hnote

  "I'M NOT THE MESSIAH!!!"
  "Well I say you are and I should know, I've followed a few."

  On the way to the bar I was working up nerve to try the
  master’s lesson on an ordinary girl. After all, you don’t 
  feel so bad disrespecting a bar girl who’s trying to get 
  you to buy her drinks — but a nice, ordinary, Southern girl?

  We went into the bar, and before I sat down, I said, 
  “Listen, before I buy you a drink, I want to know one 
  thing: Will you sleep with me tonight?”

  “Yes.”

  So it worked even with an ordinary girl! But no matter how 
  effective the lesson was, I never really used it after 
  that. I didn’t enjoy doing it that way. But it was 
  interesting to know that things worked much differently 
  from how I was brought up.

  Because our findings showing potential benefits of TNF 
  or TNF agonism for treating AI, it seems paradoxical 
  that anti-TNF therapies are a major therapeutic class 
  of drugs currently marketed for AI. TNF antagonists 
  have provided clinical benefit to about half of AI   patients,
  those with rheumatoid arthritis and Crohn's disease. Yet an 
  expanding body of research in animal models on spontaneous 
  autoimmunity suggests the opposite strategy may be 
  warranted. Furthermore, in humans, several clinical 
  observations deserve mention. First, many Crohn's and 
  rheumatoid arthritis patients never respond to TNF 
  antagonists. Second, long-term treatment with anti-TNF drugs 
  can be accompanied by onset of new or aggravated forms of 
  autoimmunity, sometimes new autoantibodies, suggesting that, 
  for some AIs, anti-TNF therapy may not be the drug of choice .