1987
DOI: 10.1016/0002-9149(87)90822-8
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An unusual variant of familial preexcitation

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Cited by 7 publications
(3 citation statements)
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“…Linkage to nine other loci (D7S495, TCRB, D7S498, D7S688, D7S505, D7S642, D7S636, D7S483, and D7S550) was then assessed (Table II). The maximum two-point LOD score, detected with locus D7S505, was 7.80 at a recombination fraction (8) of 0.0 indicating odds of > 60,000,000 to 1 that the locus responsible for disease in Family AS is on chromosome 7q3 (30). The physical location of chromosome 7 anchor marker TCRB places the disease locus at 7q35-7q36 (27).…”
Section: Resultsmentioning
confidence: 99%
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“…Linkage to nine other loci (D7S495, TCRB, D7S498, D7S688, D7S505, D7S642, D7S636, D7S483, and D7S550) was then assessed (Table II). The maximum two-point LOD score, detected with locus D7S505, was 7.80 at a recombination fraction (8) of 0.0 indicating odds of > 60,000,000 to 1 that the locus responsible for disease in Family AS is on chromosome 7q3 (30). The physical location of chromosome 7 anchor marker TCRB places the disease locus at 7q35-7q36 (27).…”
Section: Resultsmentioning
confidence: 99%
“…While most affected individuals appear to be sporadic, screening studies have suggested that at least 3% of probands have a symptomatic affected first degree relative ( 1). Reports of familial WPW have demonstrated an autosomal dominant mode of inheritance (2)(3)(4)(5)(6)(7)(8).…”
Section: Introductionmentioning
confidence: 99%
“…Since Öhnell reported familial WPW syndrome in 2 kindreds in 1944, 1 several other studies of the familial occurrence of WPW syndrome have been reported. [2][3][4][5][6][7] These studies suggested that WPW syndrome may be caused by genetic defects, based on the observations that WPW syndrome developed in infancy or childhood and in multiple generations in certain families.…”
Section: Discussionmentioning
confidence: 99%