text:
Mohamed Al-Maghout
Shade And Noon Sun - Poem by Mohamed Al-Maghout
All the fields of the world
At odds with two small lips
All the streets of history
At odds with two bare feet.
They travel and we wait
They have gallows
We have necks
They have pearls
And we have freckles and moles
They own the night, the dawn, the afternoon sun and the day
And we own skin and bones.
We plant under the noonday sun,
And they eat in the shade
Their teeth are white as rice
Our teeth dark as desolate forests,
Their breasts are soft as silk
Our breasts dusty as execution squares
And yet, we are the kings of the world:
Their homes are buried in bills and accounts
Our homes are buried in autumn leaves
In their pockets they carry the addresses
of thieves and traitors
In ours we carry the addresses
of rivers and thunderstorms.
They own windows
We own the winds
They own the ships
We own the waves
They own the medals
We own the mud
They own the walls and balconies
We own the ropes and the daggers.
And now beloved
Come, let us sleep on the pavements.
Translated by: May Jayyusi and John Heath-Stubbs
Comments about Shade And Noon Sun by Mohamed Al-Maghout
Aftab Alam Khursheed (9/24/2013 9:44:00 AM)
A beautiful poem of vivid imagery so nice nice to read Brother (Report) Reply
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COLUMBUS -- The 160th Ohio State Fair kicks off Wednesday, July 24 and continues through Aug. 4 at the Ohio Expo Center in Columbus with a spectacular midway, big-name entertainment, hundreds of exhibits and one of the largest junior fair shows in the nation.
This year's event offers new attractions, agricultural exhibits, interactive educational activities, sporting competitions, fair food and a variety of shopping opportunities.
Daily hours of operation at the 2013 Ohio State Fair are admission gates, 9 a.m. to 10 p.m. (except Aug. 4, closing at 8 p.m.); commercial buildings, 10 a.m. to 9 p.m.; Youth Center, 8 a.m. to 8 p.m.; Janis Center, 9 a.m. to 7 p.m.; and other exhibit buildings, 9 a.m. to 9 p.m.
The Mountain Dew Midway is open 10 a.m. to 11 p.m. Sunday through Thursday and 10 a.m. to midnight Friday and Saturday.
Admission price is $10 for adults (ages 13-59) and $8 for youth (age 5-12) and senior citizens (60+) while children under age 5 are free.
Ride coupons are $1 apiece with kiddie rides requiring one coupon, super kiddie and spectacular rides two coupons each and super spectacular rides three coupons. Special ride-all-day wristbands are available for $23 apiece.
Save on gate admission prices with $6 tickets available through Aug. 4 at Kroger, participating AAA locations with AAA membership and Ticketmaster outlets. Purchase ride-all-day wristband vouchers (to be redeemed at the Fair for a wristband) for only $20 at Kroger stores and Ticketmaster outlets through July 23 only.
Visit the Ohio State Fair website, ohiostatefair.com, for special discount days.
Stroller, wagon, wheelchair and locker rentals are available at the fairgrounds for a fee.
Parking is $5 per vehicle with easy access to AAA Parking Lots from Interstate 71 at the 17th Avenue exit and the Hudson Street exit at Silver Drive. Handicapped parking available. Ride the AAA Courtesy Shuttle to and from the main entrance gate and your vehicle.
The free AEP Ohio on-grounds Energy Express Shuttle make frequent stops around the perimeter of the grounds from 10 a.m. to 10 p.m. Sunday through Thursday and 10 a.m. to 11 p.m. Fridays and Saturdays.
Sporting events scheduled for this year's fair include a 5K run, July 28 (8 a.m.) at Crew Stadium; Baton twirling, July 27 (9 a.m. to 6 p.m.) at Buckeye Sports Center; Boxing, July 24-27 (6 p.m. except July 27 at noon) at ShowPlace Pavilion; Cheerleading and Dance, Aug. 4 (10 a.m.) at Buckeye Sports Center; Monster Arm Wrestling, July 28 (1 to 4 p.m.) at ShowPlace Pavilion; Power Lifting, Aug. 3 (noon) at Buckeye Building; State Taekwondo Tournament, Aug. 3 (10 a.m. to 5 p.m.) at the Buckeye Building; and wrestling, July 27-28 (9:30 a.m. and 1:30 p.m.) at the Buckeye Sports Center.
Entertainment scheduled for the WCOL Celeste Center includes:
Jeff Dunham, July at 7 p.m.
Ladies Night Out Tour featuring Eric Benet, K'Jon and Noel Gourdin, July 25 at 7:30 p.m.
Martina McBride with special guest Angie Johnson, July 26 at 7 p.m.
Will Downing and Lalah Hathaway, July 27 at 7:30 p.m.
Styx and REO Speedwagon, July 28 at 7:30 p.m.
Justin Moore with special guest The Farm, July 29 at 7 p.m.
Austin Mahone with special guest Jake Miller, July 30 at 7:30 p.m.
Carly Rae Jepsen with special guest New Hollow, July 31 at 7 p.m.
Steve Miller Band, Aug. 1 at 7 p.m.
The Oak Ridge Boys, Larry Gatlin & the Gatlin Brothers and Crystal Gayle, Aug. 2 at 7 p.m.
Hillsong Live, Aug. 3 at 7 p.m.
Visit the website ohiostatefair.com for ticket prices and additional information regarding the entertainers scheduled to perform.
For more information about the fair, call 1-888-OHO-EXPO or 1-614-644-FAIR.

subset: commoncrawl


text:
Includes Barlows in Massachusetts, Connecticut,
Ohio and Michigan as well as in New York From
the research of Kent Barlow
He married Mary Pemberton who was born c1636
He married 10 January 1688, Sarah Huxley, who was born
1675, in Hartford Connecticut
Parents of Sarah Huxley: Thomas Huxley - died 21
July 1721 Sarah Spencer - born c1646 and
died 24 October 1712
He married Mary White on 17 October 1753 in Granville
He married Phebe Doud who was born 22 January 1761
Parents of Phebe Doud:
Isaac Doud, born 30 January
1729/30 in Middletown, Connecticut and died
29 March 1761
Phebe Stow, born 19 January 1734/35 & died
03 December 1813 in Pomfet, Vermont
Married 09 December 1754 in Middletown, Connecticut
He married Nancy Crownover, who was born 20 November 1786
and died 04 December 1833
He married Mary Rockafeller, who was born 17 August 1839
in Atlas Michigan and died 29 April 1873 in Atlas Michigan
He married Lucy Ann Sayre on 23 July 1885 in Atlas Michigan
Lucy was born 22 November 1863, & died
15 December 1928
Parents of Lucy Ann Sayre: Daniel Brewster
Sayre, born October 1830 and died 20 December 1855 Caroline
He married 11 November 1909, in Ohio, Josephine Muenscher.
Josephine was born 06 August 1890 in Sandusky Ohio
and died 04 March 1933 in Rochester, New York
Barlow was foreman of the Stromberg-Carlson model shop
at the time of his retirement. His service in the field
of telephony dates back to the early days of telephone
pioneers more than 40 years ago. Most of his work has been
devoted to experimental and research aspects. His introduction
to telephone work began in 1904 in Elyria, Ohio, when he
joined the Garford Manufacturing Company. He came to Rochester
and became associated with Stromberg-Carlson in 1916.
Barlow, who is a member of the Telephone
Pioneers of America, has had a part in the growth of the
telephone to the vast system it is today. He confined himself
mostly advancements in the field during his work in the
experimental laboratory which later became the model shop.
Copy of original
September 15, 1950 Rochester Times Union Rochester New
We Congratulate Wayne B. Barlow
on his 39th Birthday Today
Wayne B. Barlow of 95 Elmcroft
Rd., won' t have much time to celebrate his 39th birthday
today. He will be hard at work on his first book, a college
text for music appreciation. It's title will be "Foundations
of Music."
Barlow walked into Eastman School of Music when he was
10 years old and took his first music lesson. He has studied
there ever since.
Following years of piano, violin and organ lessons, Barlow
received bachelor's and master's degrees in music from
Eastman School. Then followed a doctorate of philosophy
in composition, the first such degree to be awarded in
this country.
In addition to his work on his textbook, Barlow is kept
busy in his position as executive secretary of Eastman
School's graduate department. In addition to administration
work, he teaches graduate courses in music acoustics, composition,
and orchestration. Dr. Barlow also instructs in University
Extension School and is organist and director of music
of St. Thomas Episcopal Church.
In his spare time, he builds electronic equipment and
takes color photographs. His interest & skills in electronic
devices led him to develop and electronic tuner now being
used by the Rochester Philharmonic Orchestra and several
high fidelity record players used by the Eastman School.
Barlow considers his major work the "Mass in G" performed
this year by the Eastman Senior Symphony under his direction.
He said last night that a selection
he wrote in 1937, "The
Winters Passed," a rhapsody of Appalachian folk songs
for oboe and strings, was included on a recent television
drama. He explains he missed hearing the music himself, but
several of his friends called his attention to it.
Mr. Barlow and his wife, Helen, have two children, Robert,
11, and Joan, 8. Their son plays the concert harp, and their
daughter, the piano.
Mrs. Barlow is a graduate of Oberlin, and later received
a master's degree from the University of Southern California.
The Rochester Times Union Rochester, New York September
06, 1951
Copy of the original
Wayne Barlow, Eastman composer
Wayne Barlow, a composer and a faculty member of the Eastman
School of Music for 50 years, died Dec. 17 after a long
illness. He was 84.
Mr. Barlow, in 1937, was the first person in the United
Stated to receive a doctoral degree in music composition.
He served as guest composer and lecturer at many colleges
and universities around the country. In 1968, he founded
the Eastman Electronic Music Studio which combined his
childhood fascination with electronics and his love of
"He was a prolific composer who wrote very attractive
music," said Robert Freeman, the former Eastman director.
Mr. Barlow, who was born in Elyria, Ohio, graduated from
Monroe High School in Rochester. He recieved his bachelor's,
master's, and doctoral degrees from Eastmans.
He served on the Eastman faculty from 1937 to 1978. He
was chairman of the department of composition from 1968
to 1973, director of the Electronic Music Studio from 1968
to 1978 and dean of graduate studies from 1973 to 1978.
Mr. Barlow received awards and grants for work in Denmark,
Belgium, and Holland. His compositions ranged in form from
sacred music, works for full symphony orchestra and pieces
that included pre-recorded tape.
Freeman recalled a well know piece for oboe and strong
orchestra, entitled, "The Winter's Passed," which
he said probably celebrated the end of the season in Rochester.
Mr. Barlow's commissioned compositions also covered a
wide range. His commissions included works for the Indianapolis
Symphony, the Catholic Diocese of Rochester and one for
the Penfield School Distric called Woodpecker with Long
His most recent and largest combined orchestral and choral
work was The Seven Seals of Revelation, based on the Book
of Revelations and commissioned and performed by the Brevard
School of Music in North Carolina.
He served as music director at Christ Episcopal Church
and organist and choirmaster at St. Thomas Episcopal Church.
He is survived by his wife, Helen Barlow of Rochester;
a daughter, Joan B. Donat and her husband, Klaus Donat
of Arizona; and two grandchildren.
A funeral service was held Saturday at St. Paul's Episcopal
Church, 25 Westminster Road.
Rochester Democrat & Chronicle Rochester NY Tuesday,
December 24, 1995
Robert received his bachelors degree from the Eastman
School of Music, his DMA from the Juillard School of Music.
Robert W. Barlow, a prominent harpist
in New York City and native Rochesterian, died Sept. 30,
1989, at St. Vincent's Hospital in New York City after
a brief illness. He was 49.
"He wanted to use his talent to enrich the lives of
other people" said his mother, Helen Barlow of Rochester. "He
felt that he had been given a gift that he could offer to
The son of Wayne and Helen Barlow, Mr. Barlow graduated
from the then - Monroe High School, the Eastman School
of Music, and the Julliard School of Music in New York
City. He began studying the harp at the age of 8 and
made his solo debut with the Rochester Civic Orchestra
at age 15.
"While at Julliard, he studied with Marcel Grandjaney,
a noted harpist and teacher," Wayne Barlow said. "He
was commended by Grandjany for his exceptional talent and
mastery of the harp as a solo instrument."
Mr. Barlow was the first harpist with the U.S. Air Force
Symphony Band in Washington. He appeared with numerous
orchestras and toured with many leading ballet companies,
including the Russian Bolshoi Ballet and the Royal
Danish Ballet. Mr. Barlow was permanent first harpist
for the American Ballet Theater at the time of his death
and also gave lessons at his home in New York City.
Copy of Original
Mr. Barlow enjoyed art, and also built
a circular home for himself at Lake Kirk in Putnam County
his father said.
Besides his parents, Mr. Barlow is survived
by his sister and brother-in-law, Joan and Klaus Donat of
Arizona, and a niece and a nephew.
A funeral was held October 5 at St Paul Episcopal Church. Burial was in White
Haven Memorial Park, Perrinton.
Klaus, who was born in Austria, has a degree in Physics
Children of Joan and Klaus are:
Heidi Donat has studied art in California and Arizona Wolfram
Donat received his masters degree in music at the University
of Anchorage
New York Index


