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Previous Volume 334:270-271 January 25, 1996 Number 4 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.

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To the Editor: We were quite surprised that the remarkable review of mitochondrial DNA and disease by Johns (Sept. 7 issue)¹ ended with the assumption that the American cyclist Greg LeMond retired in 1994 because of a "mitochondrial myopathy." The genetics of mitochondrial DNA still present several enigmas, and certain mutations can be present at birth and become clinically manifest only in adulthood.² Nevertheless, we think that the ATP-generating capacity of Greg LeMond's muscles should have fallen below their energy threshold well before 1993, the year of his last Tour de France race. The mitochondrial genome has an underdeveloped DNA-repair . . . [Full Text of this Article]

References

This article has been cited by other articles:

• ODAWARA, M., MAKI, H., YAMADA, N. (1999). Pathogenicity of homoplasmic mitochondrial DNA mutation and nuclear gene involvement. J. Med. Genet. 36: 934-935 [Full Text]