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3 multiple tissue-specific diseases, including Emery-Dreifuss (EDMD2/3) and Limb-Girdle muscular dystro
5 r dystrophy (MD) known as autosomal dominant Emery-Dreifuss MD (EDMD-AD) and dilated cardiomyopathy a
7 tations result in laminopathies that include Emery-Dreifuss muscular dystrophy (AD-EDMD) and Hutchins
8 human diseases including autosomal dominant Emery-Dreifuss muscular dystrophy (AD-EDMD), which affec
9 disrupted the expression of genes linked to Emery-Dreifuss muscular dystrophy (EDMD) and centronucle
10 ge of diseases, including autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD) and related dis
11 en found in patients with autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD) as well as dila
17 ntified two patients with genetically proven Emery-Dreifuss muscular dystrophy (EDMD) who followed an
18 utations in nesprin-1/-2 are associated with Emery-Dreifuss muscular dystrophy (EDMD) with conduction
20 ent a diverse group of diseases that include Emery-Dreifuss muscular dystrophy (EDMD), dilated cardio
21 protein, defects in which are implicated in Emery-Dreifuss muscular dystrophy (EDMD), one of the thr
30 en shown to be altered in autosomal dominant Emery-Dreifuss muscular dystrophy (EDMD-AD) and in dilat
32 the overtly aphenotypical model of X-linked Emery-Dreifuss muscular dystrophy (Emd(-/y)) were also i
38 n and are closely linked to the pathology of Emery-Dreifuss muscular dystrophy 1 (EDMD1), a laminopat
39 ype lamins cause several diseases, including Emery-Dreifuss muscular dystrophy and Dunnigan-type fami
40 se a wide range of human diseases, including Emery-Dreifuss muscular dystrophy and Hutchinson-Gilford
41 rigidity is a nonspecific feature, found in Emery-Dreifuss muscular dystrophy and in some congenital
42 revent or delay heart failure in humans with Emery-Dreifuss muscular dystrophy and related disorders
44 des epidemiological information for X-linked Emery-Dreifuss muscular dystrophy and the collagen VI di
46 strongly support gene expression models for Emery-Dreifuss muscular dystrophy by showing that emerin
51 he natural history of cardiac involvement in Emery-Dreifuss muscular dystrophy was described in detai
52 n LB3T-Ig (R454W; LB3T-IgRW), known to cause Emery-Dreifuss muscular dystrophy when present in lamin
53 n the head or tail domain of this gene cause Emery-Dreifuss muscular dystrophy, a childhood-onset dis
55 a broad variety of human diseases, including Emery-Dreifuss muscular dystrophy, dilated cardiomyopath
56 cause a variety of human diseases including Emery-Dreifuss muscular dystrophy, dilated cardiomyopath
57 r neuromuscular disorder, autosomal dominant Emery-Dreifuss muscular dystrophy, DOK7 gene therapy lik
70 minant muscle weakness: Duchenne and Becker; Emery-Dreifuss; distal; facioscapulohumeral; oculopharyn
72 ive multicomponent behavior, as in the Blume-Emery-Griffiths model, and can straightforwardly reprodu
73 the ground state is consistent with a Luther-Emery liquid with power-law superconducting and charge d
75 alone, (2) a saline-wetted cytobrush, or (3) emery paper (600A-grit Wetordry Tri-M-ite; 3M) abrasion
78 olymerase chain reaction-based assay, 45% of emery-paper samples were found to be positive for beta-g
80 are usually closely related to their hosts (Emery's rule) [4-8] and expected to be similar due to co
81 s and their hosts are often close relatives (Emery's rule), and two main hypotheses compete to explai
82 icity within the three-band Hubbard [aka the Emery-VSA (Varma-Schmitt-Rink-Abrahams) model], using cl