David O Hutchinson
Country: New Zealand
- Autosomal dominant nemaline myopathy with intranuclear rods due to mutation of the skeletal muscle ACTA1 gene: clinical and pathological variability within a kindredDavid O Hutchinson
Department of Neurology, Auckland City Hospital, Private Bag, Auckland 92024, New Zealand
Neuromuscul Disord 16:113-21. 2006..Actin is normally present within the nucleus in only trace amounts. Mutation at postion 163 may result in intranuclear rods by virtue of its close proximity to a nuclear export signal within the actin molecule...
- Utilisation of intravenous immunoglobulin in New Zealand: a clinical auditDavid Hutchinson
Department of Neurology, Auckland City Hospital, Auckland
N Z Med J 119:U2340. 2006..To identify what diagnoses account for the utilisation of intravenous immunoglobulin (IVIG) in New Zealand (NZ), to establish regional differences in prescribing patterns, and to audit the appropriateness of its use in a subset of patients...
- Two-dimensional gel electrophoresis in inclusion body myositisD O Hutchinson
Department of Neurology, Auckland Hospital, Auckland, New Zealand
J Clin Neurosci 15:440-4. 2008..No unique spots were identified in the IBM gels. When viewed with other work, the results of this study suggest that widespread, uncontrolled activation of genes is unlikely to be a component of the pathogenesis in IBM...
- Neuromuscular disease and respiratory failureDavid Hutchinson
Department of Neurology, Auckland City Hospital, Auckland, New Zealand
Pract Neurol 8:229-37. 2008..New-onset weakness of limb and respiratory muscles in the intensive care unit is usually due to critical illness myopathy or critical illness polyneuropathy, and treatment is supportive...
- Intranuclear rod myopathy: molecular pathogenesis and mechanisms of weaknessAna Domazetovska
Institute for Neuromuscular Research, Children s Hospital at Westmead, New South Wales, Australia
Ann Neurol 62:597-608. 2007..Mutations at Val163 in ACTA1 result in pure intranuclear rod myopathy; however, the molecular mechanisms by which mutations at Val163 lead to intranuclear rod formation and muscle weakness are unknown...