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1 tem for understanding the molecular basis of adrenoleukodystrophy.
2 evelop life-threatening progressive cerebral adrenoleukodystrophy.
3 NA, is being tested in persons with cerebral adrenoleukodystrophy.
4 inical studies for the treatment of cerebral adrenoleukodystrophy.
5 azone might slow the progression of cerebral adrenoleukodystrophy.
6 isease, as devastating as childhood cerebral adrenoleukodystrophy.
7 plantation in boys with early-stage cerebral adrenoleukodystrophy.
8 evere neurological manifestation is cerebral adrenoleukodystrophy.
9 nd potential alternative approaches to treat adrenoleukodystrophy.
10 ute to the biochemical pathology of X-linked adrenoleukodystrophy.
11 inflammatory cerebral phenotypes of X-linked adrenoleukodystrophy.
12 involved in cerebral phenotypes of X-linked adrenoleukodystrophy.
13 this enzyme in the pathogenesis of X-linked adrenoleukodystrophy.
14 may be facilitated by newborn screening for adrenoleukodystrophy.
15 stem cell transplantation in adult cerebral adrenoleukodystrophy.
16 he childhood-onset cerebral form of X-linked adrenoleukodystrophy, a demyelinating disorder of the ce
22 .7 kb segment encompassing exons 7-10 of the adrenoleukodystrophy (ALD) locus of the X chromosome has
24 ansporter that is 42% identical to the human adrenoleukodystrophy (ALD) protein, which is defective i
26 all molecule inhibitors for the treatment of adrenoleukodystrophy (ALD), we conducted a high-throughp
32 el therapy in boys with early-stage cerebral adrenoleukodystrophy and evidence of active inflammation
33 nstrated by contrast enhancement in cerebral adrenoleukodystrophy and is an early sign of lesion prog
34 e therapy, most patients with early cerebral adrenoleukodystrophy and MRI abnormalities had no major
35 ents with neuroinflammatory diseases (e.g. X-adrenoleukodystrophy and multiple sclerosis) suggest tha
37 the multiple gene mutations responsible for adrenoleukodystrophy and possible mechanisms for the gen
38 Twenty patients with different phenotypes of adrenoleukodystrophy and seven age-matched controls were
40 S without recurrence of symptoms of cerebral adrenoleukodystrophy, and 1 patient died from presumed g
41 dysplasia punctata, Refsum disease, X-linked adrenoleukodystrophy, and deficiency of mitochondrial me
42 logic disorders Zellweger syndrome, neonatal adrenoleukodystrophy, and infantile Refsum disease and a
43 europathy is the late-onset form of X-linked adrenoleukodystrophy, and is considered the most frequen
45 ties may be important in the pathogenesis of adrenoleukodystrophy, and that a mutant myelin protein c
47 lateral sclerosis (ALS) and active cerebral adrenoleukodystrophy are encouraging further development
48 umulate in tissues of patients with X-linked adrenoleukodystrophy, are activated by very long-chain a
49 ctroscopy have been well studied in X-linked adrenoleukodystrophy, but no data exist on magnetic reso
56 rrier disruption marks the onset of cerebral adrenoleukodystrophy (CALD), a devastating cerebral demy
57 eported for patients with childhood cerebral adrenoleukodystrophy (CCALD) who had received haematopoi
58 deletion was diagnosed with active cerebral adrenoleukodystrophy characterized by demyelination and
59 oleukodystrophy is a severe form of X-linked adrenoleukodystrophy characterized by white-matter disea
60 ssive inflammatory demyelination in cerebral adrenoleukodystrophy coincides with blood-brain barrier
63 e partially restored in transfected X-linked adrenoleukodystrophy fibroblasts regardless of the chime
68 ts with childhood onset of cerebral X-linked adrenoleukodystrophy have been followed for 5-10 years a
72 homozygous for Zellweger syndrome, neonatal adrenoleukodystrophy, infantile Refsum's disease, and in
74 adult cerebral inflammatory form of X-linked adrenoleukodystrophy is a rapidly progressive neurodegen
78 ientific commentary on this article.X-linked adrenoleukodystrophy is caused by mutations in the ABCD1
83 imal models have been developed for X-linked adrenoleukodystrophy, metachromatic leukodystrophy and Z
86 sease progression in advanced adult cerebral adrenoleukodystrophy (n = 1), or secondary disease progr
87 m, Zellweger syndrome (ZS), through neonatal adrenoleukodystrophy (NALD) to the least severe form, in
88 linical variants within the PBDs is neonatal adrenoleukodystrophy (NALD), a disease that is usually a
89 verse event, clinically progressive cerebral adrenoleukodystrophy, occurred in six [5%] of 116 patien
91 ion of this protein in cells from a neonatal adrenoleukodystrophy patient specifically defective in P
97 somal ATP-binding cassette half-transporter, adrenoleukodystrophy protein (ALDP), are the primary cau
99 d sequence identity with two human proteins, adrenoleukodystrophy protein and peroxisomal membrane pr
101 somal-membrane proteins, including the human adrenoleukodystrophy protein, required for the efficient
102 omal disorders, is caused by the lack of the adrenoleukodystrophy protein, with an accumulation of ve
103 ing, encodes a peroxisomal membrane protein (adrenoleukodystrophy protein; ALDP) that belongs to the
104 eatment, an increase in transcription of the adrenoleukodystrophy-related gene and the peroxin gene,
106 ients with childhood-onset cerebral X-linked adrenoleukodystrophy shows the long-term beneficial effe
107 evaluate the new information about X-linked adrenoleukodystrophy that has been reported in 2002 and
108 ons in the gene encoding ALDP cause X-linked adrenoleukodystrophy; the role of ALDR and PMP70 in huma
109 data from 14 adult males with adult cerebral adrenoleukodystrophy treated with allogeneic haematopoie
110 Median age at diagnosis of adult cerebral adrenoleukodystrophy was 33 years (range 21-48 years).
111 g lesions suggestive of progressive cerebral adrenoleukodystrophy were randomly assigned (2:1 without
112 mmatory myeloneuropathic variant of X-linked adrenoleukodystrophy, where the disease process appears
113 st frequent peroxisomal disorder is X-linked adrenoleukodystrophy, which is caused by mutations in AB
114 n ABCD1 cause the neurodegenerative disease, adrenoleukodystrophy, which manifests as the spinal cord
115 used procedure for the diagnosis of X-linked adrenoleukodystrophy (X-ALD) and other peroxisomal disor
116 to study the phenotype evolution of X-linked adrenoleukodystrophy (X-ALD) and the relation between ax
117 sor imaging (DTI), in children with X-linked adrenoleukodystrophy (X-ALD) before and after haematopoi
118 assay, we determined the number of X-linked adrenoleukodystrophy (X-ALD) hemizygotes from the United