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Yesterday, May 8, 2010, the New York Yankees and the Boston Red Sox played a game at Fenway Park that celebrated the 107th anniversary of their first meeting on May 7, 1903. The Yankees won this time, but Boston won in 1903. And it wasn’t even the Yankees all those years ago; it was the New York Highlanders.
As is its custom, The New York Times published the complete box score, all the players, hits, time of the game and so forth, but because this was an anniversary, they also published the box score and a story from 1903. Another reason was that the game yesterday lasted over three hours and the game in 1903 lasted but 98 minutes, and this was part of the story. Ordinarily, I wouldn’t pay too much attention to a story like this except something caught my eye in the old box score, the kind of thing that grabs you with a glance for a reason you can’t easily explain. It was the name of the pitcher for New York. His name was Wiltse, an uncommon name.
In the early and mid-1950’s I was a baseball nut and on the evening of September 18, 1954 found myself at a meeting of the Syracuse, New York Hot Stove League with a bunch of other baseball nuts, mostly much older baseball nuts. These older guys didn’t have an excuse for their nuttiness. I did because I was only a kid. I don’t remember any of the details of that day except for one and that’s only because I have a scrap of paper inscribed George “Hooks” Wiltse New York Giants 1904-1914 September 18, 1954. He was the honored guest that evening and I got an autograph. He probably made a bit of a speech and answered questions. At the time he was 75 and his handwriting was a little shaky. As I looked at the old box score, I wondered if this was the same Wiltse that pitched for the other New York team in 1903? I was pretty sure it was.
The Baseball Encyclopedia said no. There was another Wiltse, an older brother, who bounced around for a minute or two with Pittsburgh, Philadelphis and finally New York but wasn’t nearly as good a pitcher as Hooks. The brother was known as Snake, but his name was much more unpleasant that his fastball and the game against Boston was his next to last in the bigs forever. The following year Hooks joined the Giants and, working in tandem with Christy Mathewson, the two won 435 games.
But I’m glad the name, even if it was wrong brother, caught my attention. It was fun to compare the box score and there’s no puzzle in why the game lasted so much longer in 2010. This year, the Yankees had 11 hits and 10 runs; Boston had 9 hits and 3 runs. In 1903 the Red Sox had 13 hits and 6 runs, New York had 6 hits and 2 runs. Twenty hits versus 19; 13 runs versus 8; two doubles and one home run in 2010; the same in 1903. There was one big difference; one player, Chick Stahl, hit two triples. I had to look him up; I’d never heard of Chick Stahl and in looking at his record it was puzzling to see he played for one or the other Boston teams from 1897 to 1906 and then died shortly before the 1907 season was to begin. He was only 34. There’s probably a sad field of dreams-like story there.
Back to the big difference, the length of the game. This is why. In 1903 nine men played for each team, one pitcher, each of who pitched a complete game, no substitutes, no pinch hitters, pinch runners, no designated hitters, and no relief pitchers. No trips to the pitcher’s mound, nothing that might delay the game. In 2010 there were twenty-nine players, including a pinch hitter for a designated hitter and six pitchers.
I don’t know if the game in 1903 was any better than the game in 2010, but this year’s game was certainly longer, over-thought, over-computerized, over-strategized, and employed too many people measuring the speed of fastballs and every other kind of thing. Or perhaps the thinking is that if someone is paying a lot of money for a skybox seat, they should be able to stick around as long as possible to get their money’s worth and eat every last morsel of complimentary food. But I wonder if anyone in all of major league baseball has had two triples in one game this year? I kind of doubt it and to see some guy dashing around the bases and beating the throw to third is a bit more exciting than counting pitches, the endless waiting for yet another relief pitcher to face one batter or watching some guy run slowly around the bases after a home run.
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And finally, have fun trying new and different techniques, positions, accessories, etc. There is hope for ED, and you can have a fulfilling and satisfactory sex life. Dont put too much pressure on yourself. Enjoy!
Intracavernosal administration of alprostadil (Caverject) has reported success rates of 67 to 85 percent and has been used in the treatment of erectile dysfunction for several years.11 When injected directly into the corpus cavernosum, alprostadil (prostaglandin E1) acts on the arteriolar smooth muscle cells, causing them to relax and produce an erection, usually within several minutes. Its mechanism of action is to stimulate an increase in the levels of intracellular cyclic nucleotides that cause relaxation. The usual dose is between 5 and 40 g per injection. The current average wholesale price ranges from about $86 for six of the 5-mg doses to approximately $163 for six of the 40-g doses.12 Patients usually start at 2.5 g and titrate up in 5-g increments for effect, with a maximum dose of 60 g. No more than three injections per week are recommended, with a minimum period of 24 hours between injections.13 Initial dosing and required adjustments should be carried out in the physician's office.
