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Biomedical subjects

H Mitsumoto

Publications and source records attributed to H Mitsumoto.

111 records · Page 7Linked to original sources

Myasthenia gravis therapy: immunoadsorbent may eliminate need for plasma products.

This in vitro study assessed the effectiveness of a new immunoadsorbent (Asahi IM-TR 350) in removing anti-acetylcholine receptor antibody from plasma with minimal loss of albumin. Plasma procured from a myasthenia gravis patient undergoing routine plasma exchange was perfused through the immunoadsorbent and recirculated in vitro to simulate a clinical treatment. To assess the temperature dependency of sorption, perfusion was performed at various temperatures. Plasma solute concentrations were taken before and after perfusion to calculate solute rejection coefficients. The immunoadsorbent has a high sorption capacity for anti-acetylcholine receptor antibody, while allowing a minimum loss of albumin. For patients with myasthenia gravis, this immunoadsorbent can provide an alternative to plasma exchange that does not require the use of plasma products.

Antibodies↗

Animal models of ALS.

Animal models of amyotrophic lateral sclerosis (ALS) provide a unique opportunity to study this incurable and fatal human disease both clinically and pathologically. This is particularly true for certain pathological and therapeutic studies that are impractical or impossible to perform in human patients. Nonetheless, postmortem ALS tissue remains the "gold standard" against which pathologic findings in animal models must be compared. Four natural disease models have been most extensively studied, including three mouse models: motor neuron degeneration (Mnd), progressive motor neuronopathy (pmn), wobbler, and one canine model: hereditary canine spinal muscular atrophy (HCSMA). The wobbler mouse has been the most extensively studied of these models with analyses of clinical, pathological (perikaryon, axon, muscle), and biochemical features. Experimentally induced ALS animal models have allowed controlled testing of various neurotoxic, viral and immune-mediated mechanisms. Molecular techniques have recently generated mouse models in which genes relevant to the human disease or motor neuron biology have been manipulated. The most clinically relevant of these is a transgenic mouse overexpressing the mutated SOD1 gene of FALS patients, which has already provided significant insights into mechanisms of motor neuron degeneration in this disease. Because no single animal model perfectly reflects all the clinical and pathological characteristics of ALS, study of selected features from the most relevant models will contribute to a better understanding of the pathogenesis and/or etiology of this disease.

Amyotrophic Lateral Sclerosis↗