Hesperides grapefruit body lotion series#

Novotny EJ, Singh G, Wallace DC, et al (1986) Leber's disease and dystonia: a mitochondrial disease. Mita S, Rizzuto R, Moraes CT, et al (1990) Recombination via flanking direct repeats is a major cause of large scale deletions of human mtDNA. Marzuki S, Noer AS, Lertrit P, et al (1991) Normal variants of human mitochondrial DNA and translation products: the building of a reference data base. Howell N, McCullough DA, Kubacka I, Halvorson S, Mackey D (1992) The sequence of human mtDNA: the question of errors versus polymorphisms. Analysis with restriction enzymes of four or five base pair recognition. Horai S, Matsunaga El (1986) Mitochondrial DNA polymorphism in Japanese. Hertzberg M, Mickelson KNP, Serjeantson SW, Prior JF, Trent RJ (1989) An Asian-specific 9-bp deletion of mitochondrial DNA is frequently found in Polynesians. Hasegawa H, Matsuoka T, Goto Y, Nonaka I (1991) Strongly succinate dehydrogenase-reactive blood vessels in muscles from patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. Guazzi GC, Comelio F, Ciacci G, D'Amore I, Paolini E, Federico A (1985) Epilepsy, optic atrophy, ophthalmoplegia, myopathy with raggedred fibers and increased serum pyruvate and lactate content: familial mitochondrial disorder with autosomal dominant transmission and adult onset. IRL Press, Washington DCĭubowitz V (1985) Muscle biopsy: a practical approach. Science 261:765–769ĭarley-Usmar, Rickwood D, Wilson MT (1987) Mitochondria, a practical approach. Ann Neurol 31:391–398Ĭote J, Ruiz-Carrillo A (1993) Primers for mitochondrial DNA replication generated by Endonuclease G. Cell 56:131–139Ĭiafaloni E, Ricci E, Shanske S, et al (1992) MELAS: clinical features, biochemistry and molecular genetics. Genetics 104:699–711Ĭhang DD, Clayton DA (1989) Mouse RNAse MRP RNA is encoded by a nuclear gene and contains a decamer sequence complementary to a conserved region of mitochondrial RNA substrate. FASEB J 6: 2791–2799Ĭann RL, Wilson AC (1983) Length mutations in human mitochondrial DNA.

Genetics 130:139–152īrown MD, Voljavec A, Lott M, et al (1992) Leber's hereditary optic neuropathy: a model for mitochondrial degenerative diseases. Genetics 103:287–312īallinger SW, Schurr TG, Torroni A, et al (1992) Southeast asian mitochondrial DNA analysis reveal genetic continuity of ancient mongoloid migrations. Nature 290:457–465Īquadro C, Greenberg BD (1983) Human mitochondrial DNA variation and evolution: analysis of nucleotide sequences from seven individuals. Clin Exp Neurol 21:1–25Īnderson S, Bankier AT, Barrel BG, et al (1981) Sequence and organization of the human mitochondrial genome. These considerations suggest that the 9-bp insertion is pathogenic and that the region affected by the mutation may play a previously unsuspected functional role in mtDNA gene expression.Īicardi J (1985) Some disorders of the central gray matter in children: clinical and radiological diagnosis.

Hesperides grapefruit body lotion series#

Extensive screening of a large series of DNA samples, collected from unrelated normal individuals as well as patients affected by different neurological disorders, consistently failed to detect the 9-bp insertion, with two exceptions: a patient suffering from a syndrome virtually identical to that described in our original family and a child affected by bilateral striatal necrosis, a disorder which has been attributed to impairment of mitochondrial oxidative phosphorylation. The proband and most of his maternal relatives were affected by a late-onset mitochondrial encephalomyopathy of variable severity, characterized by a unique combination of symptoms. The mutation was contained within the non-coding region between the genes specifying subunit 11 of cytochrome c oxidase and tR-NA Lys. A heteroplasmic insertion of a 9-bp tandem repeat element was detected in the mitochondrial DNA of the maternal members of a large family.