Correction for Havel and Hamilton, Arterioscler Thromb Vasc Biol 24 (2) 213-215.

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:618.)
© 2004 American Heart Association, Inc.

Correction

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In the January 2004 issue of Arteriosclerosis, Thrombosis, and Vascular Biology, in Figure 1 of the Editorial by Dr. Heistad (Arteriosclerosis, Thrombosis, and Vascular Biology, 2004; pp 1–3), the impact factor is provided for T&H,

but the legend should indicate correctly Thrombosis and Haemostasis.

In the February 2004 issue, in the Editorial by Havel and Hamilton (Hepatic Catabolism of Remnant Lipoproteins: Where the Action Is; pp 213–215), an oversight in the production process allowed the publishing of an incomplete figure.

View larger version (96K): [in this window] [in a new window]   Top left, Receptor-mediated uptake and intracellular processing of triglyceride-rich remnants and cholesteryl ester-rich LDL in rat liver (1988 version), showing passage of lipoproteins through fenestrae in the sinusoidal endothelium, followed by binding to endocytic receptors (Y) on hepatocytic microvilli projecting into the space of Disse (SD). The endocytic receptors migrate with their cargo to coated pits at the microvillar bases where they undergo endocytosis to form primary endosomes. After loss of the clathrin coat and endosome-fusion, the lipoproteins dissociate from the receptors at the acidic pH within the endosome. The lipoproteins are transported within the maturing endosomes toward the biliary (apical) pole of the cells, forming multivesicular bodies (MVB) (late endosomes), whereas the excess surface membrane resulting from endosome-fusion forms recycling endosomes that carry the receptors back to the basolateral surface of the cell (modified from Figure 1 in Havel RJ, Hamilton RL. Hepatocytic lipoprotein receptors and intracellular lipoprotein catabolism. Hepatology. 1988;8:1689–1704.). Top right (2003 version), Enlargement of a basolateral microvillus and adjacent endothelial cell . . . [Full Text of this Article]