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E. Christopher Ellison, MD; Ginny L. Bumgartner, MD, PhD

Arch Surg. 2006;141:1084.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

As demonstrated by Ho et al, CT-1 treatment in a D-gal rat model of hepatic failure had profound antiapoptotic effects and promoted cell repair and proliferation that improved survival. The beneficial effects were observed when animals were treated at 12 and 18 hours after induction of FHF but not at 6 and 24 hours. The authors deduce that the lack of improvement in survival at 6 hours may be due to early generation of suppressors of cytokine signaling and, hence, an inhibition of the beneficial CT-1 actions. If this were the case, one would expect that the suppression could be overcome by increasing the concentrations of administered CT-1, and this can and should be experimentally tested. Equally important would be the identification of such inhibitors. In addition to dose-response curves, given the few numbers of animals in the 6-hour group, it . . . [Full Text of this Article]

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