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 338:919-920 March 26, 1998 Number 13 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 Braunwald, E. PubMed Citation

To the Editor: The Shattuck Lecture by Dr. Braunwald (Nov. 6 issue)¹ provided an outstanding overview of cardiovascular medicine and science. In the section entitled "Transgenic Techniques," apolipoprotein (apo) A-I– and apo E–deficient mice are described as genetically engineered mouse models of atherosclerosis. Though that is true for apo E–deficient mice, it is not for apo A-I knockouts.

Lipoprotein risk factors for atherosclerosis include low levels of high-density lipoprotein (HDL) or high levels of apo B–containing lipoproteins, such as low-density lipoprotein (LDL) or remnant lipoproteins. In humans and mice, apo A-I levels determine HDL levels, whereas apo E is necessary . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Potier, M., Karl, M., Elliot, S. J., Striker, G. E., Striker, L. J. (2003). Response to sex hormones differs in atherosclerosis-susceptible and -resistant mice. Am. J. Physiol. Endocrinol. Metab. 285: E1237-E1245 [Abstract] [Full Text]  
• Mestroni, L. (2003). Genomic medicine and atrial fibrillation. J Am Coll Cardiol 41: 2193-2196 [Full Text]