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In this essay I’ll explain the way in which the Ouroboros in the Fourth Edition of Dungeons & Dragons differs from the original Dungeons & Dragons of its inaugural edition. The basic idea is the same: the snake consumes its own tail, and both the snake and its tail move on while becoming increasingly ever-more-intimate to each other. Both editions have two things in common, too: balance and balance. (What balance in a game is, and what is balanced, is a question for another essay, or for a whole book, or for a lifetime.)

We start with the first thing I mentioned, and that is the way that the Ouroboros of the Fourth Edition of Dungeons & Dragons is unlike its original counterpart. Most notably, the original Ouroboros is actually an undead critter; in other words, a creature that is animated by a deity. As such, it was a fairly powerful critter. I mean, even if you kill the god and set the Ouroboros to wail and gnash its teeth, someone else could basically just animate it with the same god’s power. The Fourth Edition Ouroboros is neither animated nor immortal, hence the addition of the “razor” element to the designation, to make sure the Ouroboros can’t ever be restored to a god’s favor.

The Second Thing We Have in Common is that We Both Feature Very Balanced Features. Or at Least I Do.

The original Fourth Edition Ouroboros

Nov 22, 2017
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The antimalarial drug quinine and the anti-tuberculous drug rifampicin induced increases in cyclic AMP accumulation in human erythrocytes. This response was blocked by the beta 2-agonist salbutamol. Rifampicin and quinine, which are effective in the treatment of falciparum malaria and tuberculosis, respectively, were also synergistic in their effects in increasing cyclic AMP accumulation. Treatment with these drugs increased the number of inhibitory receptors on the cell surface. In contrast, a thiosemicarbazone, a low-toxicity analog of an antimalarial drug, did not change the number of receptors. The effects of quinine, rifampicin and salbutamol on cyclic AMP accumulation showed a threshold in the concentration of the drugs required to achieve optimal stimulation of the cells. The optimal concentration in the case of quinine, an antimalarial drug, was at about 10(-4) M, in the case of rifampicin, an antituberculous drug, it was at about 0.1 micrograms/ml, and in the case of salbutamol, an inhaled beta 2-agonist, it was at about 100 micrograms/ml. Similar concentrations of these drugs were required to induce optimal inhibition of the cyclic AMP response. In patients receiving treatment with these drugs at a given concentration a decrease in the cyclic AMP response was seen to occur in parallel with increased antimalarial and/or antituberculous resistance. The changes in cyclic AMP metabolism described here may relate to the established antimalarial and anti-tuberculous activities of these drugs.

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