Gr-1+ cells are known to facilitate tumor outgrowth. As such, it is conceivable that strategies seeking to eliminate this population may have a measurable antitumor effect. In certain tumor models, the Gr-1 depleting antibody inhibited tumor outgrowth even in the absence of T cells, although the antitumor effect was more pronounced in immune competent mice (32, 33). In light of these results and to verify that MDSCs are the target of sildenafil-mediated antitumor activity, we examined the effect of antibody-mediated MDSC depletion in combination with PDE5 inhibition in vivo. BALB/c mice were challenged on day 0 with C26GM tumor and were (a) left untreated; (b) injected with 100 g of antiGr-1 antibody i.p. on days 0, 3, and 6; (c) treated with sildenafil; or (d) treated with a combination of the two treatments. As shown in Fig. 6 E, Gr-1 depletion delayed tumor outgrowth similarly to PDE5 inhibition, whereas no synergistic effect was seen with the combination. Collectively, these data demonstrate the immunosuppressive nature of Gr-1+ cells and the ability of PDE5 inhibition to reduce their suppressive phenotype in vivo.
A study published in Psychology of Men and Masculinity (2006) reported the results of an Internet survey of more than 52,000 heterosexual men and women on the topic of penis size, self-image and women's perception of, and satisfaction with, their partners' penis size. The very large sample size permitted researchers to detect the smallest differences among responses.
In the same issue of the journal, Dr. Steven A. Grover and colleagues studied a group of 3,912 Canadian men, nearly half of whom reported having erectile dysfunction in the four weeks prior to visiting their family physicians. The men's cholesterol, glucose and blood pressure measurements were taken.
The Massachusetts Male Aging Study surveyed 1709 men aged 4070 years in the greater Boston area between 1987 and 1989 and reported a prevalence of erectile dysfunction of 52%, with 9.6% of respondents reporting complete erectile dysfunction.5 In 2000 the overall prevalence of erectile dysfunction in this study population was re-estimated to be 44%.6 The Massachusetts study is important because it is the first cross-sectional, community-based, random-sample multidisciplinary survey on the topic and involved a significant cohort followed up for nearly a decade beyond the initial assessment. A survey of 3009 men aged 1870 years from all regions of Canada revealed a similar prevalence of erectile dysfunction.7
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Were talking about blood flow in the male penile shaft, explains urologist Ajay Nehra, MD, professor of urology at the Mayo Clinic in Rochester, Minn. Arteries in both the heart and the penis are lined with endothelium, says Dr. Nehra. When the endothelium in these blood vessels doesnt respond well to the release of nitric oxide (a key part of the chain reaction that allows blood to flow as needed), then blood doesnt flow into organs, including the penis.
Are there physical causes of erectile dysfunction? A prior history of cigarette smoking, heart attacks, strokes, and poor circulation in the extremities suggest atherosclerosis as the cause of the erectile dysfunction. Diminished sensation of the penis and the testicles, bladder dysfunction, and decreased sweating in the lower extremities suggest diabetic nerve damage. Loss of sexual desire and drive, lack of sexual fantasies, gynecomastia (enlargement of breasts), and diminished facial hair suggest low testosterone levels.
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Excessive stress can also lead to the blood pressure and diabetes problems that lead to the erectile dysfunction in men. Continuous exposure to the stress makes you prone to the heart disorder and thus you suffer from the creation problems during the sexual intercourse. Even short-term stress may affect sexual functioning for the reason that the body is not designed to perform sexually while fighting or running away. However, in the case of short-term stress, the body should be able to respond sexually once the stress is gone. With long-term stress, once the stress has passed, the patient may have to treat any remaining stress-related disease in order to restore sexual function.
Erection involves the integration of neural and vascular functions. In essence, an erection occurs when blood flow to the penis exceeds flow out of the penis. The cavernosal arteries supply blood to the corpora cavernosa of the penis (through the pudendal artery); the emissary veins running through the tunica albuginea allow drainage. During erection, relaxation of trabecular smooth muscle results in increased blood flow to the corpora cavernosa and expansion of the sinusoids therein. This distension causes mechanical compression of the emissary veins, which impedes their ability to drain blood and thereby results in penile rigidity8 (Fig. 1).
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