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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Body iron stores and the risk of coronary heart disease.

BACKGROUND. Recent studies have suggested an association between higher body iron stores and the risk of coronary heart disease. To assess these findings, we examined the association between transferrin saturation and the risk of coronary heart disease, myocardial infarction, overall mortality, and mortality from cardiovascular causes in a large population. METHODS. We studied a total of 4518 men and women from the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study, using a multivariate Cox proportional-hazards model. Base-line data were collected from 1971 to 1974, with follow-up through 1987. Transferrin saturation (serum iron concentration divided by total iron-binding capacity) was used as a measure of the amount of circulating iron available to tissues. RESULTS. The risk of coronary heart disease was not related to transferrin-saturation levels in white men or women. Estimates of the relative risk of coronary heart disease for the fifth quintile of transferrin saturation as compared with the first quintile were 0.72 (95 percent confidence interval, 0.51 to 1.00) for men and 0.85 (95 percent confidence interval, 0.60 to 1.21) for women. The results were similar for myocardial infarction. A significant inverse association with transferrin saturation was found for overall mortality and for mortality from cardiovascular causes in white men and women. Transferrin saturation was not associated with any of the clinical outcomes in blacks, possibly owing to the small sample. CONCLUSIONS. Higher transferrin-saturation levels were not associated with an increased risk of coronary heart disease or myocardial infarction. On the contrary, the results indicate that there may be an inverse association of iron stores with overall mortality and with mortality from cardiovascular causes.[1]


  1. Body iron stores and the risk of coronary heart disease. Sempos, C.T., Looker, A.C., Gillum, R.F., Makuc, D.M. N. Engl. J. Med. (1994) [Pubmed]
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