text:
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The Outsiders
For this column I had considered comparing the best of those on the outside looking into Cooperstown to the bottom players enshrined in the Baseball Hall of Fame. I soon realized that would be a useless exercise, however, as most everyone agrees that "better than the worst" should not be the standard. If everyone better than Rick Ferrell is to be enshrined, Cooperstown may have to invade Bowerstown, Toddsville, Hartwick and Middlefield just to make room.
Instead I decided I would just assemble a lineup of the best not in the Hall and let readers determine for themselves if any of these eight are Hall-worthy. Either this weekend or next week, maybe I will turn my attention to the pitchers but for now it's the position players. Readers of this site already have a pretty good sense of who the most glaring omissions are amongst the hurlers.
So without further ado, here is my All-Overlooked starting eight.
Ted Simmons - .285/.348/.437 - 117 OPS+ | 95.3 WARP3
Simmons played 19 seasons, was rarely injured and as his B-Ref page sponsor notes, he "had more RBIs than Bench, more runs than Carter, more hits than Berra or Fisk."
Hard to say it much better than that.
First Base
Will Clark - .303/.384/.497 - 137OPS+ | 105.2 WARP3
Clark's peak was tremendous, and there is little doubt that toiling for the better part of his career in Candlestick Park hampered the general public's appreciation for him. A terrific gloveman, Bill James famously ranked Clark among the best first baseman in baseball history in The New Bill James Historical Baseball Abstract. A Hall with Orlando Cepeda, Jim Bottomley and Tony Perez ought to be able to make some room for Clark.
Second Base
Bobby Grich - .266/.371/.424 - 125 OPS+ | 121.1 WARP3
Grich won four gold gloves, finished in the top-10 for bases on balls in a season six times (he was hit by a ton of pitches too) but failed to live up to the electorate's standards in the team-dependent numbers like runs or RBI. I would love to know why, say, Bobby Doerr has a better case than Grich.
He edged Lou Whitaker for this slot, whom Rich has convinced me should also be enshrined.
Third Base
Dick Allen - .292/.378/.534 - 156 OPS+ | 92.8 WARP3
Allen's shoddy defensive work over the course of his career harmed his candidacy but it is tough to imagine a hitter of Allen's greatness on the Cooperstown outs. His career OPS+ number is greater than Hank Aaron's.
Alan Trammell - .285/.352/.415 - 110 OPS+ | 129.4 WARP3
Trammell should be such a lock, yet he probably will not get in again. There is a tier of middle infielder that the electorate seems to overlook, whose offense does not stack up to the HOF position players further to the right of the defensive spectrum and whose defense does not stack up (at least in reputation) to their peers at their own positions. Think Trammell and Luis Aparicio, and Grich versus Bill Mazeroski.
This should be addressed.
Left Field
Tim Raines - .294/.385/.425 - 123 OPS+ | 123.9 WARP3
I would say Rich tackled this one pretty thoroughly last week.
Center Field
Andre Dawson - .279/.323/.482 - 119 OPS+ | 105.3 WARP3
I have come around on Dawson. His superior defensive work as a center fielder early in his career combined with his exceptional power numbers overcome his crummy on-base. Without injuries, I have a feeling his case would be a real slam dunk.
Right Field
Dwight Evans - .272/.370/.472 - 127 OPS+ | 120.2 WARP3
He was every bit the offensive force Jim Rice was, he played longer and won eight gold gloves. I addressed Evans's case in my first Change-Up column here at Baseball Analysts.
So have at it. Tell me why those eight do not belong in the Hall, and which position players you think are more glaring omissions.
Edit: For Will Clark/Bill James ranking accuracy
Update (01/04/08): Rob Neyer disagrees with me on Clark (he would put Keith Hernandez ahead of him), thinks Santo belongs ahead of Allen and Murphy ahead of Dawson.
As far as first base goes, a vote for Hernandez ahead of Clark places a whole lot of faith in the superiority of the mustached man's glove. Clark has him comfortably on the OPS+ front, and notched just a few less plate appearances over the course of his career. Maybe Keith really was that good a fielder but to my eye Clark looks like the superior option.
The Santo over Allen argument is all about fielding and longevity. Allen was a way better hitter (156 OPS+ vs. 125) but Santo has five gold gloves and about three full seasons worth of plate appearances over Santo. Still, I am comfy with my choice.
Murphy over Dawson is fair, but here is why I favor The Hawk. He and Murphy had similarly awesome peaks, but Dawson's was ended by a stroke of utter misfortune - his horrible knee injury on that Montreal turf. Murphy just kinda faded.
I got to watch a lot of games for two of the players listed living in both Montreal and Boston. I think Andre Dawson was one of the most exciting athletes I ever saw play. He was a great centerfielder/great arm and had amazing speed. If he played 10 years later he would have been a no doubt HOFer even with his injury history. Unfortunately for him he played in the wrong market and wrong era. Now he's known as a slow slugger on the Cubs. I think that needs to be taken into consideration as well as with his stats. I like Dwight Evans but nobody ever thought of him as HOFer while he played for the Red Sox even though he was always very good (and underappreciated).
Good choices. I particularly like the Will Clark and Dwight Evans selections.
Perhaps we don't want to go back so far, and I certainly consider Raines the left fielder most worthy, but it is too bad that Indian Bob Johnson is so neglected. Good enough to play some center field also, he played for 13 years, most of the time full-time, and had no real decline phase or preparation phase either,
Over that career, his lowest OPS+ was 125 and his best was 174 at age 38 in 525 ABs, his next to last year. He ended with a .296/.393/.506 line and an OPS+ of 138. Most years he was in the top 10 in OPS, Slugging and home runs.
Along with Sherry Magee from a still earlier era, he was a real star who is generally forgotten.
I have another comment about the HOF process. Sportswriters and sports radio are obsessed with how much money players make, whether players are worth their salaries, and which players their team should sign or keep. I'm surprised that a player's career earnings are not part of the HOF measurement since almost all of the players up for consideration are from the free agency era. Seems to me that a player's career earnings as compared to their peers reflects how much a player was valued by baseball as much as award voting (especially for position players). I'm pretty sure Jim Rice was paid more than Dwight Evans for example so it stands to reason that the Red Sox viewed him as a more valuable player. I think the high paid players are under more scrutiny and pressure than other players. Would be interesting to see over time how players measure up. I believe that the players believe that the guys who are paid the most are the best and probably would prefer that title to the other awards handed out by writers.
I love the Indian Bob case, too. I think he is unfairly punished for having accumulated some numbers during the early war years. His peak came in the mid-to-late 30's.
As you mention, his lowest OPS+ season was 125! And here we are debating slugger Jim Rice's case, with a career number of 128.
For those who like the more traditional stats, in only one year, his second, did he strike out more than he walked (58BB-60K). Otherwise, he had years with 98BB-65K (1937) and 99BB-59K (1939) and a high of 76 Ks once.
He hit over .300 five times and over .290 four more times. To start his career, he hit 20+ home runs for 9 consecutive years and totaled 8 years with 100+ RBIs (7 straight) and two more with 90+. He also scored 100 runs 6 times and had 90+ four more times. He averaged over 30 doubles per year, hitting 40 and 44 in two seasons. In 8 of those seasons he was an all-star.
In his 13 seasons, he played in 140+ games 10 times, including his last two years, and in 138 twice more. Only in 1943 did he miss substantial time appearing only in 117 games. He had over 600 plate appearances in 9 seasons and close to 600 in every season but one when he had 502.
So we have a durable player whose traditional as well as more advanced stats indicate he was an elite performer.
I think Indian Bob was ignored because he played on one of the WORST teams in American League history (that being the post-1932 Philadelphia Athletics). Talk about not getting any visibility.
I personally think Harlond Clift should be in the Hall. He did in fact play for the worst team in the AL in the 30's. I haven't had the chance to look up his numbers, but he would compare favorably with any of the 3bs in the Hall.
That's right, the more closely you look at Andre Dawson, the better his case is. A good article up at the Hardball times website today, showing his WPA numbers are very good, and that doesn't even include his defense. Bottom line, 22nd all time in extra base hits, and no 20th century CF with anything remotely like his qualifications has ever been left out of the hall.
The only thing is that OBP. I think Andre is the perfect storm of what the absolute lowest OBP (as an OF) that should be in the HOF is, and hopefully if he is elected people don't buy arguments for slow LF with similar OBP.
I totally agree with Simmons and Trammell as HOFers. Glad to see the history buffs making the case for Indian Bob. Great article.
Re Bob Johnson, John Brattain wrote a terrific guest column for this site two years ago. What held Indian Bob back more than anything else is the fact that his rookie season was at the age of 27. Johnson's rate stats were of the quality of other Hall of Famers but his counting stats came up a bit short because of the late start. He will always be a part of the Hall of the Very Good.
I agree with Will Clark being extremely underrated especially with such a great peak. But Bill James lists him at no. 14 in the 2001 historical abstract (behind Donnie Baseball strangely enough) and also lists Dick Allen at 1B, right behind Clark at no. 15. But I do wish Clarkie got more consideration than he did.
A while ago (probably at least 5 years) I made a list of, for a bunch of counting stats like HR and RBI, who had the greatest total who was not in the Hall of Fame (despite being eligible). Andre Dawson turned out to be at the top of a lot of the lists.
Mark B, thanks a lot. I edited the post. I am not sure why I thought that but I appreciate you clearing it up.
I'm from the Bay Area, so I got to see The Thrill and Big Mac at their best. I loved watching them both but I have to go with McGwire at 1b. At 2b, my favorite overlooked candidate is Joe Gordon. Gold Glove caliber D, probably would have been a 40HR/yr hitter had he not spent his prime in Yankee Stadium. James does a comparison between Doerr/Gordon in "The Politics of Glory".
On that last comment, I meant Raines and Dawson, of course.
I did not want to leave this thread without also commending you for selecting Grich. No need to review all the numbers, but he was a second baseman with power and terrific on base skills. He was also deemed an outstanding fielder. While he did have injury problems, he still managed better than 140 games in 9 of his 17 seasons and finished with an OPS+ of 125, only once under 100 (98) after his first brief appearance in the majors.
