Correction for Greilberger et al., Arterioscler Thromb Vasc Biol 17 (11) 2721-2728.

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18:1197.)
© 1998 American Heart Association, Inc.

Corrections

In our article entitled "In vitro interactions of oxidatively modified LDL with type I, II, III, IV, and V collagen, laminin, fibronectin, and poly-D-lysine" (Arterioscler Thromb Vasc Biol. 1997;17:2721–2728), several of the symbols in the figures were incorrectly assigned. The correct symbol assignment is as follows:

(1) In the legend to Figure 2, the symbol for type II collagen should be an open rhombus. (2) In the legend to Figure 6, the open circle is the symbol for native Eu³⁺-LDL; the open rhombus for ox–Eu³⁺-LDL, REM 2.0, 4 hours’ oxidation; and the open triangle for ox–Eu³⁺-LDL, REM 4.9, 24 hours’ oxidation. (3) In the legend to Figure 7, third line from above, the open triangle is the symbol for fibronectin.

Joachim Greilberger Otto Schmut Günther Jürgens

Medical School, Karl-Franzens

Universität Graz, Austria

In Table 1 of our article entitled "Serum total, free IGF-I, and IGFBP-1 levels in an elderly population: relation to cardiovascular risk factors and disease" by J.A.M.J.L. Janssen, R.P. Stolk, H.A.P. Pols, D.E. Grobbee, and S.W.J. Lamberts (Arterioscler Thromb Vasc Biol. 1998;18:277–282), an error has occurred in Table 1 on page 279. The mean free IGF-I level must be 0.092 (SE 0.004) nmol/L; range, 0.020 to 0.283 instead of 0.074 (SE 0.06) nmol/L; range, 0.02 to 0.28.

J.A.M.J.L. Janssen

Dijkzigt University Hospital

Rotterdam, The Netherlands

In our article entitled "Effect of -tocopherol (vitamin E) and ß-carotene supplementation on the incidence of intermittent claudication in male smokers" (Arterioscler Thromb Vasc Biol. 1997;17:3475–3480), a computing error was found that affected the size of the study population. However, this error caused no change in the results or conclusions of the study. The correct figures are as follows:

Twenty-six thousand eight hundred seventy-two participants of the ATBS Study had no intermittent claudication at baseline, and during follow-up, 2578 new cases of intermittent claudication were observed. Compared with placebo, the adjusted relative risk for typical intermittent claudication among those who received -tocopherol was 1.11 (95% confidence interval, 0.99 to 1.23); among those who received both -tocopherol and ß-carotene, 1.04 (0.93 to 1.16); and among those who received ß-carotene, 1.01 (0.90 to 1.13).

Markareetta Törnwall

National Public Health Institute

Helsinki, Finland

In our article entitled "Thrombin-induced thromboxane synthesis by human platelets: properties of an anion binding exosite I–independent receptor" by Ruth Ann Henriksen, Gennady P. Samokhin, and Paula B. Tracy (Arterioscler Thromb Vasc Biol. 1997;17:3519–3526), several errors were introduced during the correction stage. The correct text is as follows:

(1) In the first paragraph on page 3520, the mutation in Thrombin Quick I should be Arg382(67)Cys, where 382 indicates the position in the prothrombin sequence and 67 is the corresponding position in the chymotrypsinogen sequence. (2) The paragraph on page 3523 that appears just before the heading Effects of the Protein Kinase Inhibitor Genistein should read as follows:

The previous observation that treatment of platelets with 2.3 nmol/L thrombin for 5 minutes results in a >90% decrease in antibody binding to the PAR-1 cleavage site³⁶ suggests that functional PAR-1 would not be present after initial treatment with thrombin (Figure 2B) and is consistent with our conclusion that thrombin stimulation of platelets can occur through two receptors. To further characterize the response to thrombin after stimulation with 5 nmol/L thrombin, [Ca²⁺]_i flux, known to be stimulated by thrombin through PAR-1,³¹ was monitored in platelets loaded with fura 2. When these platelets were treated with 5 nmol/L thrombin for 2 minutes, the addition of 100 nmol/L thrombin resulted in no additional [Ca²⁺]_i flux. Thus, maximal thromboxane production is observed in response to thrombin in the absence of any additional [Ca²⁺]_i flux, further differentiating two platelet responses to thrombin.

Ruth Ann Henriksen

East Carolina School of Medicine

Greenville, North Carolina

In our article entitled "Factors of the metabolic syndrome: baseline interrelationships in the first follow-up cohort of the HDDRISC Study (HDDRISC-1)" by Francisco Leyva, Ian F. Godsland, Melek Worthington, Christopher Walton, and John C. Stevenson (Arterioscler Thromb Vasc Biol. 1998;18:208–214), the first sentence of the Acknowledgments was not complete. Full acknowledgments are as follows:

Financial support for the study was provided by the Heart Disease and Diabetes Research Trust, the Cecil Rosen Foundation, and the John Ellerman Foundation.

Ian Godsland

Imperial College of Science, Technology and Medicine

London, England

This article has been cited by other articles:

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