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1 a mouse model of Sandhoff disease, a lethal gangliosidosis.
2 neuronal apoptosis in the mouse model of GM1-gangliosidosis.
3 of Tay-Sachs disease known as variant AB GM2 gangliosidosis.
4 type II, mucopolysacharidosis type III, GM1 gangliosidosis.
6 of the cardinal pathological features of GM2 gangliosidosis, a point is reached when functional deter
8 t in the autosomal recessive disorders G(M1) gangliosidosis and Morquio B, is synthesized as an 85-kD
9 the nature of the neurological injury in GM2 gangliosidosis and the extent of its reversibility, we h
10 acid beta-galactosidase knockout mice (G(M1) gangliosidosis) and found that the acid beta-galactosida
11 ed neuron-specific Hexb production, reversed gangliosidosis, and ameliorated peripheral sensory dysfu
12 racterizes the neurodegenerative disease GM1-gangliosidosis, but whether the accumulation of GM1 is d
13 ortest lifespan, despite the fact that G(M1) gangliosidosis carrier mice with an otherwise normal gen
16 l of the human lysosomal storage disease GM1-gangliosidosis, GM1-ganglioside accumulates in the glyco
17 asts from patients with Fabry's disease, GM1 gangliosidosis, GM2 gangliosidosis (Tay-Sachs and Sandho
19 te onset Tay-Sachs (LOTS), Sandhoff] and GM1 gangliosidosis have been studied to determine whether th
20 e model of Tay-Sachs disease, a severe human gangliosidosis, indicating that this enzyme is responsib
22 roimaging which are initial findings for GM2 gangliosidosis is important from the point of diagnosis
23 read expression of betagal in the CNS of GM1 gangliosidosis mice is sufficient to achieve significant
26 give new significance to mutations in G(M1) gangliosidosis patients found in the C-terminal part of
27 the frontal cortices of postmortem human GM1 gangliosidosis, Sandhoff disease, and Tay-Sachs disease
28 ith Fabry's disease, GM1 gangliosidosis, GM2 gangliosidosis (Tay-Sachs and Sandhoff forms), metachrom
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