Good article , all of the players mentioned have some merit for the hall. The article brought up a memory of some kind of rift between Will Clark and Rafael Palmeiro, does anyone remember what that was all about ?
Am surprised nobody mentioned Santo. Among third basemen, he ranks in the top half dozen in career TOB, TB, HR, RBI, RC, XBH, and BB. He also won five Gold Gloves. Led the NL in BB 4x and TOB 3x. Played 154 or more games every year from 1961-71, including 160 or more seven times. Eight consecutive years with at least 86 BB.
Sure, Santo benefited by playing home games at Wrigley Field and his road stats aren't all that impressive, but Ernie Banks and Billy Williams also benefited in a similar manner. His omission from the HOF is not the same injustice as Blyleven's but he is enough of a borderline candidate to get some pub when it comes to players who have been overlooked by voters.
WRT: anti-Expo fervor in HOF selection.
While it would certainly be a shame if Tim Raines were not elected to the Hall of Fame, in his first year of eligibility, its premature to attempt to rectify a true shame that has yet to be committed.
Admittedly, his gimmicky comeback attempts in 1976 and 1980 detract from his resume. But 10 at bats as a publicity stunt from the mind of Bill Veeck, can't out weigh what he accomplished in the prior decades.
re: Bob Johnson, having 4 seasons during wwII (when he landed his career ops+ high) doesn't really help his case considering the competition was so weak at the time.
Outside of Raines, who I think should be in the Hall, but probably shouldn't be on this list, at least not until next week when he is "officially" rejected to members of the BBWAA, the only other player I think is Hall-worthy is Dick Allen. The others all just miss in my book.
Also, regarding Clark's ranking in the Historical Baseball Abstract, James had Clark at #14 all time (which certainly counts as one of the top first baseman ever), but he also had him behind Mattingly, who he rated at #12, but ahead of Keith Hernandez at #16.
My guess is if James did a new version, he'd have Clark just ahead of Mattingly simply because Clark played for a few more years after the Abstract was published, and by James' own admission, he was very conservative when ranking players who were still playing. Mattingly has already retired, while Clark was still active.
That said, Mattingly's ranking by someone as respected as James certainly has to make one wonder if Mattingly deserves a second look. There are 1B who are in the Hall ranked significantly lower than Mattingly, and several in front of him, such as McGwire and Bagwell, who were no doubt chemically enhanced. I don't view Mattingly as a HOFer, but I would vote for him before Jim Rice and others.
Those 4 war years were completely in line with his performance in his first 9 years. In fact, except for 1944 when he moved to Boston, they were probably slightly less impressive.
As noted, he did not arrive in the majors until he was 27, so by the war he was an older player who still performed excellently. Because he only had the 13 years, his counting stats are unimpressive, although he had more RBIs and doubles than Hank Greenberg who also played for 13 seasons, and generally on better teams. (In no way am I suggesting he was as good as Greenberg.) And nearly as many home runs as Al Simmons had in 20 years with a higher OPS+ than the great Simmons, by the way. He also had more home runs and a higher OPS+ than Goose Goslin, another outfielder who played a lot in the 1930s, and altogether for 18 years.
A hall of famer should be someone that doesn't need an argument to be made for them.
For me, any player you have to come up with reasons why they should be in the hall of fame, shouldn't be in it.
They make it in, great. Good for them and their fans.
But I ain't gonna cry myself to sleep if they don't get in.
The only guy on this list that meets my criteria of yes/no, is raines.
As for the rest of my ballot
Blylevin, TJ, goose, mcgwire, lee smith
Who are "at the bench" in this lineup?
"A hall of famer should be someone that doesn't need an argument to be made for them."
I keep on encountering this argument, and it's just plain wrong. Every player whose career value depends significantly on BB rate needs to have an argument made for them, because most BBWAA voters consider the BB a meaningless offensive stat.
In the alternate universe where OBP rather than BA was a Triple Crown stat, Raines, Grich, and Dwight Evans were all easily elected.
There are other persistent biases in the voting. Players who played their careers in horrible parks, players who were excellent all-around but didn't do one thing superbly, defensive value at offensive positions ... it's a long list.
The proposed rule of thumb might work if voters were overvaluing or undervaluing guys by just 10-20% at max, but they're not anywhere close to that.
That's a cool list, Manuel. I like it.
And I agree with Eric. There are all sorts of players who merit advocacy because of the numerous traits that contribute to teams' winning efforts that the BBWAA overlooks.
Great list.
"A hall of famer should be someone that doesn't need an argument to be made for them.
For me, any player you have to come up with reasons why they should be in the hall of fame, shouldn't be in it.
The only guy on this list that meets my criteria of yes/no, is raines.
As for the rest of my ballot
Blylevin, TJ, goose, mcgwire, lee smith"
Actually, everyone on your ballot is a perfect example of a player who needs to have arguments made for him and reasons given for election, not just because he is not already elected but because his greatness as a player is not always obvious. Someone like Raines or Blyleven does not on first glance seem to be an all-time great; it is only after analysis that their true greatness becomes clear.
Incidentally, I find this hard to believe, and I may be misunderstanding the facts, but the 2007 HOF yearbook indicates that Stan Musial was elected in 1969, but he retired after the 1963 season, 6 years earlier. That suggests he was not elected in his first year of eligibility. Is it possible that Musial was not a first ballot HOFer?
Bob: Musial was a first-ballot HOFer. He retired after the 1963 season, sat out for five years (1964-1968), and was elected in 1969. The same rules apply to all players.
Sandy Koufax: retired in 1966, voted into the HOF in his first year of eligibility in 1972.
Cal Ripken and Tony Gwynn: last season was 2001, voted into the HOF in 2007.
Tim Raines: last season 2002, eligible for the first time in 2008.
Ok, Rich, I see that. But then how is it that DiMaggio was elected in 1955 (according to the yearbook) and retired after the 1951 season?
There are some surprising names who had to wait. Mickey Cochrane was elected in 1947 after retiring in 1937. I would have thought he was a no-brainer. Dickey also had to wait from 1946-1954 and Hartnett from 1941-1955. Berra also seems to have missed on the first vote as he retired in 1965 but got in in 1972. Others who had to wait include McCovey, Greenberg, Eddie Mathews, Al Simmons, Reggie Jackson & Paul Waner. I can guess at the arguments against in each case, but I think in most cases time has erased the memory of them.
I should have checked other players before commenting on Musial. I see that you are absolutely correct. Thanks. There are a few anomalies, some due to early deaths or other factors, but that would not explain the DiMaggio case.
Joe DiMaggio is an interesting case. Excluding 1945 (when all players were eligible, including active players), one could argue that he was elected in his *third* year of eligibility.
Here are his vote totals:
Year Votes Pct 1945 1 .4% 1953 117 44.3% 1954 175 69.4% 1955 223 88.8%
When the Hall of Fame was established in 1936, all players were eligible, retired and active. Writers could vote for anybody but were discouraged from voting for current major leaguers up until 1946 when an official one-year waiting period was put into effect. The five-year waiting period was established in 1954, although an exception was made for Joe D. because of his high level of previous support. As a result, he was elected in 1955, or two years earlier than he would have under today's rules.
Thanks Rich. Interesting information.
In "The Luckiest Man Alive" Eig says that in 1939 the BWAA"voted to waive its normal election process and immediately nominate Gehrig to the baseball Hall of Fame." I assumed that meant that the rule was already in place, but apparently it wasn't.
After Lou Gehrig retired in the middle of the season in 1939, the BBWAA agreed to hold a special election for him at the Winter Meetings in December. Gehrig was the lone candidate on the ballot and was voted into the HOF. Interestingly, Gehrig's vote total has never been revealed.
The BBWAA also agreed to postpone the next regular election until 1942, as the initial quota of 10 inductees from the 20th century had been met.
Allen a way better hitter than Santo? That comment somewhat destroys the credibility of an otherwise intelligent analysis here. Allen was a marginally better hitter and a significantly inferior fielder. Certainly Santo was more superior as a fielder than Allen was as a hitter.
And if your going to throw out an intangible like Santo's career being longer, you have to give Santo credit for playing as a juvenile diabetic at a time where doing so was far more difficult than even today. But I say neither should be cut any slack so you take Santo's numbers for what they are, but longevity is still a point in his favor.
As you note, nobody was elected in 1940 or 41, but there must have been another election in 1939, probably before the Gehrig choice which was on December 7. Aside from Gehrig, which as you point out was a special case, there were 10 men elected in 1939, most of them primarily for their executive role (Comiskey, Spaulding, Bulkeley) or from the 19th century (Cummings, Radbourn, Ewing, Anson, Keeler). There were two 20th century players also in Eddie Collins and Sisler.
I probably should read some more about the actual history of the HOF. By my count, at the end of 1939, there were 26 members of the HOF, 7 primarily executives (although Spaulding played quite a bit too), 6 from the 19th century (although McGraw was probably there as a manager) and including Gehrig 13 from the 20th century (although I suppose Keeler could be considered 19th century and so could Cy Young). Eliminating Young, Keeler and Gehrig, it was indeed 10 players from the 20th century. I did not realize there was such a quota at the time.
Allen: .292/.378/.534
Santo had two seasons with an OPS+ over 156, Allen's career figure.
Yes, Bob, the voters added those other players in January 1939 via the normal channels.
I have to concur with Sully on the Allen vs. Santo issue when it comes to hitting. Now, one can favor Santo for his fielding (or for the fact that he played his entire career at the hot corner whereas Allen played more games at first base than third), but it would be next to impossible to make an objective case that he was a better *hitter* than Allen.


