Research article
Intravenous immune globulin in hereditary inclusion body myopathy: a pilot study
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* Corresponding author: William A Gahl bgahl@helix.nih.gov
1 Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA
2 Department of Genetics and Metabolism, Children's National Medical Center, Washington DC, USA
3 Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
4 Department of Rehabilitation Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, USA
5 George Washington University School of Medicine and Health Sciences, Washington DC, USA
6 University of Maryland, Department of Hearing and Speech Sciences, College Park, MD, USA
BMC Neurology 2007, 7:3 doi:10.1186/1471-2377-7-3
Published: 29 January 2007Additional files
Additional file 1:
Isoelectric focusing of serum transferrin and Apo C-III. A. Normal sialylation of transferrin (N-linked glycoprotein) in all four patients before IVIG (Pre), after IVIG loading (Mid), and after the treatment period (Post). Samples of patients 3 and 4 were electrophoresed on a gel different from the gel for samples 1 and 2. Transferrin sialo-isoforms are indicated by their charge (2–6). B. Normal sialylation of Apo C-III in all four patients before IVIG (Pre), after IVIG loading (Mid), and after the treatment period (Post). Normal control sera (NC1 and NC2) exhibit three bands; treatment with sialidase (S) reduces this to one main band and a minor band. Samples of patients 3 and 4 were electrophoresed on a gel different from the gel for samples 1 and 2. Apo C-III0 = asialo-; Apo C-III1 = monosialo-; Apo C-III2 = disialo-Apo C-III isoforms.
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