santana, just 28 and the best there is. So how can the Twins find a way to hang onto him in a world where Gil Meche is worth 11 million bucks a year and Barry Zito is worth $126 million for seven years? That's the question.
"It's not a secret, what's going on out there (in the market)," Santana says. "So what's fair is fair. I'm not asking for anything new. What I've said in the past is, the sooner they do something, the better, because I'm willing to do something. But it's going to be up to them to make something happen."
He has a way of delivering these words -- softly, calmly, soothingly -- that keep them from sounding like any kind of threat. He's going to get paid. So he has no reason to push the tension meter. Why would he want to? He isn't trying to force his way out. If anything, he's trying to savor what he has.
From the outside, these Twins might seem like just another good little team. But from the inside, the men who make up this group recognize there is something different, something powerful about the vibe that bonds them.
Redmond won a World Series in 2003 with a similar bunch of chemistry majors in Florida. Yet he still says, "This is the best group of guys, collectively, I've ever been a part of." These are men who recognize a good thing when they're living it. And Johan Santana gets that as much as any of them.
"Around here," he says, "it doesn't matter what kind of awards you've got. Once you're in there, in that clubhouse, we're all the same. We don't talk to each other different just because you won a Cy Young or American League MVP or a batting title. We put that all on the side, because we're all together. ...
"So hopefully, they can find a way to keep this group together. I know it's going to be tough for them. But I'm pretty sure they're going to try their best. We have a lot of guys here who would really love to stay here. And hopefully, they'll find a way to keep them."
But while he wonders about his teammates' future, they can't help but wonder about his -- for good reason. Because the fate of the whole franchise might rest on it.
"It'll all come down to money with Johan," Hunter says. "Barry Zito got $126 million, and you've gotta believe Johan will get more than Barry Zito. But I don't know what team he's going to get it from. I don't know if he's going to get it from the Twins. You know, at the rate we're going and what the Twins are, if you look at their past, they're going to let him go, unless they can get an extension at a discount. But Johan should be here, man. People love him here."
For some reason, the rest of America hasn't quite comprehended the magnitude of this man -- as a pitcher and as one of baseball's classiest human beings. But he is now so huge in Minnesota, they might name a lake after him one of these days -- if he stays.
"In Minnesota, I can feel it when they announce my name on the nights I'm pitching," Santana says. "And I can hear it. When I'm walking up to the bullpen to warm up, you can hear people clapping. You can see the look in people's eyes. And it's cool. I love Minnesota."
In Minnesota, they have been lucky enough to see him go out these the last three years and reach a historic level of domination. If you just look at his winning percentage (.696 or better in all three years), the innings he has pitched (228 or more in all three years) and his spectacular strikeout and hits-allowed rates, only one other pitcher in history has had three straight seasons like this -- Randy Johnson (from 2000-02).
So when you hear this man speak about getting even better, you sure do feel sorry for the hitters.
Except Johan Santana isn't speaking about them.
"When I talk about being better," he says, "I'm talking not just about baseball, but about life."
But this is already a man who seems to understand what's meaningful in life. The countryside in and around his remote home town -- Tovar, Venezuela -- was devastated by mudslides in 2005. Santana has worked tirelessly, and donated heavily, to help repair the damage. And his latest gift was particularly astonishing: He bought a fire truck from a Minnesota fire department -- and donated it to his town.
"I have some good friends who are firefighters," he says. "And when I was talking to them, it was hard to imagine what was going on in that moment (when the mudslides hit). So I just tried to help."
When you hear these stories, you understand the fascinating dynamics of his situation. "Greed" would never be a word you could use to describe Johan Santana. But he is also business-savvy enough to know what he is worth.
Then you think about his team, knowing it can't afford to lose him on one level, wondering if there is any way it can afford to keep him on another level.
So the Minnesota Twins have a lot to ponder, don't they? And while they do that pondering, the best pitcher in baseball will keep on striving to be something that barely seems possible:
Better than he already is.
Jayson Stark is a senior writer for ESPN.com.
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