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Photodynamic therapy (PDT) is an emerging cancer therapy that uses the combination of non-toxic dyes or photosensitizers (PS) and harmless visible light to produce reactive oxygen species and destroy tumors. The PS can be localized in various organelles such as mitochondria, lysosomes, endoplasmic reticulum, Golgi apparatus and plasma membranes and this sub-cellular location governs much of the signaling that occurs after PDT. There is an acute stress response that leads to changes in calcium and lipid metabolism and causes the production of cytokines and stress response mediators. Enzymes (particularly protein kinases) are activated and transcription factors are expressed. Many of the cellular responses center on mitochondria and frequently lead to induction of apoptosis by the mitochondrial pathway involving caspase activation and release of cytochrome c. Certain specific proteins (such as Bcl-2) are damaged by PDT-induced oxidation thereby increasing apoptosis, and a build-up of oxidized proteins leads to an ER-stress response that may be increased by proteasome inhibition. Autophagy plays a role in either inhibiting or enhancing cell death after PDT.
Photodynamic therapy (PDT) is a promising therapeutic procedure for the management of a variety of solid tumors and non-malignant lesions. PDT is a two-step procedure that involves the administration of a photosensitizing agent [
After the absorption of photons the PS is transformed from its ground state to its triplet excited state via a short-lived excited singlet state (
PDT as a treatment procedure has been accepted by the United States Food and Drug Administration for use in endo-bronchial and endo-esophageal cancer [
The available body of literature suggests that there is clearly no single pathway that leads to cell death after PDT. In the present review we aim to describe and summarize different cell death pathways activated by PDT [
Apoptosis is a very complex, multi-step, multi-pathway cell-death program that is genetically encoded in every cell of the body [
In mammals the Bcl-2 family has at least 20 relatives, all of which share at least one conserved Bcl-2 homology domain. The family includes four other anti-apoptotic proteins: BclXL, Bcl-w, A1 and Mcll, and two groups of proteins that promote apoptosis: the Bax and the BH3-only families [
Bcl-2 and other members of the family potently inhibit apoptosis in response to many, but not all cytotoxic insults. Bcl-2 itself is required for the survival of kidney and melanocyte stem cells and mature lymphocytes [
PDT is thought to induce photodamage of Bcl-2 and related antiapoptotic proteins and activate the proapoptotic members of the family [
In the study by He
This study documented that down-regulation of Bcl-2 with antisense oligonucleotide resulted in sensitization of PDT apoptosis-resistant cells to apoptosis; however, the overexpression of Bcl-2 in a PDT apoptosis-sensitive cell line resulted in the enhancement of the apoptotic response.
A similar approach was used in human gastric adenocarcinoma MGC803 cell line which was infected with antisense bcl-2 RNA retrovirus vector to study effect of 2-butylamino-2-demethoxy-hypocrellin A (2-BA-2-DMHA) photosensitization [
A study performed by Kim
Another work indicating possible role of Bcl-2 in PDT response was reported by Xue
The study indicating that Bcl-2 may by a potential target in PDT, was also performed by Kessel
This team provided additional evidence to the hypothesis that Bcl-2 photodamage can be a target for some photosensitizing agents by showing that the effects of the photosensitizer CPO can be mimicked by the Bcl-2 antagonist HA14-1 [
The BH3-only proteins seem to act as damage sensors and direct antagonists of the pro-survival proteins, whereas the Bax like proteins act further downstream, probably in mitochondrial disruption. The BH3-only proteins are sentinels that can detect developmental death cues or intracellular damage. In healthy cells, they are restrained in diverse ways, including sequestration by the cytoskeleton. When unleashed by death signals, they switch off survival function by inserting their BH3 domain into a groove on their pro-survival relatives [
The possible role of Bax in PDT-mediated apoptosis was showed by Srivastava
The research performed by Usuda
Accumulating evidence suggests that PDT is an efficient inducer of apoptosis in many cancer cell lines, whereas the lack of the ability to undergo apoptosis does not protect cells from lethal effects of PDT. It therefore appears that the post-mitochondrial regulators, such as Bax protein, may be in the promotion of the late events of tumor responses. Thus, tumor cells with increased Bax/Bcl-2 ratio can be more effectively treated by PDT.
Bax was found to translocate to mitochondria during apoptosis in HeLa cells after PDT with zinc (II) phthalocyanine [
It is generally recognized that mitochondria play a critical role in the apoptotic cascade by controlling the release of crucial factors involved in that process [
Another work indicating an important role of cytochrome c in PDT-induced apoptosis was carried out by Vantieghem
Another support for the hypothesis that cytochrome c plays a vital role in PDT-induced apoptosis was provided by Varnes
All death receptors belong to TNFR superfamily (tumor necrosis factor receptor) [
TNFR signaling was discovered to be an important factor in immune response and such members like Fas and APO2/TRAIL induce apoptosis through a p-53 independent mechanism. The signaling members of TNFR superfamily can be divided into two main subgroups. One class contains cytoplasmic death domain, whereas the other class does not. Death domains mediate interaction of death receptors with death-domain–containing adaptor proteins and then act in the caspase-dependent pathway. Death domain containing receptors activate the apoptotic pathway by caspase-8 mediated cleavage of the pro-apoptotic Bcl-2 superfamily member BID [
Because treatment with factors that activate death receptor signaling in cancer cells may be an effective anticancer strategy it has been investigated whether PDT can affect this pro-apoptotic pathway.
The early evidence comes from the study designed by Ahmad
To further evaluate the role of Fas in PDT mediated apoptosis, Ali
There is also strong evidence that APO2/TRAIL is involved in PDT mediated apoptosis. Schempp
Further support for this hypothesis was provided by Granville
Nuclear factor kappa B (NF-κB) is a term referring to a group of dimeric transcription factors that belong to the Rel family and are regulated via shutting from the cytoplasm to the nucleus in response to cell stimulation [
PDT produces an oxidative stress that can result in activation and translocation of NF-κB to the nucleus, as originally shown for treatment of L1210 murine leukemia cells with Photofrin and light. [
Mitogen-activated protein kinases are proline-directed Ser/Thr protein kinases activated by dual phosphorylation on both tyrosine and threonine residues [
A link between SAPK and p38 pathways and apoptosis has been suggested in several studies [
The involvement of stress kinases in PDT mediated cell death was also investigated by Chan
Ceramide is implicated in the cell-signaling pathway involved in apoptosis as it acts as a second messenger to permeabilize the outer mitochondrial membrane and facilitate the release of cytochrome c from the mitochondria [
p21/WAF1 involvement in PDT was investigated by Ahmad
Necrotic cell death has been described as a violent and quick form of degeneration affecting large fractions of cell populations, characterized by cytoplasmic swelling, destruction of organelles and disruption of the plasma membrane, leading to the release of intracellular contents and consequent inflammation [
Necrosis has been referred to as accidental cell death, caused by physical or chemical damage and has generally been considered an unprogrammed process [
Studying the factors and parameters that cause cellular necrosis after PDT is not as easy as studying those factors which lead to apoptosis. The crucial factors in determining the type of cell death, e.g., apoptosis or necrosis following PDT are: the cell type, the presence of an intact set of apoptosis machinery, the subcellular localization of the PS, the light dose applied to activate it locally, and the oxygen partial pressure [
Nagata and colleagues [
Xue and Oleinick [
Autophagy is a catabolic cellular mechanism that allows the cell to maintain a balance between the synthesis, degradation, and recycling of cellular products [
The term "autophagy" originated in 1963 at the Ciba Foundation Symposium on Lysosomes, where it was used to describe the presence of membrane vesicles that contain disintegrating organelles and cytoplasm components. Evidence soon confirmed that autophagy is an adaptive, energy-generating process. Molecular control of autophagy came into focus in the late 1990s. Signaling pathways governing this process became better understood after the identification of the target of rapamycin kinase (TOR), which controls cell growth and protein synthesis [
One of the first diseases associated with autophagy was cancer [
It is still unclear exactly how autophagy affects the outcome of PDT [
In order to understand how PDT affects autophagy it is important to take note of the PDT affected proteins that are involved in this mechanism. Many proteins, some directly involved in the autophagic process, are damaged by PDT induced ROS. Some ER and mitochondrial photosensitizers cause damage to Bcl-2, to which Beclin1 (a pro-autophagic protein) binds. The IP3 protein, a regulator of the autophagic process associated with the ER [
PDT can also affect autophagy by damaging organelles that are directly involved in the process. Several photosensitizers target autophagy-related organelles such as lysosomes and endosomes. When tetra(4-sulphonatophenyl)-porphine (TPPS4) photosensitizer is used photo-oxidation of the organelle matrix occurs [
The effects of a damaged lysosome on the autophagic process were explored in an autophagic flux study of murine hepatoma 1c1c7 cultures. These cultures were sensitized with NPe6 and irradiated with LD90 light dose. Acridine orange (AO) staining of acidic organelles was done in order to observe the effect of PDT on the lysosome. No lysosomal damage was observed when cells were exposed to either light or photosensitizer alone. In those cells that received PDT, AO staining was completely lost within an hour, and within two hours autophagosome accumulation was observed [
Based on studies with various cancer lines and photosensitizers it can be concluded that PDT directly induces autophagy. This is independent of photosensitizer target, as autophagy was observed with photosensitizers that localize in the ER, mitochondria, lysosomes, and endosomes. A second conclusion that can be drawn is that apoptosis often occurs in cells that are already undergoing autophagy and is also a result of PDT. The rates of autophagy and apoptosis depend on the cancer cell type, photosensitizer, and light dosage. Depending on cell type, autophagy will either promote or prevent cell death from PDT. In cells that are able to undergo apoptosis autophagy alleviates the destructive effects of PDT by recycling damaged organelles [
PDT can lead to all three forms of cell death, namely apoptosis, necrosis and autophagy (
It is also important to bear in mind that most of the reported
The understanding of the cascade of events playing a role in PDT-mediated apoptosis is far from complete. Defining these events will hopefully result in designing better PDT protocols, which could have wider applications as a cancer therapeutic modality.
Schematic illustration of the mechanism of Photodynamic therapy (PDT). The photosensitizer (PS) is injected systemically and after sufficient time to allow its accumulation in the lesion light is delivered to produce reactive oxygen species (ROS). The tumor cells are killed by a mixture of necrosis and apoptosis, the blood supply is damaged and the host immune system activated.
Jablonski diagram. Ground state PS absorbs a photon of correct wavelength to excite its electron to first excited singlet state that may (in addition to losing energy by heat or fluorescence emission) undergo intersystem crossing to long lived triplet state. This can undergo photochemistry by either electron transfer (Type I) or by energy transfer (Type II) to molecular oxygen to produce ROS.
Photodynamic effect. An excited triplet state can either react directly with a reductant, e.g., an organic molecule in a cellular microenvironment, acquiring a hydrogen atom or electron to form a radical and produce a superoxide anion radical (O2•-), type I reaction or, more likely, transfer its energy to molecular oxygen (3O2) and form singlet oxygen (1O2), type II reaction.
Cell death pathways in PDT. The mode of cell death observed after PDT to some extent depends on the intracellular localization of the PS and PDT related damage to that organelle. PDT with PS localizing in mitochondria will lead to loss of membrane permeability and release of pro-apoptotic mediators while ER damage will release cellular deposits of calcium. PS that accumulates in lysosomes will release proteolytic enzymes upon illumination. Lysosomes may also fuse with autophagosomes to hydrolyse damaged organelles and recycle them during autophagy. In the excess of damage the cell will not survive despite initiation of autophagy. Necrosis as well as autophagy may be a dominant cell death mode after PDT when apoptosis is dysfunctional. It should be remembered that several PS may localize in more than one organelle and the activation of cell death pathways may occur concurrently (adapted from Oleinick
Major cell death mechanism activated by Photodynamic therapy (PDT).
Cytochrome c release
Bcl-2 damage
NFκB damage
Beclin 1,
mTOR activation
Research in the Hamblin laboratory is supported by NIH grant R01AI050875, Center for Integration of Medicine and Innovative Technology (DAMD17-02-2-0006), CDMRP Program in TBI (W81XWH-09-1-0514) and Air Force Office of Scientific Research (FA9950-04-1-0079). PM is partly supported by NIH Dermatology training grant.


