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S H APPEL

Publications and source records attributed to S H APPEL.

8 recordsLinked to original sources
PubMed1964

MUTANT MICE (QUAKING AND JIMPY) WITH DEFICIENT MYELINATION IN THE CENTRAL NERVOUS SYSTEM.

Two mutant mice with deficient myelination are described. Quaking is a new autosomal recessive mutant mouse with marked tremor of the hindquarters. The mice eat, swim, breed, and nurse well even though the entire central nervous system is very deficient in myelin by histological and chemical criteria. Myelin formation is impaired; no destruction is seen. Peripheral nerves are myelinated. Jimpy, a known sex-linked mutation, has similar but more severe symptoms and similar pathology, with the additional feature of sudanophilic (nonpolar) lipid distributed in some white-matter tracts. Both mutants offer new opportunities for study of the formation and functions of myelin.

Animals↗
PubMed1964

THE APPLICATION OF TISSUE CULTURE TO THE STUDY OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS. II. SERUM FACTORS RESPONSIBLE FOR DEMYELINATION.

1. In the presence of a source of complement, the gamma 2 globulin fraction of rabbit EAE serum results in complete demyelination of myelinated cultures of rat cerebellum. Exposure of the serum to homologous or heterologous brain specifically removes the myelinotoxic activity whereas exposure to non-nervous tissue does not. Polylysine has no effect upon the cultures or upon the demyelinative potency of EAE, whereas heparin inhibits activity presumably through an effect on complement. 2. With the fluorescent antibody technique, the EAE globulins are specifically localized to the myelin sheaths and glial cell membranes during the process of demyelination. As demyelination proceeds, the globulins become localized within the neuroglia in a homogeneous manner which contrasts sharply with the punctate pattern observed in control experiments. 3. The "delayed sensitivity" and classical antibody interpretations of experimental allergic encephalomyelitis are discussed. It is suggested that several factors may be responsible for the pathogenesis of EAE, one of which may well be a myelinotoxic antibody.

Animals↗