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When F.C. Revved Up to Ignore Info on Football Dangers
Editor,
I appreciated your column about football injuries. In the mid 80's when my wife was school board chairman a child from Winchester ruptured his spleen during a Mustang game and died on the way home.
At that time our local team had not been winning very often, and the preparation of the athletic fields was a major budget expense. Concurrently my pediatric journals had several articles about the frequency and severity of football injuries. I mentioned to my wife, the chairman, that Falls Church should seriously reevaluate its commitment to football. She said that if I felt strongly about it I should make a presentation to the school board. I agreed and spent time gathering facts and prepared a statement for the meeting.
The word had apparently leaked out about my intentions, so when I arrived at the council chamber the left and center sections were totally full. Cheerleaders in uniform, football players in uniform shirts, parent athletic boosters in team shirts and enough students and parents were there to fill every available seat in those sections. The right side of the chamber was totally empty. When I arrived someone came over to me, pointed to the empty section and said, "Dr. Salsbury, that is your side." When the time came I made my presentation with lots of statistics and a recommendation that we put more emphasis on other less injurious sports. Then the other pro football side spoke-one after another. After well over an hour there were still many waiting to speak, and the board needed a break. After a break many more spoke about the value and importance of football. One woman said that it wasn't our child that died, so why should our football program suffer. The board voted unanimously to continue its support to the football program. The audience cheered, and I left quietly through a different door.
Because of comments such as yours parents, coaches and trainers are much more aware of the dangers of repeated head trauma than they were 30 years ago. This is a major advance in public awareness that will benefit scores of young athletes who insist they are immortal.
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Outlawing Football Would Drive It Underground
Editor,
The News-Press hit the trifecta for the week of December 8.
First, since I am not a citizen of the City of Falls Church, I am not represented by or have the right to vote for David Snyder. But I have the privilege of calling him a friend. A good friend who speaks with knowledge and wisdom. So when he speaks out for the good of the community, listen carefully, learn and act. His recent commentary should convince you to support his ideas about a light rail system that will benefit us all. Thanks, Dave!
As for Nicholas Benton's coluimne on outlawing football.
Dear Mr. Benton, My high school's first principal lost his son in a high school game therefore my school never did have a team. But injuries are sometimes the collateral damage of contact sports which is more than just a game. It's a business that employs tens of thousands of people at many levels and generates billions of dollars in revenue not just for owners and players but for vendors, advertisers, consumer products.
If the game were made illegal it would go underground, drop regulations, change the rules and cause greater damage to the participants. These contact sports are evolving and have made and are making changes to make them safer but not totally free from injury. Evolution takes time, and if we outlaw too many activities we'll spend the rest of our lives...reading your editorials. And when Helen Thomas asks the musical question, "Is that all there is?", about who the Republicans will choose to be their standard bearer...maybe the question should read, "Who will be their substandard bearer?"
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The Falls Church News-Press welcomes Letters to the Editor. Deadline for Letters is 5 p.m. Monday each week. Letters should be 350 words or less. All letters printed become property of the Falls Church News-Press and may be edited for clarity and length. Click via our form or use one of the contact methods below.
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To listen to us campaign for City Council, you'd think the only problem we have in the City of Falls Church is a lack of development and that our success ...
Paul Handly | Thursday, 29 March 2012
Having finished the "long" (60-day) session of the General Assembly, both Houses of the General Assembly adjourned to consider competing budgets. The subcommittees of the two budget committees, Senate Finance an...
Jim Scott | Tuesday, 3 April 2012
Spring? Summer? What happened to winter? March's abnormally warm weather brought out gorgeous blossoms and early garden preparations, but it also brought a handful of residential burglaries to our community. Je...
Penny Gross | Thursday, 29 March 2012
The New York Times had a revealing article that stated: "Big business groups like the Chamber of Commerce spent millions of...
Wayne Besen | Wednesday, 4 April 2012
President Obama's forceful speech and Q & A at the Associated Press luncheon Tuesday included a sorely-needed critique of the ...