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MOTLEY CRUE: The Final Tour Starts
Photo by Michael Loccisano/Getty Images
For Motley Crue, the end of life on the road begins tonight (Wednesday).
The Final Tour, with opening act Alice Cooper, gets under way in Grand Rapids, Michigan. The group has scheduled 72 dates in North America this year, wrapping up November 22nd in Spokane, Washington.
The Crue promises to that this will be their final tour, even signing contracts saying none of them can tour using the Crue name in the future. Singer Vince Neil says signing the deal was a way to protect themselves and their fans.
In other Crue news, the band's autobiography, The Dirt, has just been released as an E-book. A film adaptation of the book is slated to be released in 2015.


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Savage Mark II FV Scope Mounting ??
I have just purchased a Savage Mark II FV and a BSA PT624X44MD Platinum Target Scope. Can someone give me a recommendation on what mounting rings to get for it. I know the scope has 1 inch tubes but not sure on the height i should be buying. I will be using the rifle for bench rest style shooting.
Does this scope have "Side Focus" or Front Bell "Adjustable Focus"? Also if it has Bull Barrel, it could make a difference. For my Simmons 4-12x44 w/SF, it required HIGH rings(Ruger 77/22 with taper barrel, rings came with rifle). For my Weaver V16 4-16x42 w/A/O it took HIGH rings(Weatherby 243 with taper barrel), because it has A/O(adjustable objective). I have a Marlin 17HMR and mounted a BSA Sweet 17, 3-12x40 w/A/O and it too took high rings and clears bull barrel by 1/8". I use Weaver Quad Lok rings and they work very well from WalMart at a reasonable price of $11. So if your scope has front bell Adjustable Objective on top of 44MM lens, you might need to go to "Extra High" rings to clear barrel.
my $.02
Here is how i decide,
Set scope on table, measure the distance from the botton of the tube to table. get rings that are at least 1/8" taller than that and you should be good for clearance of most any barrel.
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Insight into the role of the epicardium in cardiac development and regeneration has significantly improved over the past ten years. This is mainly due to the increasing availability of new mouse models for the study of the epicardial lineage. Here we focus on the growing understanding of the significance of the epicardium and epicardially-derived cells in the formation of the atrioventricular (AV) junction. First, through the process of epicardial epithelial-to-mesenchymal transformation (epiEMT), the subepicardial AV mesenchyme is formed. Subsequently, the AV-epicardium and epicardially-derived cells (EPDCs) form the annulus fibrosus, a structure important for the electrical separation of atrial and ventricular myocardium. Finally, the AV-EPDCs preferentially migrate into the parietal AV valve leaflets, largely replacing the endocardially-derived cell population. In this review, we provide an overview of what is currently known about the regulation of the events involved in this process.
The heart develops from two populations of cardiogenic anterior lateral plate mesodermal cells, known as the First Heart Fields (FHFs), which join at the ventral embryonic midline to form the primary heart tube (reviewed in [
The AV valves are crucial structures in the developed 4-chambered heart. When properly formed, they prevent retrograde flow of blood from ventricles to atria during ventricular systole. The first step in AV valve development is the formation of the AV cushions. The AV cushions initially form as a result of an accumulation of cardiac jelly in the AV canal and subsequently become populated by endocardially-derived mesenchymal cells as the result of endocardial epithelial-to-mesenchymal transformation (or endoEMT) [
While there are many aspects to the development of the AV junction, in this contribution we specifically focus on the role of the epicardium and epicardially-derived cells (EPDCs) in this process. We will refer to the EPDCs at the AV junction as AV-EPDCs. The AV-EPDCs derive from the AV-epicardium, which, just like the rest of the epicardium, with the exception of the epicardium found on the outflow tract [
Our understanding of the role of the epicardium in heart development has been greatly advanced by the development and use of mouse models in which cre-recombinase is expressed in epicardial and/or epicardially-derived cells. These "epicardial-cre" mice include the cGATA5Cre [
Epicardially-derived cells contribute to the parietal leaflets of the atrioventricular (AV) valves. This figure shows a transverse section of a 17ED mouse heart from a cross between a male Wt1Cre mouse and a female R26mT/mG reporter mouse. This cell-lineage tracing model shows that the epicardially-derived cells (in red) at the AV junction (AV-EPDCs) preferentially contribute to the right parietal (rpAV) and left parietal (lpAV) leaflets of the AV valves in a mouse heart at 17 embryonic days of development. The myocardial structures are stained for the myosin heavy chain with MF20 (green), the section was counterstained with DAPI (blue in B) to stain all nuclei. AoAV = aortic leaflet of left AV valve; AS = atrial septum; LA = left atrium; LV = left ventricle; lpAV = left parietal AV valve leaflet; PuV = pulmonary vein; RA = right atrium; RV = right ventricle; rpAV = right parietal AV valve leaflet; septAV = septal leaflet of right AV valve.
As the epicardium proper is forming, the tissues at the AV junction are undergoing significant remodeling. Whereas at the interior side of the AV junction, endoEMT is responsible for the generation of the endocardially-derived mesenchyme of the AV cushions, the epicardial EMT (epiEMT) taking place at the exterior AV junction (or AV groove) is responsible for the accumulation of epicardially-derived mesenchyme in the AV sulcus. Subsequently, a subpopulation of these AV-EPDCs starts to penetrate the lower boundary of the AV canal myocardium, resulting in the formation of the annulus fibrosus and in the incorporation of the primary AV canal myocardium into the atrial chambers [
Cascade of events involving the epicardial and epicardially-derived cells in the development of the AV junction. The epicardium plays a crucial role in virtually all aspects of the development of the structures at the AV junction. While insight into the molecular mechanisms that control the formation of the epicardium proper as well as epicardial EMT is steadily growing, virtually nothing is known about the molecular mechanisms that govern the formation of the annulus fibrosus and the ones that are involved in the migration of AV-EPDCs into the parietal AV valve leaflets.
The first step in the series of epicardial-related events that regulate the remodeling of the AV junction is the formation of the AV epicardial epithelium (or AV epicardium) itself. This process is initiated when cells from the proepicardium reach the myocardial surface of the heart around ED9.5. For many years it was believed that the mechanism through which this is achieved is fundamentally different between the mammalian and the avian heart. Specifically, it was thought that while in the avian heart the proepicardium is making contact with the heart proper via protruding proepicardial villi, the primary mechanism of how the proepicardial cells reach the heart in the mammalian heart is by the release of proepicardial vesicles into the pericardial cavity that subsequently "land" on the myocardial surface to form the epicardium [
The second step in the cascade of epicardial-related events at the AV junction is the formation of epicardially-derived cells forming the mesenchyme of the AV sulcus (or AV-EPDCs). This process is initiated by epicardial epiEMT and is followed by the expansion of the AV-EPDC population by proliferation. The AV-EPDCs in the AV sulcus form an important pool of precursor cells for the development of a number of structures at the AV junction. Not only do the AV-EPDCs play a critical role in the formation of the annulus fibrosus and contribute to the development of the parietal AV valve leaflets [
It is well recognized that a number of genes expressed at relatively high levels in the AV junctional myocardium are important in the regulation of endoEMT in the AV cushions. In particular the roles of Tgfβ2 and Bmp2 are well recognized in this process [
Schematic representation of the contribution of the AV epicardium and the epicardially-derived cells to the development of the AV junction. After formation of the epicardial epithelium (green), epiEMT generates a population of AV-EPDCs (green cells in panel A) that, as far as their gene expression profile is concerned, are still very similar to the epicardium itself. However, when the AV-EPDCs migrate further into the AV sulcus and approach the AV myocardium (red cells), the molecular profile of the AV-EPDCs changes drastically as the expression of genes characteristically found in the mesenchyme of the annulus fibrosus (e.g., MMP2) and the AV cushions (e.g., Sox9) is upregulated. These "differentiated" AV-EPDCs (red cells in panel A) then penetrate the AV myocardium to form the annulus fibrosus (panel B) and migrate into the parietal AV valve leaflets where they intermingle with the endocardially-derived mesenchymal cells (ENDCs; blue cells in panels A and B).
Previously, it has been described that when ventricular EPDCs migrate into the ventricular wall they gradually lose expression of Wt1 and Raldh2 and that they gain expression of mesenchymal cell markers such as Sox9 [
In studies using the Wt1CreERT2/+ mouse in conjunction with the Rosa26mT/mG reporter mouse, the Pu lab was the first to unambiguously show that EPDCs contribute to the formation of the annulus fibrosus in the mammalian heart [
The role of the epicardium in the development of the AV valve leaflets has been an area of interest for years. In a 1986 paper on the formation of the mitral valve [
The initial studies on the fate of EPDCs in the developing heart using avian models strongly suggested that EPDCs were able to migrate into the AV cushions [
Much of what is currently known regarding the genes involved in epiEMT and EPDC contribution to the fibroblast populations of the developing heart is based on studies of the epicardium covering the ventricles [
The preferential contribution of EPDCs to the parietal leaflets of the AV valves presents several questions concerning the role of EPDCs in AV valve development, including: (i) what determines the migration of EPDCs into the AV valve leaflets; (ii) do the EPDCs in the parietal leaflets regulate the process that leads to the reduction of endocardially-derived cells in these leaflets; (iii) what are the similarities and differences in the molecular and functional characteristics of the epicardially- and endocardially-derived cells that reside in the AV valves; and (iv) what differences in gene expression, if any, exist between the parietal leaflets and the "septal" leaflets of the AV valves? Although we have previously established that the EPDCs in the parietal leaflets express many of the same proteins that are also expressed by the endocardially-derived valve interstitial cells in the AV leaflets (e.g., collagen I, periostin, vimentin, filamin A, and sox9 [
Finally, in addition to understanding the molecular differences in the endocardially-derived and epicardially-derived cells of the AV valves, it is important for future research to address what role the AV-EPDCs play in AV valve development and maturation. Removal of the proepicardium in avian embryos results in a spectrum of cardiac defects, including thin myocardium, abnormal outflow tract septation, failure of coronary plexus formation, failure of the AV cushions to fuse, and enlargement of the AV cushions [
The authors would like to acknowledge the financial support by the following grants: NIH NCRR C06-RR018823, NIH-NCRR C06-RR015455, the "South Carolina COBRE for Developmentally Based Cardiovascular Diseases", P30 GM103342-01 (A.W.), NIH R01HL033756-30 (A.W.), American Heart Association Grant-in-Aid 13GRNT16220004 (A.W.), American Heart Association Predoctoral Grant 12PRE11340000 (M.L.), European Community's Sixth Framework Program Grant LSHM-CT-2005-018630 (M.J.B.v.d.H.), Netherlands Heart Foundation Grant 1996M002 (M.J.B.v.d.H.). This publication was supported by Project 1233 from the South Carolina Clinical & Translational Research (SCTR) Institute, with an academic home at the Medical University of South Carolina CTSA, NIH Grant Numbers UL1RR029882 and UL1TR000062 (A.W.). The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NHF, NIH and AHA.
The authors declare no conflict of interest.


