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  • and by analysis of 370 levitra online purchase Nelson and Bruschi TNF genotype in patients presenting with severe acetaminophen-induced hepatotoxicity. The authors note that ISIS 22113 was not effective at higher doses of acetaminophen, which “suggests that a reduction of Fas expression can reduce the severity of liver damage caused by low dose, but cannot completely block the effects of high doses of .” Furthermore, the relative effectiveness of Fas-directed antisense treatments with a more clinically relevant protocol was not examined. Any reductions to the severity of hepatotoxicity would constitute an improvement on current N-acetylcysteine strategies , under these more clinically realistic scenarios. The redundancy in function of proinflammatory mediators is illustrated by the wellconducted TNF/lymphotoxin-α knockout studies of Boess et al. The failure of ISIS 22063 and TNF receptor knockouts to prevent hepatotoxicity at higher doses of acetaminophen argues for the importance of other mediators in the acetaminophen-generated extrinsic pathway, taken collectively.

    Both studies concluded that TNF, or more widely sepsis, was unlikely to be a primary factor in this form of hepatotoxicity. The complex interrelationship between acetaminophen and the extrinsic immune response is also highlighted by an observation that acetaminophen itself can inhibit Fas/CD85 activation at the level of downstream caspase4 activation thereby blocking resultant apoptosis. It would have been of particular interest to determine the relative effectiveness of ISIS 22063 given at increasing intervals after acetaminophen exposure.

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