Nicholas F. Benton | Wednesday, 4 April 2012
As a father, I know how strongly we all want the best possible future for our children, one that's happy, ...
James Moran | Tuesday, 3 April 2012
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The following cell lines were used: CT26, a carcinogen-induced, undifferentiated colon carcinoma obtained from BALB/c mice (51); TS/A, a mouse mammary adenocarcinoma derived from BALB/c mice (52); MCA203, a C57BL/6-derived fibrosarcoma (53); and B16-GM, a C57BL/6 melanoma cell line genetically modified to secrete GM-CSF (54). The 4T1-HA cell line was obtained by lentiviral transduction of 4T1 mammary carcinoma and was provided by K. Whartenby (Johns Hopkins University, Baltimore, MD). These cell lines were grown in DMEM or RPMI 1640 (Invitrogen) with 10% FBS (Invitrogen). The C26GM cell line derived from the C26 colon carcinoma was genetically modified to produce GM-CSF (8) and was grown in the presence of 800 µg/ml G418.
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Evidence of an immune-mediated, antitumor effect of PDE5 inhibition is further shown by tetramer analysis on splenocytes obtained from sildenafil-treated, CT26WT tumor- bearing mice, which revealed a higher number of CTLs specific for AH-1 (unpublished data), a CT26 tumor-associated antigen, as compared with their untreated counterparts (19). To confirm immune-mediated antitumor activity in the sildenafil-treated groups, we performed an in vivo cytotoxicity assay. BALB/c mice were injected with PBS (naive), vaccinated with -irradiated CT26WT or C26GM, or challenged with CT26WT or C26GM tumors on day 0. On day 12 (CT26WT) or day 5 (C26GM), all mice received carboxyfluorescein diacetate succinimidyl ester (CFSE)–labeled splenocytes pulsed with the MHC class I–restricted AH-1 peptide (CFSEhigh), admixed with CFSE-labeled splenocytes pulsed with the irrelevant hemagglutinin (HA)-peptide (CFSElow). In vivo T cell cytotoxicity was determined 40 h later (Fig. 2). These time points were chosen based on the kinetics of tumor outgrowth observed in Fig. 1 A and Fig. 1 B, respectively, when tumor size significantly differed between untreated and sildenafil-treated mice. As expected, an endogenous AH1-specific immune response was observed in the vaccinated mice as compared with their tumor-bearing counterparts. PDE5 inhibition in the vaccine-primed mice failed to augment antigen-specific CD8 responsiveness compared with no treatment. In contrast, tumor-bearing mice treated with sildenafil early after tumor challenge generated antigen-specific immunity that was significantly greater then that observed in their untreated counterparts and similar, or even superior, to that induced by vaccination. Collectively, this is the first indication that PDE5 inhibitors can modulate antitumor immunity. Because the sildenafil-mediated antitumor immune response does not completely eradicate tumors, tumor escape mechanisms may be associated with their outgrowth. To test this hypothesis, the parental CT26WT cell line, as well as the CT26 tumor removed on day 24 from sildenafil-treated mice (either AH-1 pulsed or unpulsed), and BALB/c splenocytes were incubated with either AH-1 peptide-primed (Fig. S1 C) or tumor-primed (Fig. S1 D) effector T cells. Although effector T cells recognized the parental CT26WT line and released IFN- in the assay, they failed to recognize the sildenafil-derived tumor. Its recognition, however, was restored by loading the sildenafil-derived tumor with the AH-1 peptide. (Fig. S1, C and D). These results suggest that the immune response in sildenafil-treated mice does not result in complete tumor eradication but rather in the selection of antigen-escape variants.
CORRESPONDENCE Ivan Borrello: borreiv@jhmi.edu
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The Falls Church News-Press welcomes Letters to the Editor. Deadline for Letters is 5 p.m. Monday each week. Letters should be 350 words or less. All letters printed become property of the Falls Church News-Press and may be edited for clarity and length. Click via our form or use one of the contact methods below.