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I'm trying to print downloaded photos that is on the screen. Not individual
ones but what is on the monitor screen. Each picture has a number below it to
identify the picture.
1. I hit "PrintScn Sys Rq" key once. Open Inranview software. Click on
Edit, but there was no paste option. The infranview screen says I have no
2. So the problem is getting my screen photo on the clipboard. What am i
doing wrong?


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While most in the liberal media are downright ignoring President Obama's attack on religious institutions -- via the mandate that they cover contraceptives in their health insurance plans, even if doing so violates church teaching -- MSNBC's Martin Bashir mentioned the issue in today's "Clear the Air" commentary that closes his eponymous program.
Of course, true to MSNBC form, Bashir ignored the legitimate policy and religious liberty implications of Gingrich's complaint to dredge up Gingrich's past moral failings, namely his adulteries, as a way of fatally wounding the messenger and hence, Bashir hopes, negating the message [MP3 audio available here; video posted below page break]:
MARTIN BASHIR: It's now time to clear the air and in the world of the Republican primaries, our most bitter presidential candidate – Newt Gingrich – is back doing what he loves best: accusing the president of being hateful of religion.
This time, it's the issue of contraception and the idea that, under the president's reform of health care, all hospitals, including religious institutions, will be required to provide contraception.
But to hear Newt Gingrich on the subject, well, this is a declaration of war by the president.
NEWT GINGRICH from February 5 Meet the Press: "You know he's basically declared war on the Catholic Church. The fact is – what you're saying is there cannot be a genuinely Catholic University, there cannot be a genuinely Catholic hospital that in fact, it will have to be subordinated to the rules of a secular government."
BASHIR: What's interesting about Gingrich is the way he sounds so theologically robust. But one wonders if Mr. Gingrich was using the rhythm method himself when he was committing adultery with his Catholic mistress Callista. You see, here's the problem, the vast majority of Catholics and evangelicals in America actually use contraception.
According to a report by the Guttmacher Institute, which studies sexual and reproductive health, among sexually active women, 68 percent of Catholics are using a highly effective method of birth control, such as the pill, sterilization or an IEUD [sic]. The figure is 73 percent for mainline Protestants and 74 percent for evangelicals. But according to Newt Gingrich, the president is waging a war against religion.
Of course, Newt knows exactly what he's doing. He's desperately trying to gloss over his serial adultery and multiple marriages and to now sound like a man who's standing firm on Scripture and tradition.
But which version of the Bible does Newt Gingrich actually follow?
Last year marked the 400th anniversary of the first publication – in 1611 – of the King James version of the Bible. It remains one of the most pre-eminent books in the English language.
Thirty years [sic] later, in 1631, the royal printers in London were asked to produce a reprint. Everything went well, apart from a single mistake. The compositors accidentally omitted the word "not" from the Seventh Commandment. So, "Thou shalt not commit adultery," became "thou shalt commit adultery."
And while I cannot be certain, I have a sneaking suspicion that Newt Gingrich much prefers the 1631 King James version, above all others.
Bashir, himself a practicing Christian and a formerly serious journalist, should know better. Shame on him.
<<Like this post? Help us take on media bias by donating to NewsBusters (there's also a PayPal option on that page). Without the support of our readers, NewsBusters would not be possible.>>


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On Tue, 2010-01-26 at 17:10 +0000, Greg Stark wrote: > Postgres: Liberate Your Data! I like it. It may not even need the "!". Also, it looks like it would translate well into many languages. Regards, Jeff Davis
Next: From: Peter Eisentraut Date: 2010-01-27 21:31:54 Subject: Re: Wanted: new project slogan Previous: From: Jeff Davis Date: 2010-01-27 20:55:07 Subject: Re: Wanted: new project slogan


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Sasha summarises Professor James Coyne's recent no-holds-barred talk on the PACE trial and points you to the slides, video, audio and transcript.
Discuss the article on the Forums.
DSM5 - Ticket back to Reevesville
Discussion in 'Action Alerts and Advocacy' started by Khalyal, Feb 12, 2010.
Page 8 of 9
Page 8 of 9


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Triumph Thunderbird
Sport Tuning Tips
Reviews Home
Here are
some Triumph Thunderbird Sport tuning tips from "J.B.":
I live in England and have
a '99 T'Bird Sport.
Couple of hints for you,
just reading the excellent article on valve clearance
adjustment, which I had a go at myself not so long ago.
Couple of things I found out about this engine:
I really do understand the
frustration with the lack of clearance under the frame
tube, so I found that it is really much easier to remove
the coolant junction pipe that is bolted to the left hand
side of the
cylinder head, it takes two minutes, and whilst still
attached to the hose, it will fold neatly out of the way
to allow you to work. Once removed, dry thoroughly
around the mating area and when bone dry cover the hole
with gaffer tape, err, believe me stuff can fall in there!
The engine goes
"quiet" when the valve tappet clearances are too
tight! Honest, so be very suspicious of an overly
quiet engine - the healthy rustle is what you want to
The engine power is largely
restricted by the awful exhaust system (especially the
downpipes/header pipes), and of course the standard
Best Regards, J.B.
Thanks J.B. for sending
these tips!


