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1 t these ophthalmologic manifestations, as in Leber's hereditary optic neuropathy.
2 ad drusen, compressive optic neuropathy, and Leber's hereditary optic neuropathy.
3 and 4917 may play a role in the etiology of Leber's hereditary optic neuropathy.
4 A G11778A mutation, the most common cause of Leber's hereditary optic neuropathy.
5 gene products as well as pathophysiology of Leber's hereditary optic neuropathy and chronic progress
6 nclude disorders of the optic nerve, such as Leber's hereditary optic neuropathy and Kjer-type optic
8 inal ganglion cell function and death, as in Leber's hereditary Optic Neuropathy and suggests novel t
9 ns the three primary pathogenic mutations of Leber's hereditary optic neuropathy, and by correlating
10 otal reports support the use of idebenone in Leber's hereditary optic neuropathy, but this has not be
11 placebo-controlled trial in 85 patients with Leber's hereditary optic neuropathy due to m.3460G>A, m.
12 g the mutation at position 11778 that causes Leber's hereditary optic neuropathy has been transferred
15 1) presented with symptoms characteristic of Leber's hereditary optic neuropathy (LHON) 2 years befor
17 ed mitochondrial optic neuropathies, such as Leber's hereditary optic neuropathy (LHON) and Autosomal
20 DNA (mtDNA) mutations in the pathogenesis of Leber's hereditary optic neuropathy (LHON) has yet to be
21 e mildly deleterious mtDNA mutations causing Leber's hereditary optic neuropathy (LHON) have demonstr
31 drial genome in subunits of Complex I causes Leber's Hereditary Optic Neuropathy (LHON), a specific d
39 d human mutated mtDNA levels responsible for Leber's hereditary optic neuropathy (LHOND), and neuroge
40 skeletal muscle mitochondrial function in 10 Leber's hereditary optic neuropathy patients/carriers wi
41 trolled trial in the mitochondrial disorder, Leber's hereditary optic neuropathy, provides evidence t
42 ation of an MS-like illness in patients with Leber's hereditary optic neuropathy who carry a mitochon
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