FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 342:823 March 16, 2000 Number 11 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited Related Article by Zipfel, G. J. PubMed Citation

To the Editor: In their review of recent evidence indicating that gelsolin limits excitotoxic necrosis while probably enhancing ischemia-induced apoptosis in cerebral ischemia, Zipfel et al. (Nov. 11 issue)¹ suggest that "the concurrent administration of an antiapoptotic agent may produce further benefits." I assume that they refer to caspase inhibitors, since gelsolin is specifically cleaved by caspase 3 and may in turn activate caspase 3 in a "feedfoward" manner if cleaved. Indeed, the possibility that caspase inhibitors could be used therapeutically in a variety of neurologic and nonneurologic diseases associated with excessive apoptosis has raised high hopes.² However, two notes . . . [Full Text of this Article]

References

This article has been cited by other articles:

• de Perrot, M., Liu, M., Waddell, T. K., Keshavjee, S. (2003). Ischemia-Reperfusion-induced Lung Injury. Am. J. Respir. Crit. Care Med. 167: 490-511 [Abstract] [Full Text]