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Course Reserves
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- Interlibrary BorrowingMake an Interlibrary Borrowing request to obtain materials not owned by the JFKU Libraries & Learning Resource Centers
- Direct DeliveryUse Direct Delivery to request to have books mailed to your home, or to have articles or book chapters scanned and emailed to you.
Research Help
Librarians are available to meet with you to assist with research, help you find specific materials, help with APA, and more.
Please see our Ask a Librarian page for contact information. For in depth consultations, please make an appointment.


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A 34-year-old man sought by police vice officers for allegedly forcing minor girls into prostitution has been arrested on suspicion of burglary after leading police on a foot chase through suburban backyards, authorities said.
Leroy Bragg was arrested Tuesday night after being shot with a stun gun, Hawthorne police Lt. Gary Tomatani told the Daily Breeze in Torrance.
He had been sought by Los Angeles police vice officers who specifically target men suspected of kidnapping teen girls and forcing them into prostitution.
Bragg, a Hawthorne resident, is suspected of kidnapping a 14-year-old Upland girl earlier this week, Los Angeles police Detective Hector Sanchez said. The girl has not been found, but investigators believe she is out of harm's way, Sanchez said.
Bragg is also a suspect in a number of other kidnappings.
"This has the potential to be a human trafficking investigation," Sanchez said. "It involves multiple juveniles."
Bragg was held on suspicion of burglary at the LAPD's 77th Street Division jail. More serious charges were pending as state and other authorities investigate.
Sanchez told the newspaper many of the young victims come from broken homes and have psychological problems. Pimps supply them with drugs and abuse them.
"When girls get exploited like this, they have a lot of things to worry about," he said. "So when they see the police a lot of times, even though we are there to rescue them, they are trained to dislike us by their pimp."
Police declined to release more specific details because the case is under investigation.


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Annual General Meeting 2017
Tuesday, 3rd October 2017
3rd July 2017
Together with Mazars we have created a board effectiveness review to enable a board to stand back and assess its strengths and areas for development. Download your copy and have your whole board complete the questionnaire.
29th June 2017
24th May 2017
27th April 2017
Our Corporate Governance Expert Group works with boards, investors and regulators to promote high quality corporate governance by quoted companies.
Our Secondary Markets Expert Group deals with issues arising from the European and UK government and regulators that affect secondary markets and the ability of small and mid-size quoted companies to raise finance.
Our Legal Expert Group ensures that new and revised regulations that affect small and mid-size quoted companies are proportionate and appropriate for the sector.
Our Share Schemes Expert Group examines all aspects of share scheme regulation to ensure that they remain cost effective and easy to implement for small and mid-size quoted companies.
Our Tax Expert Group campaigns to introduce measures that encourage investment in the small and mid-size quoted company sector and reduce the tax burden.
Our Corporate Finance Expert Group deals with issues that affect the primary markets for small and mid-size quoted companies.
Our Financial Reporting Expert Group campaigns for proportionate reporting standards for small and mid-size quoted companies.
Tuesday, 3rd October 2017
Thursday, 29th June 2017


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MobileRead's Tenth Birthday Giveaway!
View Single Post
Jade Aislin
Posts: 163
Karma: 3100
Join Date: Sep 2011
Device: Kobo Auro H2O, PRS-T1
Happy birthday!
I stumbled onto calibre as a way to organize my reading frenzy. So naturally, I frequent the calibre section, specifically the
area. I've also used the '
Which (ereader) should I buy?
' section to finally decide on a new ereader.
Both sections have great people on it who are willing to answer any question. The calibre plugin section has lots of great plugins that make calibre work even better for my needs. The people on the other section give great advice to anyone who is unsure of what ereader to get.
It's hard to think of anything that changing could help. However, I noticed some of the specific ereader forums don't have subforums. For example, there's an apple forum, but there is none for those people who are looking for iPad 2 help. The sony section has a feature that allows the reader to see which version of the sony ereader the person is talking about, but it still does not have a sub forum. When I go looking for information on my Sony PRS T1, I have to slog through questions about other ereaders before I can find anything that relates to the one I own. Sub forums for specific ereaders (when there is more than one in a forum section) might be useful.
Jade Aislin
View Public Profile
Find More Posts by Jade Aislin
Track Posts by Jade Aislin via RSS


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Legg Mason Open Rehearsal Series
Offering serious music students in middle, high school and college a "behind-the-scenes look" at a working BSO rehearsal. Open Rehearsals at the Joseph Meyerhoff Symphony Hall are free, but seating is limited to 500 attendees. Please bring your valid student/school ID to the rehearsal.
Please note that some of the works on the concert program may not be rehearsed at the Open Rehearsal.
To reserve tickets, students and teachers may contact the BSO Education Department by phone: 410.783.8118 or email: firstname.lastname@example.com.
Rimsky-Korsakov's ScheherazadeThursday, March 30, 10 am
Marin Alsop, conductor
Jennifer Koh, violin
Barber: Adagio for Strings
Steven Mackey: Beautiful Passing (BSO Premiere)
Rimsky-Korsakov: Scheherazade
Till Eulenspiegel's Merry PranksFriday, May 12, 10 am
Markus Stenz, conductor
Andrew Balio, trumpet
Mozart: Symphony No. 29
Haydn: Trumpet Concerto
Detlev Glanert: Frenesia (BSO Premiere)
Strauss: Till Eulenspiegel Merry Pranks


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Go ahead.... pinch yourself. You're not dreaming!
There is no water more beautiful anywhere in the world than in the Exumas, the magical island chain that encompasses the Central Bahamas. The opulent sapphire color that caresses the stunning, pearl-white sandy beaches of this picturesque archipelago, made up of 365 islands and tiny islets known as "cays," has earned - and rightfully so - a distinctive name all its own: Exuma Blue. Whether you are enjoying a relaxing stroll along the beach or taking a boat tour through the Exuma Cays, you will be awestruck by the many exquisite shades of the sparkling, crystalline blue waters of the Exumas.
But don't take our word for it........come see for yourself! At Cottage Cut Villas, we offer you your own private slice of beachfront paradise. With direct flights from such major cities as Miami, Fort Lauderdale, Atlanta, and Toronto, in as little time as it takes you to lock your office, drive home, pack your toothbrush and bathing suit, and book your tickets, you could already be here... kicked back under a beach umbrella, with your toes buried in the warm, soft sand and a delectable ice-cold beverage in your hand.
At Cottage Cut Villas, we have your utmost relaxation and enjoyment in mind. Each air-conditioned villa has been designed to cater to your every need: 2 spacious bedrooms with 2 queen-size beds and a large private bath in each; television and internet; a fully stocked kitchen with a complete set of pots and pans, cutlery, table dishes, and utensils; and to ensure that you get as much beach time as possible, we have even included an automatic dishwasher! The living and dining areas are quite roomy for families, and the back deck provides plenty of space for those who wish to enjoy the refreshing tropical evening breezes and spectacular sunsets. And there is even an outdoor BBQ grill for those adventurous souls who insist on "roughing it" island style!
Although each villa comes with its own million-dollar beachfront view, you will be delighted to learn that vacationing at Cottage Cut Villas won't bankrupt your wallet. In fact, you will find that the nightly rates at Cottage Cut Villas are much less than what you would pay for a single bedroom unit at many of the local hotels. See Rates.
If your idea of a beach vacation includes boating, kayaking, Scuba diving, or just strolling the beach looking for seashells, you have come to the right place! Let us introduce you to the many unique and exciting things to do at Cottage Cut Villas, in George Town, Exuma!
So............ come on!! What are you waiting for? Let us help you plan that affordable vacation you've been dreaming of!!
Call or email us today, or visit us on Facebook.
** We are delighted to offer a grand-opening discount of 10% to all guests who book a minimum 4-night stay with us between now and December 31, 2011. See rates.


