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1 is the most common molecular abnormality in Pelizaeus Merzbacher disease.
2 ertain human demyelinating diseases, such as Pelizaeus-Merzbacher disease.
3 y linked to another myelin-related disorder, Pelizaeus-Merzbacher disease.
4 of misfolded proteins in the leukodystrophy Pelizaeus-Merzbacher disease activates this stress respo
5 oteolipid protein gene is the major cause of Pelizaeus-Merzbacher disease, an X-linked central nervou
6 g with severe leukodystrophy compatible with Pelizaeus-Merzbacher disease and peripheral neuropathy c
7 elin, including Charcot-Marie-Tooth disease, Pelizaeus-Merzbacher disease and Vanishing White Matter
11 The shaking (sh) pup, an animal model of Pelizaeus-Merzbacher disease, is characterized by severe
13 ical to the initiation of myelination, as in Pelizaeus-Merzbacher Disease, or to enzymatic deficienci
14 nstrate UPR activation in the leukodystrophy Pelizaeus-Merzbacher disease (PMD) as well as in three m
25 continuum of phenotypes ranging from severe Pelizaeus-Merzbacher disease (PMD) to uncomplicated HSP
26 t families with an atypically severe form of Pelizaeus-Merzbacher disease (PMD) who have three, and i
28 In man, mutations of these proteins cause Pelizaeus-Merzbacher disease (PMD), an X-linked dysmyeli
29 astic paraplegia type 2 (SPG2) is allelic to Pelizaeus-Merzbacher disease (PMD), with both conditions
33 e embryonic myelin-deficient rat, a model of Pelizaeus-Merzbacher disease, was performed to assess th
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