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1 rains from this mouse model of Tay-Sachs and Sandhoff disease.
2 storage diseases: NPC, mucolipidosis IV, and Sandhoff disease.
3 ivation also was detected in a human case of Sandhoff disease.
4 -deficient mice, a model of the neuronopathy Sandhoff disease.
7 in neurodegeneration using a mouse model of Sandhoff disease, a prototypical neuronopathic lysosomal
10 n as the AB variant), Tay-Sachs disease, and Sandhoff disease are the major forms of the GM2 ganglios
14 GM2 gangliosidoses, including Tay-Sachs and Sandhoff diseases, are neurodegenerative lysosomal stora
16 olipid storage diseases, NPC2 deficiency and Sandhoff disease, characterized by sphingolipid traffick
17 he results indicate that the pathogenesis of Sandhoff disease involves an increase in MIP-1alpha that
21 that their lack of storage in Tay-Sachs and Sandhoff diseases is due to functional redundancy in the
22 crophage/microglial population in the CNS of Sandhoff disease mice is compounded by the infiltration
24 sphingosine kinase 1 (Sphk1) was deleted in Sandhoff disease mice, a milder disease course occurred,
29 ganglioside accumulation in a mouse model of Sandhoff disease might be associated with the accumulati
30 is phenotype is not seen in the Tay-Sachs or Sandhoff disease model mice or in the corresponding huma
36 ents a 22-month-old girl with infantile type Sandhoff disease that was hospitalized for generalized s
37 exb gene (hexb-/-), a model of Tay-Sachs and Sandhoff disease, versus the functionally normal heteroz
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