Increased Apolipoprotein E ~4 in Epilepsy with Senile Plaques
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چکیده
Dubowics V. Muscle biopsy: a practical approach. 2nd ed. London: Bailliere Tindall, 1985:340-343 Consalez GG, Thomas NST, Stayton CL, et al. Assignment of Emery-Dreifuss muscular dystrophy to the distal region of Xq28: the results of a collaborative study. Am J Hum Genet 199 1 ;48:468 -480 Yates JRW, Warner JP, Smith JA, et al. Emery-Dreifuss muscular dystrophy: linkage to markers in distal Xq28. J Med Genet 1993;30:108-111 Bione S, Maestrini E, Rivella S, et al. Identification of a novel X-linked gene responsible for Emery-!.h-eifuss muscular dystrophy. Nat Genet 1994;8:323-327 Nagano A, Koga R, Ogawa M, et al. Enierin deficiency at the nuclear membrane in patients with Emery-Dreifuss muscular dystrophy. Nat Genet 1996;12:254-259 Manila1 S, Nguen chi Man, Sewry CA, Morris GE. The EmeryDreifuss muscular dystrophy protein, emerin, is a nuclear membrane protein. Hum Mol Genet 1996;5:801-808 Bione S. Small K, Aksmanovic VMA, et al. Identification of new mutations in the Emery-Dreifuss muscular dystrophy gene and evidence for genetic heterogeneity of the disease. Hum Mol Genet 19959: 1 859 -1 863 Klauck SM, Wilgenbus P, Yates JRW, et al. Identification of novel mutations in three families with Emery-Dreifuss muscular dystrophy. Hum Mol Genet 1995;4:1853-1857 Nigro V, Bruni P, Ciccodicola A, et al. SSCP detection of novel mutations in patients with Emery-Dreifuss muscular dystrophy: definition of a small C-terminal region required for emerin function. Hum Mol Genet 1995;4:20032004 Chomczynski P, Sacchi N. Single-step method of RNA isolation by acid guanidium thiocyanate-phenol-chloroform extraction. Anal Biochem 1987;162:156-159 Sambrook J , Fritsch EF, Maniatis 1. Molecular cloning: a laboratory manual. 2nd ed. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press, 1989 Hopkins IC, Jackson JA, Elsas LJ. Emery-Dreifuss humeroperoneal muscular dystrophy: an X-linked myopathy with unusual contractures and bradycardia. Ann Neurol 1981;10:230237 1~393-396
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