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Lack of involvement of neuronal nitric oxide synthase in the pathogenesis of a transgenic mouse model of familial amyotrophic lateral sclerosis. [Neuroscience. 1999]
Lack of involvement of neuronal nitric oxide synthase in the pathogenesis of a transgenic mouse model of familial amyotrophic lateral sclerosis.
Facchinetti F, Sasaki M, Cutting FB, Zhai P, MacDonald JE, Reif D, Beal MF, Huang PL, Dawson TM, Gurney ME, et al. Neuroscience. 1999; 90(4):1483-92.
Cu/Zn superoxide dismutase (SOD1) mutations associated with familial amyotrophic lateral sclerosis (ALS) affect cellular free radical release in the presence of oxidative stress. [Amyotroph Lateral Scler Other ...]
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Review [Amyotrophic lateral sclerosis: recent insights from transgenic animal models with SOD1 mutations]. [Rinsho Shinkeigaku. 2004]
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Administration of nitric oxide synthase inhibitors does not alter disease course...
Administration of nitric oxide synthase inhibitors does not alter disease course of amyotrophic lateral sclerosis SOD1 mutant transgenic mice.
Ann Neurol. 1999 Mar ;45(3):413-4.

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J Recept Signal Transduct Res. 1999 Jan-Jul ;19(1-4):573-88.

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Mannose-binding lectin (MBL) deficiency. Variant alleles in a midwestern populat...
Mannose-binding lectin (MBL) deficiency. Variant alleles in a midwestern population of the United States.
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Automated collection of quality-of-life data: a comparison of paper and computer...
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Administration of nitric oxide synthase inhibitors does not alter disease course of amyotrophic lateral sclerosis SOD1 mutant transgenic mice.

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