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1 ), which had been detected in a patient with sporadic amyotrophic lateral sclerosis.
2 otrophic lateral sclerosis and patients with sporadic amyotrophic lateral sclerosis.
3 t common genetic abnormality in familial and sporadic amyotrophic lateral sclerosis (ALS) and frontot
4 mately 20-50% of familial and up to 5-20% of sporadic amyotrophic lateral sclerosis (ALS) cases, maki
6 d peroxidation, in the lumbar spinal cord of sporadic amyotrophic lateral sclerosis (ALS) patients ve
8 D1) could be pathogenic in both familial and sporadic amyotrophic lateral sclerosis (ALS) through eit
10 as been directly linked to both familial and sporadic amyotrophic lateral sclerosis (ALS), a devastat
11 Here we use cross-ethnic genetic data in sporadic amyotrophic lateral sclerosis (ALS), an adult-o
12 may influence pathophysiologic mechanisms in sporadic amyotrophic lateral sclerosis (ALS), the associ
19 ostmortem brain samples from 9 patients with sporadic amyotrophic lateral sclerosis and from 9 contro
20 s to first degree relatives of patients with sporadic amyotrophic lateral sclerosis attending a speci
21 ndividuals who had originally presented with sporadic amyotrophic lateral sclerosis, but who subseque
22 fication of TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis cases confirms it
23 e been observed in cytoplasmic inclusions in sporadic amyotrophic lateral sclerosis cases, suggesting
26 27/63 (43%) familial, 35/500 (7%) cases with sporadic amyotrophic lateral sclerosis/motor neuron dise
27 cerebrospinal fluid (CSF) of a patient with sporadic amyotrophic lateral sclerosis (sALS) compared w
29 otassium (K+) currents have been reported in sporadic amyotrophic lateral sclerosis (SALS) phenotypes
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