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Customer Care
- We do not accept exchanges at this time.
- We accept returns within thirty (30) days of purchase on regular priced items.
- All sale items are final sale.
- Merchandise must NOT have been WORN, WASHED or ALTERED; and MUST HAVE ORIGINAL HANG TAG ATTACHED.
- Any merchandise returned missing hang tags; in a dirty, worn or poor condition; or without any Return Authorization cannot be refunded. It is then up to the customer to arrange shipping if they would like the item sent back to them.
US & Canada Hassle-Free Returns
- We offer FREE RETURNS (from USA & Canada) for online store credit. We also take care of returns for a refund to your original method of payment (ie. credit card) and will require a handling and processing fee of $5.99 which will be deducted from the amount refunded to you. Original shipping charges are non-refundable.
- If you would like to return an item, please email email@example.com, quoting your order #, within thirty (30) days from the date of receiving your order, so we can issue a Return Authorization # and a UPS return shipping label. Please follow return instructions and do not send back without receiving shipping instructions.
- Returns cannot be processed over the phone.
International Returns
- If you would like to return an item, please email email@example.com, quoting your order #, within thirty (30) days from the date of receiving your order, so we can issue a Return Authorization #. Please follow return instructions and do not send back without receiving shipping instructions. Please write your Return Authorization # on the outside of your package.
- You will receive your refund in the original form of payment. Unfortunately we cannot refund duties, taxes or shipping charges.
Refunds and Processing
- For any items returned outside the 30-day window, refunds are no longer applicable. For items returned between 30-60 days, a store credit will be offered. No refunds or store credits can be offered on items outside the 60-day window.
- Orders are processed within a few hours of receipt. If you need to cancel or change an order, you must make any changes within 2 hours of your order time otherwise your order might already be packed and ready to ship or already in transit.
- The MICHI corporate office and michiny.com can only accept returns of product bought directly from our office or online store. We do not accept returns or exchanges of items purchased at any other retail or online location for any reason. All returns must be made at the store where the garment was originally purchased. The return policy of that retailer will apply.
- For hygienic reasons, please make sure that swimwear and any bottoms are tried on over your own underwear. In the interests of hygiene, we will refuse returns of items where it's obvious that this hasn't been done, or if the hygienic strip has been removed or replaced.
- Once your return has been received and it complies with our returns policy, we will refund you by your original payment method. Unfortunately we cannot refund duties, taxes or shipping charges.
- Gift cards are non-returnable and non-refundable.
- Store Credit can only be used online at our website, www.michiny.com
- Store Credit cannot be transferred to another person.
- Store Credit may not be purchased and is only provided when previously purchased items have been returned.
- Store Credit may be used to purchase gift cards to our store.
- Any purchase amounts that exceed the value of the Store Credit will require an additional method of payment for the remaining balance due.
- Store credit never expires.
- Store credit is provided in U.S. Dollars.
- Hand or machine wash cold, with like colors.
- Bras are ideally washed inside a mesh laundry bag.
- Hang or lay flat to dry.
- Do not put in the dryer.
- Do not dry clean.
- Do not bleach.
I just ordered a new item but my order is taking longer than normal. Is there an issue?
Please note that orders placed during new collection launches may take longer than usual to process and prepare to ship, due to high volume. We do our best to deliver within the delivery time indicated on your order shipments and will inform you if we cannot meet the delivery date.
I am a Canadian but my order shows up in USD?
Given that MICHI is sold globally, all of our online store transactions are completed in US dollars. We are working on a Canadian online store to launch in the near future.
My order won't go through! What's going on?
If you're still receiving an error message after reviewing your credit card information, billing and shipping address, make sure you're using the latest version of your web browser. If the issue persists, please contact your credit card company to ensure there are no holds placed on your card.
Oops! I need to change something on my order.
If you need to change or cancel your order, please contact us immediately at firstname.lastname@example.com. Ensure the subject line has your order number and "Change to Order" in it.
I just made a MICHI purchase. Can I add something else?
Unfortunately, we cannot add items to an existing order. Please place a new order for the item contact us immediately at firstname.lastname@example.com. We'll be happy to waive shipping on this additional order if it was placed within 24 hours of the original order.
My favourite item is sold out! Will it come back in stock?
If the style/size you are looking for is showing as sold out, please contact us at firstname.lastname@example.com to be added to the waitlist so that we can notify you when we get more stock. If that style is no longer being produced, our Customer Service rep will let you know!
When is your next collection launching?
We create two collections per year: Spring/Summer and Fall/Winter. For the inside scoop, sign-up for our MICHI newsletter to hear about exclusive news and releases. Go to our homepage, scroll to the very bottom and enter your email address.
Can I return items that were purchased on sale?
All sale items are final sale and cannot be returned.
I sent my item back for a refund. How long until I get my money back?
Once we have received your package, your refund will be processed within 3 business days. You will be notified via email when this transaction has taken place. Please note that it may take a few business days for the refund to show up on your bank statement.
When will my order ship?
Most orders ship within 1-3 business days of purchase. Shipping times may vary due to availability of merchandise. Remember, orders are not shipped on the weekends or holidays!
Feel free to add a note when placing your order to let us know if you need your MICHI pieces for a specific date! We will do our best to make sure you get it in time.
Where is my order confirmation?
As soon as your order ships, you should receive an email confirmation to the email address you entered on your order. If for some reason, you did not receive an email, please check your junk folder and add firstname.lastname@example.com to your safe sender list.
Will my parcel be charged International taxes and duties?
International orders outside Canada and the US, may be subject to import duties and taxes, which are applied once a shipment reaches your country. MICHI cannot control these potential charges and is not responsible for any duties/taxes applied to your package. To avoid any surprises, please contact your local customs office to determine the charges before you place your order with us! If you refuse a shipment from MICHI, you are responsible for the original shipping charges, any import fees, duties and/or taxes that are incurred on the package, and the cost of returning the package to us. This amount will be deducted from your merchandise refund.
If you want us to re-send the package, you will also be responsible for the shipping costs for a second try!


text:
Ask Health Experts and Get Answers to Your Health Question ASAP
Do you have any boil, abrasion, dandruff on scalp? Are you diabetic?
Dr. Arun
I do not have boils or dandruff, and I'm not diabetic. There is a small abrasion that has been ongoing for over a year that is on the scalp.
The site of this lump denote lymph node enlargement which do get painful if there is an infective problem going on in the draining area (scalp and neck). Usually they are self limiting and resolve on their own. Taking Advil or Motrin would help in resolution. If they persist or symptoms get increased, you will need a course of antibiotics. A small consideration would be of carbuncle or boil which may sometimes initially mimic the acute lymphadenitis (lymph node inflammation).
Please feel free for your follow up questions.
In next 2-3 days it should get better marginally. This would indicate, it is going in remission. If gets worse, in 2-3 days, you will need an evaluation by a doctor. If it is getting better in next couple of days it should go away in a week or so.
Feel free to ask if you have queries.


text:
The Hall H panel for the Aaron Johnson starrer at the San Diego convention is set for Saturday, July 20.
To build fans' anticipation for "Godzilla", Legendary Pictures debuts new Comic-Con poster and a concept art via Skreeonk.com. Though none of them features a full-body shot of the titular monster, fans are still able to at least create their own chilling imagination of how the creature eventually looks like through each snap of body part.
Prior to the official start of the convention on Wednesday, Legendary has built "Godzilla Encounter" to let every Comic-Con attendee feel the Godzilla experience. Fans can secure a pass by visiting the Legendary Booth (#3920) at the convention. For those who unfortunately cannot come to San Diego, there are some snaps courtesy of Collider that can be checked out.
"Godzilla" will hold a Hall H panel at the pop culture event on Saturday, July 20, starting at 10:45 A.M. According to the studio's announcement on Twitter, there will also be cast signing that fans surely cannot miss.
Directed by Gareth Edwards, the upcoming movie stars Aaron Johnson, Elizabeth Olsen, Juliette Binoche, Ken Watanabe and Sally Hawkins.
"Godzilla", which is co-written by Drew Pearce, Frank Darabont and Max Borenstein, is scheduled to stomp theaters in the U.S. on May 16, 2014.


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SAN DIEGO ---- The Padres are expected to introduce their new ownership group at a news conference Wednesday morning at Petco Park.
Major League Baseball's owners approved the O'Malley group earlier this month in Denver, leaving final closing of the $800 million sale as the last obstacle before majority owner John Moores could officially hand off the franchise to former Dodgers owner Peter O'Malley, his sons Brian and Kevin O'Malley, his nephews Peter and Tom Seidler, San Diego businessman Ron Fowler and golfer Phil Mickelson.
The sale was expected to close before Friday. The $800 million price tag includes the $200 million the team received up front as part of its 20-year, $1.2 billion deal with Fox Sports San Diego.
Fowler, chief executive of Del Mar's Liquid Investments, was set to become the controlling owner and executive chairperson.
CEO Tom Garfinkel and general manager Josh Byrnes are expected to retain their positions under the new ownership group.
The O'Malley group is the fifth group to assume ownership of the Padres, following C. Arnholt Smith (1969), McDonald's founder Ray Kroc (1974) and his wife Joan after his death (1984), TV producer Tom Werner (1990) and Moores, who bought the franchise for between $70 and $90 million in 1994.


text:
Nick Kasparie
Nick Kasparie [T. F. B.] (3-30-94 / Quincy, IL.)
Biography of Nick Kasparie
Nick Kasparie Poems
Place Of Dignity
Eyes of gold will seek what troubles the meek Those in the valley aspire to the peak It's hard to get there with these weights on my feet I've been running forever on this hopeless street
Life's Cage (The Short One)
Life's cage is true belligerence And ignorance, its Lock The young die bold The old die cold
An Epigram
To hurry passion is a fault, unwise To wait too long has led to my demise
Kelsey…Kelsey, my heart seems to say In the dead of the night Or the brightness of day Kelsey…Kelsey, the beat never stops
Sonnet Ii
The Sword That's Sheathed I am not one who walks through desert storms I am no hero searching for the truth I walk down paths with those who misinformed
Hero's Path
In one long note, the song is sung. The hopeful dirge has now begun. What started with a coward's cry continues with an honest lie Would arrows shot in parallel bring forth an end to actions fell The first struck hard into the lamb, and soon the second's sure to land
Relief to know these things that grow, Unconscious worries that come and go, Will soon subside and fear abide To rules they've made about suicide
The flower planted long ago Has reached its bitter end No longer is it beautiful It's withered now and gone
Impatience with a body ever slumping and resisting That emotion of a moving, never-ceasing human being In the energetic body of a person caffeinated While this sluggish couch potato on his journeys fabricated
One Last Chance
I didn't know then and I can't say that now, I know all the ins and the outs or the how, But I'm living and learning while still missing you, And it seems pretty clear that you're missing me too.
The shell lies deep beneath the sand It's hidden from the hands of man And long it lies without a touch Awaiting your elusive clutch
A letter on a paper is a pretty petty thing If just a few are added then some words will coalesce And from the words come stanzas as our poem starts to dress With similes to follow and a meter for the ring
Upon Heaven's Doorstep
In haste, you fled, Another dead Among the rest, From Peter's test.
Thoughts Of Nothing Much
His head's a wisp of smoke And it floats above the earth It doesn't see the purpose Of ground or trees or dirt
PoemHunter.com Updates
Check out
Classic Poets
Footsteps of Angels
Henry Wadsworth Longfellow
A Song About Myself
John Keats
A Very Short Song
Dorothy Parker
Relief to know these things that grow,
Unconscious worries that come and go,
Will soon subside and fear abide
To rules they've made about suicide
Hope: it flows, it ebbs and grows
The day of light and dark of night
Coincide at once in me
The frightful dangers soon will flee