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Heart disease among some Japanese may be due to sequencing variation inside a gene

April 9, 2003 (San Diego, CA) -- Previously published epidemiological studies have shown that there are ethnic differences in the prevalence of certain arrhythmogenic (heart-related) diseases. More recent reports indicate that mutations of the human gene SCN5A are linked to heart diseases, such as long QT syndrome type 3 (LQT3) and Brugada syndrome (BS). In a new study being presented today, researchers are suggesting that the sequencing variability inside a disease gene may also play a role in pinpointing heart disease among some ethnic groups.

A New Study
The authors of "A Collection of Nucleotide Variations in SCN5A, A Major Arrhythmogenic Gene, Among the Japanese," are Junko Masuda, George Koike, Hitoshi Kamiunten, and Akira Takeshita, Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan. Dr. Koike will present their findings on behalf of his colleagues during the American Physiology Society (APS) conference, Experimental Biology 2003, being held April 11-15, at the San Diego Convention Center, San Diego, CA.

Methodology
The SCN5A gene (sodium channel, voltage-gated, type V, alpha polypeptide) is responsible for the initial upstroke of the heart's action potential. Mutations of the gene cause a wide variety of arrhythmias, including LQT3, BS, idiopathic ventricular fibrillation and conduction disorder.

During the search for variation in SCN5A, some patients enrolled in a Japanese study were selected for further review: (1) two unrelated long QT syndrome type-3 patients; (2) two unrelated Brugada syndrome patients; and (3) two healthy subjects. Researchers prepared genomic DNA from the blood samples taken from the study subject. All exons covering entire coding region and exon-intron boundaries of SCN5A gene were amplified using PCR technology, and followed by direct sequencing analysis.

Results
The results showed that there were
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Contact: Donna J. Krupa
djkrupa1@aol.com
American Physiological Society
9-Apr-2003


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